1
|
YALÇIN KS, KASAPOĞLU B, ALANLI R, KÜÇÜKAY MB, YOZGAT A, KEKİLLİ M, KOŞAR A. The effect of lactose intolerance on plasma glucose levels and related biochemical parameters. JOURNAL OF HEALTH SCIENCES AND MEDICINE 2022. [DOI: 10.32322/jhsm.1094124] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/05/2022] Open
Abstract
Aim: To determine the effect of lactose intolerance on serum glucose levels and related biochemical parameters in the adult population who refrain from consuming milk and milk products.
Material and Method: This retrospective, observational study was conducted in a tertiary care hospital between January 2016 and December 2019 with 296 participants. Plasma glucose, calcium, 25-hydroxyvitamin D3, folate, vitamin B12, thyroid-stimulating hormone (TSH), and ferritin levels were controlled. Patients with positive lactose intolerance test results were accepted as the study group and negative results were accepted as the control group, and data of two groups were compared.
Results: Of the total 296 participants 212 (71.7%) were found to have lactose intolerance and 84 (28.3%) were found to be normal. In the lactose intolerant group, blood glucose levels were significantly lower than the control group (5.14±0.53 mmol/L versus 5.47±0.54 mmol/L, p
Collapse
|
2
|
Yan LH, Mu B, Pan D, Shi YN, Yuan JH, Guan Y, Li W, Zhu XY, Guo L. Association between small intestinal bacterial overgrowth and beta-cell function of type 2 diabetes. J Int Med Res 2020; 48:300060520937866. [PMID: 32691685 PMCID: PMC7375730 DOI: 10.1177/0300060520937866] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/30/2022] Open
Abstract
Aims Previous studies suggest that small intestinal bacterial overgrowth (SIBO) is associated with type 2 diabetes. However, few studies have evaluated the association between SIBO and beta-cell function in type 2 diabetes. The aim of this study was to evaluate whether beta-cell function was associated with SIBO. Materials and methods One hundred four patients with type 2 diabetes were included in this study. Based on the presence of SIBO, the patients were divided into SIBO-positive and SIBO-negative groups. Oral glucose tolerance tests were performed. Insulin sensitivity was measured using 1/homeostasis model assessment of insulin resistance (1/HOMA-IR) and the insulin sensitivity index (ISIM). Insulin release was calculated by HOMA-β, early-phase insulin secretion index InsAUC30/GluAUC30, and total-phase insulin secretion index InsAUC120/GluAUC120. Results Compared with the SIBO-negative group, patients in the SIBO-positive group showed a higher glucose level at 120 minutes, HbA1c, 1/HOMA-IR, and ISIM and a lower HOMA-β level, early-phase InsAUC30/GluAUC30, and total-phase InsAUC120/GluAUC120. Multiple linear regression analysis showed that body mass index, glucose at 0 minutes, and SIBO were independently associated with the early-phase and total-phase insulin secretion. Conclusion SIBO may be involved in lower levels of insulin release and worse glycemic control.
Collapse
Affiliation(s)
- Li-Hui Yan
- NHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin, China
| | - Biao Mu
- NHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin, China.,Tianjin University of Traditional Chinese Medicine, Tianjin, China
| | - Da Pan
- NHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin, China.,Tianjin University of Traditional Chinese Medicine, Tianjin, China
| | - Ya-Nan Shi
- NHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin, China
| | - Ji-Hong Yuan
- NHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin, China
| | - Yue Guan
- NHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin, China
| | - Wang Li
- NHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin, China
| | - Xiao-Yi Zhu
- NHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin, China
| | - Lei Guo
- NHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin, China
| |
Collapse
|
3
|
Imamura T, Sato M, Go H, Ogasawara K, Kanai Y, Chishiki M, Maeda H, Haneda K, Kashiwabara N, Goto A, Momoi N, Hosoya M. Volumetric Analysis of Gallbladder in Extremely Premature Infants. J Med Ultrasound 2017; 25:138-144. [PMID: 30065478 PMCID: PMC6029299 DOI: 10.1016/j.jmu.2017.03.004] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/30/2016] [Accepted: 01/25/2017] [Indexed: 11/26/2022] Open
Abstract
Background: We hypothesized that gallbladder (GB) volume is affected by serial changes during the early infancy period in extremely premature infants. Methods: We conducted a prospective study of extremely premature infants admitted to the neonatal intensive care unit of Fukushima Medical University Hospital, Fukushima City, Japan between January 2014 and December 2015. GB volume was measured by an abdominal ultrasound ellipsoid method between Day 0 and Day 56 after birth within 60 minutes before enteral feeding. We calculated GB volume (mL)/weight (kg), which was evaluated as GV/W. Results: Intotal, 30 infants were included. Themediangestationalageoftheinfantswas 26 weeks 5 days (range, 23 weeks 1 day–28 weeks 6 days), and the median birth weight was 731 g (range, 398–1220 g). The detection rate of GB decreased in the infants over time; the rates were > 93% between Day 0 and Day 7 and < 77% between Day 10 and Day 56 after birth. GV/W decreased in the infants over time. The median GV/W values were 0.18 (range, 0.05 –0.59) in infants on admission and constantly < 0.05 in those between Day 10 and Day 56 after birth. There was no correlation of GV/W with clinical variables after birth. Conclusion: It is considered that GB volume is not affected by serial changes without nonfavor-able course of enteral nutrition.
Collapse
|
4
|
Zhao M, Liao D, Zhao J. Diabetes-induced mechanophysiological changes in the small intestine and colon. World J Diabetes 2017; 8:249-269. [PMID: 28694926 PMCID: PMC5483424 DOI: 10.4239/wjd.v8.i6.249] [Citation(s) in RCA: 48] [Impact Index Per Article: 6.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/06/2017] [Revised: 04/05/2017] [Accepted: 05/05/2017] [Indexed: 02/05/2023] Open
Abstract
The disorders of gastrointestinal (GI) tract including intestine and colon are common in the patients with diabetes mellitus (DM). DM induced intestinal and colonic structural and biomechanical remodeling in animals and humans. The remodeling is closely related to motor-sensory abnormalities of the intestine and colon which are associated with the symptoms frequently encountered in patients with DM such as diarrhea and constipation. In this review, firstly we review DM-induced histomorphological and biomechanical remodeling of intestine and colon. Secondly we review motor-sensory dysfunction and how they relate to intestinal and colonic abnormalities. Finally the clinical consequences of DM-induced changes in the intestine and colon including diarrhea, constipation, gut microbiota change and colon cancer are discussed. The final goal is to increase the understanding of DM-induced changes in the gut and the subsequent clinical consequences in order to provide the clinicians with a better understanding of the GI disorders in diabetic patients and facilitates treatments tailored to these patients.
Collapse
|
5
|
Rana SV, Malik A, Bhadada SK, Sachdeva N, Morya RK, Sharma G. Malabsorption, Orocecal Transit Time and Small Intestinal Bacterial Overgrowth in Type 2 Diabetic Patients: A Connection. Indian J Clin Biochem 2016; 32:84-89. [PMID: 28149017 DOI: 10.1007/s12291-016-0569-6] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/03/2016] [Accepted: 04/22/2016] [Indexed: 01/19/2023]
Abstract
Type 2 diabetes mellitus consists of dysfunctions characterized by hyperglycemia and resulting from combination of resistance to insulin action and inadequate insulin secretion. Most of diabetic patients report significant gastrointestinal symptoms. Entire GI tract can be affected by diabetes from oral cavity to large bowel and anorectal region. Proteins, carbohydrates, fats, and most fluids are absorbed in small intestine. Malabsorption may occurs when proper absorption of nutrients does not take place due to bacterial overgrowth or altered gut motility. The present study was planned to measure various malabsorption parameters in type 2 diabetic patients. 175 patients and 175 age and sex matched healthy controls attending Endocrinology Clinic in PGI, Chandigarh were enrolled. Lactose intolerance was measured by using non-invasive lactose hydrogen breath test. Urinary d-xylose and fecal fat were estimated using standard methods. Orocecal transit time and small intestinal bacterial overgrowth were measured using non-invasive lactulose and glucose breath test respectively. Out of 175 diabetic patients enrolled, 87 were males while among 175 healthy subjects 88 were males. SIBO was observed in 14.8 % type 2 diabetic patients and in 2.8 % of controls. There was statistically significant increase (p < 0.002) in OCTT in type 2 diabetic patients compared with controls. OCTT was observed to be more delayed (p < 0.003) in patients who were found to have SIBO than in patients without SIBO. Lactose intolerance was observed in 60 % diabetic patients and 39.4 % in controls. Urinary d-xylose levels were also lower in case of diabetic patients but no significant difference was found in 72 h fecal fat excretion among diabetic patients and controls. Urinary d-xylose and lactose intolerance in SIBO positive type 2 diabetic patients was more severe as compared to SIBO negative diabetic patients. From this study we can conclude that delayed OCTT may have led to SIBO which may have instigated the process of malabsorption among type 2 diabetic patients.
Collapse
Affiliation(s)
- S V Rana
- Department of Gastroenterology, Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh, 160012 India
| | - Aastha Malik
- Department of Gastroenterology, Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh, 160012 India
| | - Sanjay K Bhadada
- Department of Endocrinology, Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh, 160012 India
| | - Naresh Sachdeva
- Department of Endocrinology, Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh, 160012 India
| | - Rajesh Kumar Morya
- Department of Gastroenterology, Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh, 160012 India
| | - Gaurav Sharma
- Department of Gastroenterology, Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh, 160012 India
| |
Collapse
|
6
|
Ouyang X, Li S, Foreman R, Farber J, Lin L, Yin J, Chen JDZ. Hyperglycemia-induced small intestinal dysrhythmias attributed to sympathovagal imbalance in normal and diabetic rats. Neurogastroenterol Motil 2015; 27:406-15. [PMID: 25630445 DOI: 10.1111/nmo.12506] [Citation(s) in RCA: 18] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/31/2014] [Accepted: 12/07/2014] [Indexed: 01/16/2023]
Abstract
BACKGROUND Hyperglycemia is known to induce dysrhythmias in the stomach; however, it is unknown whether they are also induced in the small intestine. Autonomic dysfunction is commonly noted in diabetes but the role it plays in hyperglycemia-induced dysrhythmias remains unknown. This study aimed to explore the effects of hyperglycemia on intestinal myoelectrical activity and the role of autonomic functions in hyperglycemia. METHODS Small intestinal myoelectrical activity (slow wave and spike activity) and autonomic functions (assessed by the spectral analysis of heart rate variability) were measured in Goto-Kakizaki diabetic rats and control rats treated with acute glucagon. Blood glucose was measured and its correlation with intestinal slow waves was determined. KEY RESULTS (1) The diabetic rats showed reduced regularity in intestinal slow waves in fasting and fed states (p < 0.001 for both), and increased sympathovagal balance (p < 0.05) in comparison with the control rats. The regularity in intestinal slow waves was negatively correlated with the HbA1c level in all rats (r = -0.663, p = 0.000). (2) Glucagon injection in the control rats induced transient hyperglycemia, intestinal slow wave dysrhythmias and impaired autonomic functions, similar to those observed in the diabetic rats. The increase in blood glucose was correlated with the decrease in the regularity of intestinal slow waves (r = -0.739, p = 0.015). CONCLUSIONS & INFERENCES Both spontaneous and glucagon-induced hyperglycemia results in slow wave dysrhythmias in the small intestine. Impairment in autonomic functions (increased sympathovagal balance) may play a role in hyperglycemia-induced dysrhythmias.
Collapse
Affiliation(s)
- X Ouyang
- Nanjing Medical University, Nanjing, Jiangsu, China; Veterans Research and Education Foundation, VA Medical Center, Oklahoma City, OK, USA; Diabetes Care & Research Center, Jiangsu Province Institute of Geriatrics, Nanjing, Jiangsu, China; Department of Physiology, University of Oklahoma, Oklahoma City, OK, USA
| | | | | | | | | | | | | |
Collapse
|
7
|
Zhao J, Chen P, Gregersen H. Stress-strain analysis of jejunal contractility in response to flow and ramp distension in type 2 diabetic GK rats: effect of carbachol stimulation. J Biomech 2013; 46:2469-76. [PMID: 23932327 DOI: 10.1016/j.jbiomech.2013.07.019] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/01/2013] [Revised: 07/09/2013] [Accepted: 07/09/2013] [Indexed: 12/16/2022]
Abstract
Investigation of intestinal motility in a genetic model of GK rats abandons the possible neurotoxic effect of streptozotocin in streptozotocin-induced diabetic model. Seven GK male rats (GK group) and nine normal Wistar rats (Normal group) were used in the study. The motility experiments were carried out in an organ bath containing physiological Krebs solution. Before and after 10(-5)M carbachol application, the pressure and diameter changes of jejunum were obtained in relation to (1) basic contraction, (2) flow-induced contraction with different outlet resistance pressures and (3) contractions induced by ramp distension. The frequency and amplitude of contractions were analyzed from pressure-diameter curves. Distension-induced contraction thresholds and maximum contraction amplitude of basic and flow-induced contractions were calculated in terms of stress and strain. (1) The contraction amplitude increased to the peak value in less than 10s after adding carbachol. More than two peaks were observed in the GK group. (2) Carbachol decreased the pressure and stress threshold and Young's modulus in the GK group (P<0.01). (3) Carbachol increased the maximum pressure and stress of flow-induced contractions at most outlet pressure levels in both two groups (P<0.001). Furthermore, the flow-induced contractions were significantly bigger at low outlet pressure levels in GK group (P<0.05 and P<0.01). (4) The contraction frequency, the strain threshold and the maximum contraction strain did not differ between the two groups (P>0.05) and between before and after carbachol application (P>0.05). In GK diabetic rats, the jejunal contractility was hypersensitive to flow and distension stimulation after carbachol application.
Collapse
Affiliation(s)
- Jingbo Zhao
- Mech-Sense, Department of Gastroenterology, Aalborg University Hospital, DK 9000 Aalborg, Denmark; Clinical Institute, Aarhus University, 8200 Aarhus N, Denmark; The College of Bioengineering, Chongqing University, Chongqing, China.
| | | | | |
Collapse
|
8
|
Faria M, Pavin EJ, Parisi MCR, Lorena SLS, Brunetto SQ, Ramos CD, Pavan CR, Mesquita MA. Delayed small intestinal transit in patients with long-standing type 1 diabetes mellitus: investigation of the relationships with clinical features, gastric emptying, psychological distress, and nutritional parameters. Diabetes Technol Ther 2013; 15:32-8. [PMID: 23126582 DOI: 10.1089/dia.2012.0158] [Citation(s) in RCA: 21] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/19/2022]
Abstract
BACKGROUND Studies on small intestinal transit in type 1 diabetes mellitus have reported contradictory results. This study assessed the orocecal transit time (OCTT) in a group of patients with type 1 diabetes mellitus and its relationships with gastrointestinal symptoms, glycemic control, chronic complications of diabetes, anthropometric indices, gastric emptying, small intestinal bacterial overgrowth (SIBO), and psychological distress. SUBJECTS AND METHODS Twenty-eight patients with long-standing (>10 years) type 1 diabetes mellitus (22 women, six men; mean age, 39 ± 9 years) participated in the study. The lactulose hydrogen breath test was used to determine OCTT and the occurrence of SIBO. The presence of anxiety and depression was assessed by the Hospital Anxiety and Depression scale. Gastric emptying was measured by scintigraphy. Anthropometric indices included body mass index, percentage body fat, midarm circumference, and arm muscle area. RESULTS There was a statistically significant increase in OCTT values in diabetes patients (79 ± 41 min) in comparison with controls (54 ± 17 min) (P=0.01). Individual analysis showed that OCTT was above the upper limit (mean+2 SD) in 30.8% of patients. All anthropometric parameters were significantly decreased (P<0.05) in patients with prolonged OCTT in comparison with those with normal OCTT. In contrast, there was no statistically significant association between prolonged OCTT and gastrointestinal symptoms, peripheral neuropathy, diabetic retinopathy, glycated hemoglobin, delayed gastric emptying, SIBO, anxiety, or depression. CONCLUSIONS Small bowel transit may be delayed in about one-third of patients with long-standing type 1 diabetes mellitus. This abnormality seems to have a negative effect on nutritional status in these patients.
Collapse
Affiliation(s)
- Mariza Faria
- Division of Gastroenterology, Department of Clinical Medicine, Faculty of Medical Sciences, State University of Campinas, Campinas, São Paulo, Brazil
| | | | | | | | | | | | | | | |
Collapse
|
9
|
Comparison of complications attributable to enteral and parenteral nutrition in predicted severe acute pancreatitis: a systematic review and meta-analysis. Br J Nutr 2010; 103:1287-95. [PMID: 20370944 DOI: 10.1017/s0007114510000887] [Citation(s) in RCA: 47] [Impact Index Per Article: 3.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/15/2022]
Abstract
Enteral nutrition (EN) reduces infectious complications and mortality compared with parenteral nutrition (PN) in patients with predicted severe acute pancreatitis. However, to date the complications attributable to the administration of EN and PN in this patient group have not been comprehensively studied. The aim of the study was to systematically review the complications related to the use of nutrition in patients with predicted severe acute pancreatitis receiving EN v. PN. The Cochrane Library, MEDLINE and Scopus were searched. Randomised controlled trials (RCT) of EN v. PN in predicted severe acute pancreatitis were selected. Pooled estimates of complications were expressed as OR with corresponding 95 % CI. Data from five RCT were meta-analysed. Diarrhoea occurred in six of ninety-two (7 %) patients receiving PN and twenty-four of eighty-two (29 %) patients receiving EN (OR 0.20; 95 % CI 0.09, 0.43; P < 0.001). Hyperglycaemia developed in twenty-one of ninety-two (23 %) patients receiving PN and nine of eighty-two (11 %) receiving EN (OR 2.59; 95 % CI 1.13, 5.94; P = 0.03). Given a significant reduction in infectious complications and mortality associated with the use of EN over PN that has been consistently demonstrated in previous studies, the former should be the treatment of choice in acute pancreatitis. Further clinical studies should investigate the strategies to mitigate the complications of enteral tube feeding in patients with acute pancreatitis.
Collapse
|
10
|
Effect of duodenal glucose and acute hyperglycemia on rectal perception and compliance in response to tension-controlled rectal distension in healthy humans. Dig Dis Sci 2008; 53:1624-31. [PMID: 17932756 DOI: 10.1007/s10620-007-0032-x] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/26/2007] [Accepted: 09/19/2007] [Indexed: 01/01/2023]
Abstract
BACKGROUND Acute changes in blood glucose concentration affect gastrointestinal motor and sensory function. Tone and distensibility contribute to intact rectal function. AIMS To test the effects of duodenal glucose (euglycemic hyperinsulinemia), intravenous glucose (hyperglycemic hyperinsulinemia), and saline (euglycemic normoinsulinemia as control) on rectal perception and compliance in response to tension-controlled rectal distension. METHODS During duodenal glucose at 2 kcal min(-1), marked hyperglycemic clamp (approximately 13 mmol L(-1)), or saline as control, responses to fixed-tension rectal distension, applied by means of a computerized tensostat, were compared randomized on three separate days in eight healthy subjects. RESULTS At discomfort level (score 3 on the 0-4 rectal score scale), perception of rectal distension was significantly higher during euglycemic hyperinsulinemia (45 +/- 3 g cm(-2) tolerance) and significantly lower during hyperglycemia (83 +/- 4 g cm(-2) tolerance), both reaching significance versus control (64 +/- 6 g cm(-2) tolerance; P < 0.05). At this level, no relevant variations of rectal compliance were seen, which were 10.3 +/- 1 mL mmHg(-1) during duodenal glucose, 9.5 +/- 1 mL mmHg(-1) for the group with hyperglycemia, and 9.7 +/- 2 mL mmHg(-1) for the control. CONCLUSION Duodenal glucose provokes rectal hypersensitivity whereas acute hyperglycemia contributes to rectal hyposensitivity. Despite different rectal tenso-sensitivity, rectal compliance remains virtually unchanged. Any dysfunction may cause rectal complaints.
Collapse
|
11
|
Tily FE, Thomas S. Glycemic effect of administration of epinephrine-containing local anaesthesia in patients undergoing dental extraction, a comparison between healthy and diabetic patients. Int Dent J 2007; 57:77-83. [PMID: 17506466 DOI: 10.1111/j.1875-595x.2007.tb00442.x] [Citation(s) in RCA: 15] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/15/2023] Open
Abstract
OBJECTIVES To compare the effect of administration of epinephrine (in the dental local anesthetic solution) on blood glucose concentration in healthy and diabetic dental patients after extraction. To determine if there is any correlation between blood glucose level changes and the number of carpules injected, number of teeth extracted and the gender of the patient. MATERIALS AND METHOD An open study of 60 patients (30 healthy and 30 diabetics) visiting the Oral Surgery clinic of Ajman University of Science and Technology. A drop of blood was taken from the tip of the patient's finger and placed on a glucometer strip to determine the pre-operative blood glucose level. Dental local anaesthesia (1.8 ml carpule each) containing 1:80,000 epinephrine was injected either through infiltration or block. Extraction was carried out atraumatically and 10 minutes post-extraction the glucose measurement was taken. RESULTS The difference in the blood glucose levels pre- and post operatively were not significantly different (p > 0.05) when a comparison was made between the healthy and diabetic groups. Comparison of glucose changes in diabetics who had taken their hypoglycaemic medication and those who had not, showed a significant difference (p < 0.05). Statistical analysis showed no correlation between the blood glucose level changes and the number of carpules used, number of teeth extracted and gender. CONCLUSION Dental local anaesthetic solution containing epinephrine is safe to use in all healthy and diabetic patients (irrespective of their gender), excepting those diabetics who have not taken their pre-operative hypoglycaemic medication. There is no relation between the post-extraction glucose changes and the number of carpules used, number of teeth extracted or gender.
Collapse
Affiliation(s)
- Fatima Ebrahim Tily
- Department of Surgical Science, Faculty of Dentistry, Ajman University of Science & Technology, Dubai, UAE
| | | |
Collapse
|
12
|
Abstract
Gastrointestinal (GI) sensory-motor abnormalities are common in patients with diabetes mellitus and may involve any part of the GI tract. Abnormalities are frequently sub-clinical, and fortunately only rarely do severe and life-threatening problems occur. The pathogenesis of abnormal upper GI sensory-motor function in diabetes is incompletely understood and is most likely multi-factorial of origin. Diabetic autonomic neuropathy as well as acute suboptimal control of diabetes has been shown to impair GI motor and sensory function. Morphological and biomechanical remodeling of the GI wall develops during the duration of diabetes, and may contribute to motor and sensory dysfunction. In this review sensory and motility disorders of the upper GI tract in diabetes is discussed; and the morphological changes and biomechanical remodeling related to the sensory-motor dysfunction is also addressed.
Collapse
Affiliation(s)
- Jingbo Zhao
- Center of Excellence in Visceral Biomechanics and Pain, the Research Building room 404, Aalborg Hospital, Sdr. Skovvej 15, DK-9000 Aalborg, Denmark.
| | | | | | | |
Collapse
|
13
|
Young A. Effects on digestive secretions. ADVANCES IN PHARMACOLOGY (SAN DIEGO, CALIF.) 2005; 52:123-50. [PMID: 16492544 DOI: 10.1016/s1054-3589(05)52007-6] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 05/06/2023]
Abstract
Rat amylin subcutaneously injected into rats dose-dependently inhibits pentagastrin-stimulated gastric acid secretion and protects the stomach from ethanol-induced gastritis. The ED50s for these actions (0.050 and 0.036 microg, respectively) are the lowest for any dose-dependent effect of amylin thus far described, and their similar potencies are consistent with a mechanistic (causal) association. At higher amylin doses, inhibition of gastric acid secretion was almost complete (93.4%). Gastric injury (measured by a subjective analog scale) was inhibited by up to 67%. The observation that effective doses of amylin result in plasma concentrations of 7-10 pM (i.e., within the reported range; Pieber et al., 1994) supports the interpretation that inhibition of gastric acid secretion and maintenance of gastric mucosal integrity are physiological actions of endogenous amylin. The pharmacology of these responses fits with one mediated via amylin-like receptors. Rat amylin inhibited CCK-stimulated secretion of pancreatic enzymes,amylase, and lipase by up to approximately 60% without having significant effect in the absence of CCK. ED50s for the effect were in the 0.1-0.2 microg range, calculated to produce plasma amylin excursions within the physiological range. Effects of informative ligands are consistent with the concept of amylin receptor mediation. Amylin was effective in ameliorating the severity of pancreatitis in a rodent model. The amylin analog pramlintide inhibited gallbladder emptying in mice as measured by total weight of acutely excised gallbladders. Amylin inhibition of gastric acid secretion, pancreatic enzyme secretion, and bile secretion likely represents part of an orchestrated control of nutrient appearance. Modulation of digestive function fits with a general role of amylin in regulating nutrient uptake. Rate of ingestion, rate of release from the stomach, and rate of digestion of various food groups appear to be under coordinate control.
Collapse
Affiliation(s)
- Andrew Young
- Amylin Pharmaceuticals, Inc., San Diego, California, USA
| |
Collapse
|
14
|
Zhang Q, Horowitz M, Rigda R, Rayner C, Worynski A, Holloway RH. Effect of hyperglycemia on triggering of transient lower esophageal sphincter relaxations. Am J Physiol Gastrointest Liver Physiol 2004; 286:G797-G803. [PMID: 15068963 DOI: 10.1152/ajpgi.00383.2003] [Citation(s) in RCA: 21] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
Acute changes in blood glucose concentration have major effects on gastrointestinal motor function. Patients with diabetes mellitus have an increased prevalence of gastroesophageal reflux. Transient lower esophageal sphincter (LES) relaxation (TLESR) is the most common sphincter mechanism underlying reflux. The aim of this study was to investigate the effect of acute hyperglycemia on triggering TLESRs evoked by gastric distension in healthy volunteers. TLESRs were stimulated by pressure-controlled and volume-controlled (500 ml) gastric distension using an electronic barostat and performed on separate days. On each day, esophageal manometry was performed in the sitting position during gastric distension for 1 h under euglycemia (5 mM), and either marked hyperglycemia (15 mM) or physiological hyperglycemia (8 mM) in randomized order was maintained by a glucose clamp. Marked hyperglycemia doubled the rate of TLESRs in response to both pressure-controlled [5 (3-10.5, median or interquartile range) to 10 (9.5-14.5) per hour, P < 0.02] and volume-controlled [4 (2.5-7.5) to 10.5 (7-12.5) per hour, P < 0.02] gastric distension but had no effect on basal LES pressure. Physiological hyperglycemia had no effect on the triggering of TLESRs or basal LES pressure. In healthy human subjects, marked hyperglycemia increases the rate of TLESRs. Increase in the rate of TLESRs is independent of proximal gastric wall tension. Mechanisms underlying the effect remain to be determined. Hyperglycemia may be an important factor contributing to the increased esophageal acid exposure in patients with diabetes mellitus.
Collapse
Affiliation(s)
- Qing Zhang
- Dept. Gastroenterology, Hepatology and General Medicine, Royal Adelaide Hospital, North Terrace, Adelaide, SA 5000, Australia
| | | | | | | | | | | |
Collapse
|
15
|
Damci T, Nuhoglu I, Devranoglu G, Osar Z, Demir M, Ilkova H. Increased intestinal permeability as a cause of fluctuating postprandial blood glucose levels in Type 1 diabetic patients. Eur J Clin Invest 2003; 33:397-401. [PMID: 12713453 DOI: 10.1046/j.1365-2362.2003.01161.x] [Citation(s) in RCA: 33] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/20/2022]
Abstract
BACKGROUND In diabetic patients, postprandial glucose levels, which have a major impact on metabolic control, are determined by the rate of nutrient delivery into the intestine, absorption of nutrients from the small intestine, and the metabolism of the absorbed nutrients by the liver. The present study addresses whether Type 1 diabetic patients have increased intestinal permeability and intestinal permeability predicts postprandial glucose variability. MATERIAL AND METHODS Thirty Type 1 diabetic patients together with 15 sex- and age-matched healthy controls were enrolled in the study. After an overnight fasting all patients and controls received 100 micro Ci 51Cr of EDTA as a radioactive tracer and the percentage of the isotope excreted in a 24-h urinary specimen was the permeability measure. Instant blood glucose was measured just before the test, and the patients performed and recorded self-monitoring of fasting and 2nd-hour postprandial blood glucose levels during the following week. RESULTS We found that intestinal permeability is increased in Type 1 diabetic patients compared with age- and sex-matched healthy controls. Increased intestinal permeability is related at least in part to the instant blood glucose level and the presence of diabetic autonomic neuropathy. CONCLUSION Increased intestinal permeability leads to higher variation in postprandial blood glucose levels, thereby worsening metabolic control.
Collapse
Affiliation(s)
- T Damci
- Istanbul University, Istanbul, Turkey.
| | | | | | | | | | | |
Collapse
|
16
|
Bytzer P, Talley NJ, Hammer J, Young LJ, Jones MP, Horowitz M. GI symptoms in diabetes mellitus are associated with both poor glycemic control and diabetic complications. Am J Gastroenterol 2002; 97:604-11. [PMID: 11922554 DOI: 10.1111/j.1572-0241.2002.05537.x] [Citation(s) in RCA: 128] [Impact Index Per Article: 5.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
Abstract
OBJECTIVE Diabetes mellitus is associated with an increased prevalence of GI symptoms, but the mechanisms underlying symptoms are poorly defined and controversial. We aimed to determine whether there is a relationship between GI symptoms and both diabetic complications and glycemic control. METHODS We performed a cross-sectional questionnaire study of 1101 subjects with diabetes mellitus recruited from outpatient clinics (n = 209) and the community (n = 892). Data on eight GI symptom groups, complications of diabetes (retinopathy, neuropathy, nephropathy), and self-reported glycemic control were obtained from a validated questionnaire. Glycated hemoglobin was measured in 463 of the subjects, The association between diabetic complications, glycemic control, and GI symptoms was assessed using logistic regression analysis, adjusted for demographic and clinical factors. RESULTS Of the 1101 subjects, 57% reported at least one complication. Diabetic complications were independently associated with both symptom complexity (number of symptom groups reported) (adjusted odds ratio = 1.92 per symptom group [95% CI = 1.51-2.45]) and seven of the eight GI symptom groups. For all symptom groups, the association was explained by self-reported symptoms of peripheral neuropathy. Poor glycemic control measured by both self-report and Hb A1c was an independent risk factor for upper GI symptoms, whereas other potential risk indicators, including duration and type of diabetes, were not significant. CONCLUSIONS GI symptoms in diabetes mellitus may be linked to diabetic complications, particularly peripheral neuropathy, and to poor glycemic control.
Collapse
Affiliation(s)
- Peter Bytzer
- Department of Medicine, University of Sydney, Nepean Hospital, NSW, Australia
| | | | | | | | | | | |
Collapse
|
17
|
Abstract
BACKGROUND The aim of the study was to evaluate the incidence and prognosis of abdominal pain in patients with diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar nonketotic state (HHS). Abdominal pain, sometimes mimicking an acute abdomen, is a frequent manifestation in patients with DKA. The prevalence and clinical significance of gastrointestinal symptoms including abdominal pain in HHS have not been prospectively evaluated. MATERIALS AND METHODS This is a prospectively collected evaluation of 200 consecutive patients with hyperglycemic crises admitted to a large inner-city teaching hospital in Atlanta, GA.We analyzed the admission clinical characteristics, laboratory studies, and hospital course of 189 consecutive episodes of DKA and 11 cases of HHS during a 13-month period starting in October 1995. RESULTS Abdominal pain occurred in 86 of 189 patients with DKA (46%). In 30 patients, the cause of abdominal pain was considered to be secondary to the precipitating cause of metabolic decompensation. Five of them required surgical intervention including 1 patient with Fournier's necrotizing fasciitis, 1 with cholecystitis, 1 with acute appendicitis, and 2 patients with perineal abscess. The presence of abdominal pain was not related to the severity of hyperglycemia or dehydration; however, a strong association was observed between abdominal pain and metabolic acidosis. In DKA patients with abdominal pain, the mean serum bicarbonate (9 +/- 1 mmol/L) and blood pH (7.12 +/- 0.02) were lower than in patients without pain (15 +/- 1 mmol/L and 7.24 +/- 0.09, respectively, both P <.001). Abdominal pain was present in 86% of patients with serum bicarbonate less than 5 mmol/L, in 66% of patients with levels of 5 to less than 10 mmol/L, in 36% of patients with levels 10 to less than 15 mmol/L, and in 13% of patients with bicarbonate levels 15 to 18 mmol/L. Patients with DKA and abdominal pain had a more frequent history of alcohol (51%) and cocaine abuse (13%) than those without abdominal pain (24% and 2%, respectively, both P <.001). One patient with HHS reported nausea and vomiting on admission, but abdominal pain was not reported in any patient with HHS. CONCLUSIONS Gastrointestinal manifestations including abdominal pain are common in patients with DKA and are associated with severe metabolic acidosis and with a history of alcohol or cocaine abuse, but not with the severity of hyperglycemia or dehydration. Our study indicates that investigation of the etiology of abdominal pain in DKA should be reserved for patients without severe metabolic acidosis or if the pain persists after the resolution of ketoacidosis.
Collapse
Affiliation(s)
- Guillermo Umpierrez
- Department of Medicine and Preventive Medicine, University of Tennessee Health Science Center, Memphis 38163, USA
| | | |
Collapse
|
18
|
Ishiguchi T, Tada H, Nakagawa K, Yamamura T, Takahashi T. Hyperglycemia impairs antro-pyloric coordination and delays gastric emptying in conscious rats. Auton Neurosci 2002; 95:112-20. [PMID: 11871775 DOI: 10.1016/s1566-0702(01)00383-6] [Citation(s) in RCA: 56] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/15/2023]
Abstract
Delayed gastric emptying has been shown in diabetes. Although it has been proposed that hyperglycemia, and not only autonomic neuropathy, contributes to the pathogenesis of delayed gastric emptying, the inhibitory mechanism of hyperglycemia on gastric emptying remains unclear. We studied the effects of hyperglycemia per se on gastric emptying and postprandial gastric motility in conscious rats. Liquid and solid gastric emptying were compared between saline-infused rats and D-glucose-infused rats. Two strain gauge transducers were implanted on the antrum and pylorus and the postprandial antro-pyloric coordination was compared between euglycemia and hyperglycemia. D-glucose infusion for 30 min increased blood glucose level from 5.4 +/- 0.5 to 13.0 +/- 1.3 mM and significantly delayed gastric emptying. Forty minutes after the feeding, contractions with low frequency (<3 cycles min(-1)) and high amplitude (>15 g) of the antrum were observed. This period reflects the emptying process of the gastric content and the coordination between the antrum and pylorus was frequently observed. D-glucose infusion significantly reduced feeding-induced antral contractions and abolished the number of episodes of antro-pyloric coordination. Sham feeding-induced gastric contractions were also significantly reduced by hyperglycemia. Postprandial antro-pyloric coordination was not observed in vagotomized rats, suggesting a mediation of vagus nerve. It is concluded that hyperglycemia impairs antral contractions and antro-pyloric coordination in rats. The inhibitory effect of hyperglycemia on gastric emptying is mediated, at least in part, via impaired vagal activity.
Collapse
|
19
|
Ishiguchi T, Nakajima M, Sone H, Tada H, Kumagai AK, Takahashi T. Gastric distension-induced pyloric relaxation: central nervous system regulation and effects of acute hyperglycaemia in the rat. J Physiol 2001; 533:801-13. [PMID: 11410636 PMCID: PMC2278658 DOI: 10.1111/j.1469-7793.2001.t01-1-00801.x] [Citation(s) in RCA: 34] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/15/2023] Open
Abstract
1. The pylorus plays an important role in the regulation of gastric emptying. In addition to the autonomic neuropathy associated with long-standing diabetes, acute hyperglycaemia per se has effects on gastric emptying. In this study, the role of the central nervous system in modulating the effects of hyperglycaemia on gastric distension-induced pyloric relaxation was investigated. 2. Gastric distension-induced pyloric relaxation was significantly reduced by subdiaphragmatic vagotomy, hexamethonium (20 mg kg(-1)) and N (G)-nitro-L-arginine methyl ester (L-NAME; 10 mg kg(-1)), a nitric oxide synthase (NOS) biosynthesis inhibitor, in anaesthetized rats. In contrast, neither splanchnectomy nor guanethidine (5 mg kg(-1)) had an effect. 3. An intravenous (I.V.) infusion of D-glucose (20 %) for 30 min, which increased blood glucose concentrations from 5.4 to 12.8 mM, significantly inhibited gastric distension-induced pyloric relaxation. 4. An intracerebroventricular (I.C.V.) injection of D-glucose (3 micromol) also significantly inhibited gastric distension-induced pyloric relaxation without affecting peripheral blood glucose concentrations. 5. I.V. infusion of D-glucose significantly elevated hypothalamic neuropeptide Y (NPY) concentrations. 6. Intracerebroventricular (I.C.V.) administration of NPY (0.03--3 nmol) and a Y1 receptor agonist, [leu(31), pro(34)] NPY (0.03--3 nmol), significantly inhibited gastric distension-induced pyloric relaxation in a dose-dependent manner. 7. I.C.V. administration of a Y1 receptor antagonist, BIBP 3226 (30 nmol), and of a NPY antibody (titre 1:24 000, 3 microl) abolished the inhibitory effects of hyperglycaemia on gastric distension-induced pyloric relaxation. 8. Taken together, these findings suggest that gastric distension-induced pyloric relaxation is mediated via a vago-vagal reflex and NO release. Acute hyperglycaemia stimulates hypothalamic NPY release, which, acting through the Y1 receptor, inhibits gastric distension-induced pyloric relaxation in rats exposed to acute elevations in blood glucose concentrations.
Collapse
Affiliation(s)
- T Ishiguchi
- Department of Internal Medicine, The University of Michigan Health System, Ann Arbor, MI, USA
| | | | | | | | | | | |
Collapse
|
20
|
Rayner CK, Samsom M, Jones KL, Horowitz M. Relationships of upper gastrointestinal motor and sensory function with glycemic control. Diabetes Care 2001; 24:371-381. [PMID: 11213895 DOI: 10.2337/diacare.24.2.371] [Citation(s) in RCA: 305] [Impact Index Per Article: 12.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
Acute changes in the blood glucose concentration have a major reversible effect on esophageal, gastric, intestinal, gallbladder, and anorectal motility in both healthy subjects and diabetic patients. For example, gastric emptying is slower during hyperglycemia than euglycemia and accelerated during hypoglycemia. Acute hyperglycemia also affects perceptions arising from the gastrointestinal tract and may accordingly, be important in the etiology of gastrointestinal symptoms in diabetes. Elevations in blood glucose that are within the normal postprandial range also affect gastrointestinal motor and sensory function. Upper gastrointestinal motor function is a critical determinant of postprandial blood glucose concentrations by influencing the absorption of ingested nutrients. Interventions that reduce postprandial hyperglycemia, by modulating the rate of gastric emptying, have the potential to become mainstream therapies in the treatment of diabetes.
Collapse
Affiliation(s)
- C K Rayner
- University of Adelaide Department of Medicine, Royal Adelaide Hospital, South Australia, Australia
| | | | | | | |
Collapse
|
21
|
Duggirala R, Mitchell BD, Blangero J, Stern MP. Genetic determinants of variation in gallbladder disease in the Mexican-American population. Genet Epidemiol 2000; 16:191-204. [PMID: 10030401 DOI: 10.1002/(sici)1098-2272(1999)16:2<191::aid-gepi6>3.0.co;2-6] [Citation(s) in RCA: 33] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]
Abstract
Since there have not been any studies that quantify the influence of genetic factors on gallbladder disease (GBD) in humans using information from families, we utilized pedigree data to explore the genetic control of variation in liability to GBD. Using an extension of a variance components approach, we performed genetic analyses of GBD using information from 32 low-income Mexican-American families with two slightly different general models incorporating several sex-specific GBD risk factors. After evaluating the relative magnitudes of the covariate effects from these two models, we identified a parsimonious model including only significant predictors of GBD. According to this model, heritability for GBD was high (h2 = 0.44+/-0.18), after accounting for the significant effects of age, leptin in both sexes, total cholesterol, and HDL cholesterol in males only. We have shown quantitatively that variation in GBD is under strong genetic control. However, there are two major limitations to our findings: (1) since GBD was defined by a self-reported clinical history rather than an ultrasound examination, the prevalence of GBD could have been underestimated; and (2) since our design did not allow for shared environmental effects, our estimate of heritability may have been inflated.
Collapse
Affiliation(s)
- R Duggirala
- Department of Medicine, University of Texas Health Science at San Antonio 78284-7873, USA
| | | | | | | |
Collapse
|
22
|
Abstract
The inhibitory activity of several crude drugs on alpha-glucosidases, which are the key enzymes for carbohydrate digestion and the prevention of diabetic complications, was investigated. Several crude drugs including Terminaliae Fructus, Mori Cortex Radicis, Caesalpiniae Lignum and Gyrophora esculenta potently inhibited maltase and sucrase isolated from rat intestine, while Arecae Semen and Corni Fructus remarkably inhibited alpha-amylase. Caesalpiniae Lignum and Gyrophora esculenta exhibited significant reductions of blood glucose elevation in mice loaded with maltose and sucrose.
Collapse
Affiliation(s)
- H J Choi
- East-West Medical Research Institute, Kyung-Hee University, Seoul, Korea
| | | | | |
Collapse
|
23
|
van Erpecum KJ, Venneman NG, Portincasa P, Vanberge-Henegouwen GP. Review article: agents affecting gall-bladder motility--role in treatment and prevention of gallstones. Aliment Pharmacol Ther 2000; 14 Suppl 2:66-70. [PMID: 10903008 DOI: 10.1046/j.1365-2036.2000.014s2066.x] [Citation(s) in RCA: 21] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/17/2023]
Abstract
Various agents may either enhance or impair post-prandial gall-bladder motility, and they are identified in this review. When studying the impact of medication on gall-bladder motility, the effects on interdigestive gall-bladder and intestinal motility should also be taken into account. Patients at high risk of gallstone disease, and patients who are treated chronically with gall-bladder motility inhibiting drugs, may benefit from improved gall-bladder motility using a prokinetic agent. However, there are no long-term studies to prove that such a strategy prevents gallstone formation.
Collapse
Affiliation(s)
- K J van Erpecum
- Gastrointestinal Research Unit, University Medical Center, Utrecht, The Netherlands.
| | | | | | | |
Collapse
|
24
|
Annese V, Bassotti G, Caruso N, De Cosmo S, Gabbrielli A, Modoni S, Frusciante V, Andriulli A. Gastrointestinal motor dysfunction, symptoms, and neuropathy in noninsulin-dependent (type 2) diabetes mellitus. J Clin Gastroenterol 1999; 29:171-177. [PMID: 10478880 DOI: 10.1097/00004836-199909000-00014] [Citation(s) in RCA: 65] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/27/2022]
Abstract
Although relatively frequent. diabetic involvement of digestive tract motility has not been investigated extensively in different organs. The authors studied esophageal, gastric, and gallbladder motor function in 35 type 2 (noninsulin-dependent) diabetic patients to determine the extent of gut involvement. Of these patients, 27 (77%) had peripheral neuropathy, 12 (34%) had both peripheral and autonomic neuropathy, and 22 (63%) had gastrointestinal symptoms. Esophageal manometric abnormalities were recorded in 18 patients, and delayed radionuclide emptying of the esophagus was documented in 16 patients, with a 83% concordance between the two tests. Scintigraphic gastric emptying of solids was delayed in 56% of patients, whereas gallbladder emptying after cholecystokinin stimulation was reduced in 69% of them. In 74% of patients at least one of the viscera under investigation showed abnormal motor function; however, only 36% of patients displayed involvement of the three organs. Gastrointestinal symptoms, duration and therapy of diabetes, previous poor glycemic control, and retinopathy did not correlate with the presence or the extent of motor disorders. Neuropathy was not predictive of gastrointestinal involvement and its extent; however, when motor abnormalities were present in patients with neuropathy, these were usually more severe. Gastrointestinal motor disorders are frequent and widespread in type 2 diabetics, regardless of symptoms. Autonomic neuropathy has a poor predictive value on motor disorders (0.75 for the esophagus, 0.5 for the stomach, 0.8 for the gallbladder), thus suggesting the coexistence of other pathophysiologic mechanisms.
Collapse
Affiliation(s)
- V Annese
- Section of Gastroenterology, CSS-IRCSS, San Giovanni Rotondo Hospital, Italy
| | | | | | | | | | | | | | | |
Collapse
|
25
|
Russo A, Smout AJ, Kositchaiwat C, Rayner C, Sattawatthamrong Y, Semmler J, Horowitz M, Sun WM. The effect of hyperglycaemia on cerebral potentials evoked by rapid rectal distension in healthy humans. Eur J Clin Invest 1999; 29:512-518. [PMID: 10354213 DOI: 10.1046/j.1365-2362.1999.00487.x] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
BACKGROUND Acute hyperglycaemia affects the perception of sensations arising from the gastrointestinal tract. The mechanisms responsible for this effect are unknown. Recordings of cerebral evoked potentials (EPs) can be used to assess the integrity of visceral afferent pathways. Our aim was to determine whether hyperglycaemia affects EPs elicited by rectal distension in healthy humans. MATERIALS AND METHODS Twelve healthy men, aged 19-31 years, were studied. A manometric catheter, incorporating a rectal balloon, was positioned 7-10 cm from the anal verge. Balloon distensions at both 'low' ( approximately 20 mL) and 'high' ( approximately 28 mL) volumes were performed, in a single-blind, randomized order, during both euglycaemia (4 mmol L-1) and hyperglycaemia (12 mmol L-1). EPs were recorded from a midline scalp electrode (Cz, International 10-20 system) and averaged for each series of 50 distensions. EP latencies and interpeak amplitudes were calculated. RESULTS Polyphasic EPs were recorded in all but one subject. Although the blood glucose concentration had no significant effect on the latencies of the EP peaks elicited by either 'low'- or 'high'-volume balloon distension, the interpeak amplitude (P1-N1) was greater during hyperglycaemia than during euglycaemia at the 'low' balloon volume (6.3 +/- 1.2 microV vs. 4.8 +/- 1.0 microV, P < 0.05). The blood glucose concentration had no significant effect on the perception of rectal balloon distension. CONCLUSIONS We conclude that in normal subjects acute hyperglycaemia increases the amplitude of the cerebral EP elicited by rectal balloon distension at low balloon volumes, suggesting that the effects of hyperglycaemia on gastrointestinal sensation may be mediated by central mechanisms.
Collapse
Affiliation(s)
- A Russo
- Department of Medicine, University of Adelaide, Royal Adelaide Hospital, Adelaide, Australia
| | | | | | | | | | | | | | | |
Collapse
|
26
|
Dobson CL, Davis SS, Chauhan S, Sparrow RA, Wilding IR. The effect of oleic acid on the human ileal brake and its implications for small intestinal transit of tablet formulations. Pharm Res 1999; 16:92-6. [PMID: 9950285 DOI: 10.1023/a:1018827030210] [Citation(s) in RCA: 21] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/12/2022]
Abstract
PURPOSE A human volunteer study was carried out to investigate whether activation of the ileal brake mechanism affects the transit of tablets through the small intestine. METHODS Oleic acid, which has previously been shown to activate the brake, was delivered to the small intestine in a modified release capsule at doses of 300 mg, 600 mg and 1200 mg. The effect of the oleic acid was determined by measuring the transit of two sets of radiolabelled tablets by gamma scintigraphy. One set of tablets was dosed with the capsule and the other one hour later. RESULTS The results show that in the majority of the volunteers small intestinal residence time was greater with the oleic acid than control. The effect was most pronounced in the tablets given concomitantly with the capsule and with the higher doses of oleic acid. CONCLUSIONS The ileal brake, activated by oleic acid, can slow the transit of tablets through the small intestine.
Collapse
Affiliation(s)
- C L Dobson
- School of Pharmaceutical Sciences, Nottingham University, UK
| | | | | | | | | |
Collapse
|
27
|
Lam WF, Gielkens HA, de Boer SY, Lamers CB, Masclee AA. Influence of hyperglycemia on the satiating effect of CCK in humans. Physiol Behav 1998; 65:505-11. [PMID: 9877417 DOI: 10.1016/s0031-9384(98)00189-9] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/15/2023]
Abstract
In the present study the effects of intraduodenal (i.d.) fat (endogenous CCK) and of CCK infusion on satiety were studied during normo-and hyperglycemic conditions. Eight healthy subjects participated in two protocols consisting of two experiments each. First protocol: (a) normoglycemia (control) with i.d. emulsified fat (i.d. fat) infusion, (b) acute hyperglycemia (HG) with plasma glucose levels stabilized at 15 mmol/L and i.d. fat infusion. In the second protocol the effect of exogenous cholecystokinin (CCK) on satiety was studied during normo- and hyperglycemia. Intraduodenal fat (Intralipid 10%) was infused at a dose of 1 g/h via a nasoduodenal tube in the first protocol, whereas in the second protocol CCK-33 was infused intravenously at a dose of 0.5 IDU/kg x h. Satiety was scored using visual analog scales (VAS). Plasma CCK levels were determined at regular intervals. During infusion of i.d. fat and i.v. CCK the VAS scores of wish to eat, hunger, and prospective feeding decreased significantly (p<0.05) in the normoglycemic experiments. During hyperglycemia satiety did not significantly change in the basal period; however, the scores of wish to eat, hunger, and prospective feeding increased significantly (p<0.05) when i.d. fat or i.v. CCK was administered. Plasma CCK levels in the basal and the stimulated period were not significantly different between normo- and hyperglycemia. In summary, the present study shows that in healthy humans volunteers 1) during normoglycemic conditions satiety can be induced by very low dose of i.d. fat and by CCK infusion, 2) during hyperglycemia the effect of i.d. fat and CCK on satiety are reversed, resulting in increased appetite.
Collapse
Affiliation(s)
- W F Lam
- Department of Gastroenterology-Hepatology, Leiden University Medical Center, The Netherlands
| | | | | | | | | |
Collapse
|
28
|
Andrews JM, Rayner CK, Doran S, Hebbard GS, Horowitz M. Physiological changes in blood glucose affect appetite and pyloric motility during intraduodenal lipid infusion. Am J Physiol Gastrointest Liver Physiol 1998; 275:G797-G804. [PMID: 9756511 DOI: 10.1152/ajpgi.1998.275.4.g797] [Citation(s) in RCA: 12] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
We evaluated the effects of varying blood glucose concentration within the normal postprandial range and its interaction with small intestinal nutrients on antropyloric motility and appetite. Eight healthy males (19-40 yr) underwent paired studies, with a blood glucose level of 5 or 8 mmol/l. Manometry and visual analog scales were used to assess motility and appetite, during fasting and intraduodenal lipid infusion (1.5 kcal/min). In the fasting state, antral waves were suppressed at 8 mmol/l compared with 5 mmol/l (P = 0.018). However, pyloric motility was no different between the two blood glucose concentrations. Hunger was no different at 5 mmol/l compared with 8 mmol/l, but fullness was greater at 8 mmol/l (P = 0. 01). During intraduodenal lipid infusion, antral waves were suppressed (P < 0.035) and isolated pyloric pressure waves (IPPWs) were stimulated (P < 0.02) compared with during the fasting state, with no difference between blood glucose concentrations, although the temporal patterning of IPPWs varied between blood glucose concentrations. The amplitude of IPPWs was greater at 5 mmol/l compared with 8 mmol/l (P < 0.001), and hunger decreased at 8 mmol/l compared with 5 mmol/l (P = 0.02). We conclude that "physiological" hyperglycemia modifies gastric motor and sensory function and that synergy exists between blood glucose concentration and small intestinal nutrients in modulating gastric motility and appetite.
Collapse
Affiliation(s)
- J M Andrews
- Departments of Medicine and Gastrointestinal Medicine, Royal Adelaide Hospital, North Terrace, Adelaide, South Australia 5000, Australia
| | | | | | | | | |
Collapse
|
29
|
Gielkens HA, van Oostayen JA, Frölich M, Biemond I, Lamers CB, Masclee AA. Dose-dependent inhibition of postprandial gallbladder motility and plasma hormone secretion during acute hyperglycemia. Scand J Gastroenterol 1998; 33:1074-9. [PMID: 9829363 DOI: 10.1080/003655298750026787] [Citation(s) in RCA: 16] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/04/2023]
Abstract
BACKGROUND Actual blood glucose concentrations influence gastrointestinal function. We investigated whether in healthy subjects the inhibitory effect of acute hyperglycemia on gallbladder motility is dose-dependent. METHODS Seven healthy volunteers were studied on four separate occasions in random order during euglycemia and during hyperglycemic clamping, at 4 mmol/l, 8 mmol/l, 12 mmol/l, and 16 mmol/l, respectively. Gallbladder volumes (ultrasonography) and plasma hormone release were studied before and after ingestion of a meal. RESULTS Postprandial gallbladder contraction was significantly (P < 0.05) and dose-dependently inhibited during the hyperglycemic experiments at 8, 12, and 16 mmol/l (56%+/-8%, 49%+/-8%, and 30%+/-5%, respectively) compared with euglycemia (68%+/-6%). Postprandial cholecystokinin release was significantly (P < 0.05) reduced compared with euglycemia only at a plasma glucose level of 16 mmol/l (116+/-28 versus 159+/-13 pmol x l(-1) x 120 min). Plasma pancreatic polypeptide secretion, as an indirect measure of vagal-cholinergic tone, was significantly (P < 0.05) and dose-dependently reduced during hyperglycemia at 8, 12, and 16 mmol/l. CONCLUSION In healthy subjects acute hyperglycemia significantly and dose-dependently inhibits postprandial gallbladder motility. Future studies on gallbladder motility should take into account the influence of plasma glucose, because already at postprandial glucose levels gallbladder motility is reduced.
Collapse
Affiliation(s)
- H A Gielkens
- Dept. of Gastroenterology-Hepatology, Leiden University Medical Center, The Netherlands
| | | | | | | | | | | |
Collapse
|
30
|
Gielkens HA, Lam WF, Coenraad M, Frölich M, van Oostayen JA, Lamers CB, Masclee AA. Effect of insulin on basal and cholecystokinin-stimulated gallbladder motility in humans. J Hepatol 1998; 28:595-602. [PMID: 9566827 DOI: 10.1016/s0168-8278(98)80282-1] [Citation(s) in RCA: 38] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
BACKGROUND/AIMS Acute hyperglycemia inhibits gallbladder contraction. In non-diabetic subjects this inhibitory effect may result from endogenous hyperinsulinemia. Therefore we investigated the effects of acute hyperglycemia and euglycemic hyperinsulinemia on basal and cholecystokinin-stimulated gallbladder motility. METHODS Gallbladder volume (ultrasonography) and duodenal bilirubin output were studied simultaneously in nine healthy volunteers (age 20-52 years) on 3 separate occasions in random order during: (a) saline infusion (control), (b) hyperglycemic hyperinsulinemic clamping (HG; plasma glucose at 15 mmol/l), and (c) euglycemic hyperinsulinemic clamping (HI; plasma insulin at 150 mU/l, glucose at 4-5 mmol/l). After a 2-h basal clamp period, cholecystokinin was infused intravenously for 60 min at 0.25 IDU x kg(-1) x h(-1), followed by another 60 min at 0.5 IDU x kg(-1) x h(-1). RESULTS HI and HG significantly (p<0.05) reduced basal duodenal bilirubin output compared to control, while basal gallbladder volume did not change. At the low dose cholecystokinin, gallbladder emptying during HG (25+/-3%) and HI (39+/-4%) was significantly (p<0.01) reduced compared to control (61+/-4%). The inhibitory effect of HG was significantly (p<0.05) stronger compared to HI. Duodenal bilirubin output during the low dose cholecystokinin was significantly (p<0.05) reduced by HG, but not by HI. No inhibitory effect of HG and HI on gallbladder emptying and duodenal bilirubin output was observed with the high dose of cholecystokinin. CONCLUSIONS In healthy subjects acute hyperglycemia and euglycemic hyperinsulinemia reduce basal duodenal bilirubin output and inhibit gallbladder emptying stimulated by low dose cholecystokinin. These results suggest that insulin is involved in the inhibitory effect of hyperglycemia on basal and cholecystokinin-stimulated gallbladder motility.
Collapse
Affiliation(s)
- H A Gielkens
- Department of Gastroenterology-Hepatology, Leiden University Medical Center, The Netherlands
| | | | | | | | | | | | | |
Collapse
|
31
|
Gielkens HA, Verkijk M, Lam WF, Lamers CB, Masclee AA. Effects of hyperglycemia and hyperinsulinemia on satiety in humans. Metabolism 1998; 47:321-4. [PMID: 9500570 DOI: 10.1016/s0026-0495(98)90264-5] [Citation(s) in RCA: 38] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]
Abstract
Hyperglycemia may influence satiety. One mechanism by which glucose could influence food intake is hyperinsulinemia. Therefore, we investigated the short-term effects of acute hyperglycemia and euglycemic hyperinsulinemia on satiety. Six healthy volunteers (aged 20 to 26 years) were studied for 240 minutes on three separate occasions in random order during (1) intravenous (i.v.) saline (control), (2) acute hyperglycemic hyperinsulinemia (HG) with plasma glucose at 15 mmol/L, and (3) euglycemic hyperinsulinemia (HI) with plasma insulin at 80 mU/L and glucose at 4 to 5 mmol/L. Subjective criteria for appetite like the wish to eat, prospective feeding intentions ("How much food do you think you can eat?"), and feelings of hunger and fullness were scored on a 100-mm visual analog scale (VAS) at 30-minute intervals. Appetite was also measured every 60 minutes with the use of a food selection list (FSL). Appetite (prospective feeding intentions, feelings of hunger, and the wish to eat) gradually increased over basal levels during control conditions and HI. In contrast, prospective feeding intentions and feelings of hunger gradually decreased during HG and were significantly (P < .05) reduced versus basal and control levels during the last hour of the experiment. The wish to eat followed the same pattern. Feelings of fullness did not significantly change in all three experiments. Total food selection was not significantly decreased during HG, but the preference for fat-rich or carbohydrate-rich items tended to be reduced. The study suggests that in humans hyperglycemia induces satiety. This effect seems not to be mediated by insulin, since HI had no effect on appetite. However, a potentiating effect of endogenous insulin on the satiating effect of high blood glucose levels cannot be excluded.
Collapse
Affiliation(s)
- H A Gielkens
- Department of Gastroenterology-Hepatology, Leiden University Medical Center, The Netherlands
| | | | | | | | | |
Collapse
|
32
|
Avşar E, Ersöz O, Karişik E, Erdoğan Y, Bekiroğlu N, Lawrance R, Akalin S, Ulusoy NB. Hyperglycemia-induced attenuation of rectal perception depends upon pattern of rectal balloon inflation. Dig Dis Sci 1997; 42:2206-12. [PMID: 9398796 DOI: 10.1023/a:1018898130049] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
This study investigated the effects of acute hyperglycemia on conscious rectal perception in response to two different rectal distension paradigms. Eleven healthy males were studied in random order on two separate days during euglycemia and hyperglycemia with blood glucose concentrations clamped to 3.8 +/- 0.6 and 14.8 +/- 0.86 mmol/liter, respectively. In order to evoke sensory responses, rapid phasic and ramplike distensions were applied to an intrarectal balloon. Rectal sensation thresholds for initial sensation, sensation of stool and discomfort, and sensory intensities were recorded. Additionally, anorectal motor responses were investigated during phasic distension. Acute hyperglycemia did not modify rectal sensory pressure thresholds and perception scores in response to phasic distension. Neither did hyperglycemia alter the resting anal sphincter pressure, the pressure threshold for eliciting the rectoanal inhibitory reflex, or the maximal anal squeeze pressure. In contrast, hyperglycemia attenuated rectal perception in response to ramplike distension. The pressure thresholds, 10.0 +/- 1.8 and 17.0 +/- 3.6 mm Hg for initial sensation and discomfort, respectively, during hyperglycemia were significantly higher than the corresponding thresholds of 4.4 +/- 1.4 and 11.4 +/- 1.9 mm Hg observed during euglycemia (P < 0.01). Higher rectal pressures were observed at all intensities of sensation of stool and discomfort during hyperglycemia than those obtained during euglycemia (P < 0.01). Hyperglycemia did not alter the compliance of the rectum. The results of this study demonstrate that acute hyperglycemia attenuates rectal perception, and this attenuation depends upon the type of distension employed. Our findings also demonstrate that anal sphincter motor function is not appreciably modified by hyperglycemia.
Collapse
Affiliation(s)
- E Avşar
- Department of Internal Medicine, University of Marmara Medical School, Istanbul, Turkey
| | | | | | | | | | | | | | | |
Collapse
|
33
|
Rosa-e-Silva L, Troncon LE, Oliveira RB, Foss MC, Braga FJ, Gallo Júnior L. Rapid distal small bowel transit associated with sympathetic denervation in type I diabetes mellitus. Gut 1996; 39:748-56. [PMID: 9014777 PMCID: PMC1383402 DOI: 10.1136/gut.39.5.748] [Citation(s) in RCA: 32] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/03/2023]
Abstract
BACKGROUND The pattern of progression of a meal from the stomach to the caecum in diabetes mellitus is controversial and the differential roles of transit through the jejunum and the ileum have not been investigated in diabetes. AIMS To determine gastric emptying and transit rates through proximal and distal regions of the small bowel in type I diabetic patients. SUBJECTS The study included six diabetic patients with evidence of autonomic neuropathy (DM-AN group), 11 diabetics without autonomic dysfunction (DM group), and 15 control volunteers. METHODS Gastric emptying and small bowel transit of a liquid meal were evaluated scintigraphically in these subjects. Transit through regions of interest corresponding to the proximal and distal small intestine up to the caecum was determined and correlated with gastric emptying rates, cardiovascular measurements of autonomic function, and the occurrence of diarrhoea. RESULTS Gastric emptying and transit through the proximal small bowel were similar in the three groups. The meal arrived to the caecum significantly earlier in DM-AN patients (median; range: 55 min; 22-->180 min) than in the DM group (100 min; 44-->180 min, p < 0.05) or in controls (120 min; 80-->180 min, p < 0.02). Accumulation of chyme in the distal small bowel was decreased in DM-AN patients, who showed values for peak activity (30%; 10-55%) significantly lower than in the DM group (49%; 25-77%, p = 0.02) and controls (50%; 30-81%, p = 0.02). In DM patients (n = 17), the time of meal arrival to the caecum was significantly correlated with both orthostatic hypotension (coefficient of contingency, C = 0.53, p < 0.01) and diarrhoea (C = 0.47, p < 0.05), but not with gastric emptying rates. CONCLUSIONS Patients with type I diabetes mellitus and sympathetic denervation have abnormally rapid transit of a liquid meal through the distal small bowel, which may play a part in diarrhoea production.
Collapse
Affiliation(s)
- L Rosa-e-Silva
- Department of Clinical Medicine, Ribeirão Preto Medical School, University of São Paulo, Brazil
| | | | | | | | | | | |
Collapse
|
34
|
Russo A, Fraser R, Horowitz M. The effect of acute hyperglycaemia on small intestinal motility in normal subjects. Diabetologia 1996; 39:984-989. [PMID: 8858222 DOI: 10.1007/bf00403919] [Citation(s) in RCA: 30] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
The effects of hyperglycaemia on postprandial small intestinal motor activity are unclear. Duodenal and jejunal pressures and duodeno-caecal transit were measured in eight healthy male volunteers during euglycaemia (blood glucose 4-6 mmol/l) and hyperglycaemia (blood glucose 12-15 mmol/l). Duodenal and jejunal pressures were recorded with a manometric assembly during intraduodenal infusion of 100 ml nutrient liquid comprising 14% protein, 31.5% fat and 54.5% carbohydrate together with 15 glactulose. Duodeno-caecal transit was determined by a breath hydrogen technique. The number of duodenal (p < 0.05) and jejunal (p < 0.01) pressure waves, excluding phase III episodes was reduced during hyperglycaemia compared to euglycaemia Hyperglycaemia was associated with earlier onset of phase III activity (30 +/- 12 vs 132 +/- 20 min; p < 0.05) Duodeno-caecal transit was slower during hyperglycaemia when compared to euglycaemia (114 +/- 17 vs 49 +/- 6 min, p < 0.01). We conclude that induced hyperglycaemia has major effects on postprandial small intestinal motility. The reduction in duodenal and jejunal motor activity is likely to explain the retardation of small intestinal transit during hyperglycaemia.
Collapse
Affiliation(s)
- A Russo
- University Department of Medicine, Royal Adelaide Hospital, Australia
| | | | | |
Collapse
|
35
|
Masclee AA, Gielkens HA, Lam WF, de Boer SY, Lamers CB. Effects of parenteral nutrients on gastrointestinal motility and secretion. SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY. SUPPLEMENT 1996; 218:50-5. [PMID: 8865451 DOI: 10.3109/00365529609094731] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 02/02/2023]
Abstract
BACKGROUND The stimulation of gastrointestinal motility and secretion during nutrient digestion is generally divided into a cephalic, gastric and intestinal phase. Little is known about the effects of macronutrients on gastrointestinal function during the postabsorptive or circulatory phase of digestion. METHODS Review of studies investigating the effects of circulating macro-nutrients such as fat, amino acids and glucose on gastrointestinal motility and secretion. RESULTS Intravenous infusion of fat emulsions delays gastric emptying and interrupts the interdigestive intestinal motor pattern. Intravenous amino acids, administered in high doses, stimulate gastric acid secretion, pancreatic secretion, gallbladder contraction, and intestinal motility. Patients receiving total parental nutrition (TPN) have inert gallbladders and are at risk of developing gallbladder sludge and stones. Administering a proportion of the daily amino acid requirement by rapid intravenous infusion may prove useful in the prevention of sludge and stone formation during TPN by promoting gallbladder contraction. Intravenous infusion of glucose, already at physiological postprandial plasma levels, inhibits gastrointestinal motility and secretion. The inhibitory effect of glucose is dose-dependent, that is, more pronounced at higher plasma glucose levels. Recent studies have indicated that in patients with diabetes mellitus alterations in gastrointestinal function are related to the degree of hyperglycaemia. CONCLUSIONS Nutrients during the circulatory phase of digestion influence gastrointestinal motility and secretion. Knowledge of these effects is relevant for conditions with increased plasma levels of macro-nutrients such as in patients with diabetes mellitus or during total parenteral nutrition.
Collapse
Affiliation(s)
- A A Masclee
- Dept. of Gastroenterology and Hepatology, University Hospital Leiden, The Netherlands
| | | | | | | | | |
Collapse
|