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Sadeghi A, Nouri F, Taherifard E, Shahlaee MA, Dehdari Ebrahimi N. Estimates of global and regional prevalence of Helicobacter pylori infection among individuals with obesity: a systematic review and meta-analysis. Infection 2024; 52:1223-1234. [PMID: 38594573 DOI: 10.1007/s15010-024-02244-7] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/22/2023] [Accepted: 03/18/2024] [Indexed: 04/11/2024]
Abstract
PURPOSE The prevalence of obesity is an escalating concern in modern populations, predominantly attributed to the widespread adoption of sedentary lifestyles observed globally. Extensive research has established a significant association between obesity and Helicobacter pylori (H. pylori). Nonetheless, a comprehensive assessment of the global prevalence of H. pylori among individuals with obesity remains undetermined. METHODS A systematic search strategy was applied to PubMed, Scopus, and Web of Science. The resulting records were screened using the Rayyan online tool for the management of systematic reviews. Freeman-Tukey double arcsine transformation was used. Subgroup analyses (continent, regional classifications, developmental status, religion, global hemisphere, income, access to international waters, and H. pylori eradication) and multivariate meta-regression (latitude, longitude, male-to-all ratio, mean age, and body mass index) were done to estimate the effects of the moderators. Risk of bias assessment was done using JBI checklist for prevalence studies. RESULTS A total of 472,511 individuals with obesity from 208 studies were included. The global estimation of H. pylori prevalence among individuals with obesity was 32.3% (95% CI 26.9%, 38.0%). South America had the highest prevalence. Based on the different classifications of countries, resource-rich, low-/middle-income, developing, and Islamic countries had the highest prevalence. Lower pooled prevalence was observed in the studies with adequate sample sizes (n ≥ 270). CONCLUSION The findings have the potential to influence future health policies for preventing and treating H. pylori infection. However, there is variability among the included studies, indicating the need for more population-based research.
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Affiliation(s)
- Alireza Sadeghi
- Student Research Committee, Shiraz University of Medical Sciences, Shiraz, Iran.
- Transplant Research Center, Shiraz University of Medical Sciences, Shiraz, Fars, Iran.
- Gastroenterohepatology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
| | - Fatemeh Nouri
- Student Research Committee, Shiraz University of Medical Sciences, Shiraz, Iran
| | - Ehsan Taherifard
- Student Research Committee, Shiraz University of Medical Sciences, Shiraz, Iran
| | | | - Niloofar Dehdari Ebrahimi
- Student Research Committee, Shiraz University of Medical Sciences, Shiraz, Iran.
- Transplant Research Center, Shiraz University of Medical Sciences, Shiraz, Fars, Iran.
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Gold-Smith FD, Chand SK, Petrov MS. Post-pancreatitis diabetes mellitus: towards understanding the role of gastrointestinal motility. MINERVA GASTROENTERO 2018; 64. [DOI: 10.23736/s1121-421x.18.02507-2] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 08/30/2023]
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Chen J, Chen L, Sanseau P, Freudenberg JM, Rajpal DK. Significant obesity-associated gene expression changes occur in the stomach but not intestines in obese mice. Physiol Rep 2016; 4:4/10/e12793. [PMID: 27207783 PMCID: PMC4886165 DOI: 10.14814/phy2.12793] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/03/2016] [Accepted: 04/07/2016] [Indexed: 12/15/2022] Open
Abstract
The gastrointestinal (GI) tract can have significant impact on the regulation of the whole‐body metabolism and may contribute to the development of obesity and diabetes. To systemically elucidate the role of the GI tract in obesity, we performed a transcriptomic analysis in different parts of the GI tract of two obese mouse models: ob/ob and high‐fat diet (HFD) fed mice. Compared to their lean controls, significant changes in the gene expression were observed in both obese mouse groups in the stomach (ob/ob: 959; HFD: 542). In addition, these changes were quantitatively much higher than in the intestine. Despite the difference in genetic background, the two mouse models shared 296 similar gene expression changes in the stomach. Among those genes, some had known associations to obesity, diabetes, and insulin resistance. In addition, the gene expression profiles strongly suggested an increased gastric acid secretion in both obese mouse models, probably through an activation of the gastrin pathway. In conclusion, our data reveal a previously unknown dominant connection between the stomach and obesity in murine models extensively used in research.
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Affiliation(s)
- Jing Chen
- Computational Biology, Target Sciences, GlaxoSmithKline, King of Prussia, Pennsylvania
| | - Lihong Chen
- Enteroendocrinology DPU, GlaxoSmithKline, Research Triangle Park, North Carolina
| | - Philippe Sanseau
- Computational Biology, Target Sciences, GlaxoSmithKline, King of Prussia, Pennsylvania
| | | | - Deepak K Rajpal
- Computational Biology, Target Sciences, GlaxoSmithKline, King of Prussia, Pennsylvania
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Kulkarni BV, LaSance K, Sorrell JE, Lemen L, Woods SC, Seeley RJ, Sandoval D. The role of proximal versus distal stomach resection in the weight loss seen after vertical sleeve gastrectomy. Am J Physiol Regul Integr Comp Physiol 2016; 311:R979-R987. [PMID: 27581811 DOI: 10.1152/ajpregu.00125.2016] [Citation(s) in RCA: 11] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/30/2016] [Revised: 08/26/2016] [Accepted: 08/27/2016] [Indexed: 12/16/2022]
Abstract
The mechanisms involved in the weight loss seen after vertical sleeve gastrectomy (VSG) are not clear. The rat stomach has two morphologically and functionally distinct proximal and distal parts. The rat model for VSG involves complete removal of the proximal part and 80% removal of the distal part along the greater curvature. The purpose of this study was to understand the potential independent contributions of removal of these distinct gastric sections to VSG outcomes. We prepared four surgical groups of male Long-Evans rats: VSG, sham surgery (control), selective proximal section removal (PR), and selective distal section removal (DR). Gastric emptying rate (GER) was highest after VSG compared with all other groups. However, PR, in turn, had significantly greater GER compared with both DR and sham groups. The surgery-induced weight loss followed the same pattern with VSG causing the greatest weight loss and PR having greater weight loss compared with DR and sham groups. The results were robust for rats fed regular chow or a high-fat diet. Body mass analysis revealed that the weight loss was due to the loss of fat mass, and there was no change in lean mass after the surgeries. In conclusion, removal of the proximal stomach contributes to most, but not all, of the physiological impact of VSG.
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Affiliation(s)
- Bhushan V Kulkarni
- Department of Surgery, University of Michigan, Ann Arbor, Michigan.,Department of Internal Medicine, University of Cincinnati, Cincinnati, Ohio; and
| | - Kathleen LaSance
- Department of Radiology, Vontz Core Imaging Laboratory, University of Cincinnati, Cincinnati, Ohio
| | - Joyce E Sorrell
- Department of Internal Medicine, University of Cincinnati, Cincinnati, Ohio; and
| | - Lisa Lemen
- Department of Radiology, Vontz Core Imaging Laboratory, University of Cincinnati, Cincinnati, Ohio
| | - Stephen C Woods
- Department of Psychiatry, University of Cincinnati, Cincinnati, Ohio
| | - Randy J Seeley
- Department of Surgery, University of Michigan, Ann Arbor, Michigan.,Department of Internal Medicine, University of Cincinnati, Cincinnati, Ohio; and
| | - Darleen Sandoval
- Department of Surgery, University of Michigan, Ann Arbor, Michigan; .,Department of Internal Medicine, University of Cincinnati, Cincinnati, Ohio; and
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Hoffman I, Tack J. Assessment of gastric motor function in childhood functional dyspepsia and obesity. Neurogastroenterol Motil 2012; 24:108-12, e81. [PMID: 22103293 DOI: 10.1111/j.1365-2982.2011.01813.x] [Citation(s) in RCA: 28] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
BACKGROUND The aim was to compare gastric emptying rate and nutrient tolerance during a satiety drinking test in children with functional dyspepsia (FD) and obesity and to study the relationship between daily caloric intake and the satiety drinking test. METHODS A total of 28 dyspeptic children (22 girls, mean age 12.5 ± 3.1 years) and 15 obese children (five girls, 13.3 ± 1.8 years) were studied. The patients underwent an octanoic acid gastric emptying breath test and a satiety drinking test. Prior to both tests, a dyspepsia questionnaire was filled out to calculate the mean calorie intake. KEY RESULTS The most prevalent dyspeptic symptoms were early satiety (96.4%), postprandial fullness (89.2%), and epigastric pain (78.6%), followed by nausea (50%). All dyspeptic and obese children (n = 43) started the satiety drinking test and 41 children completed the test until a score of 5 was reached. The maximum ingested volume in FD was significantly lower than in obesity or in age-matched healthy controls (252 ± 85 vs 479 ± 199 and 359 ± 29 mL respectively, both P < 0.05). As a group, dyspeptic children had significantly slower gastric emptying than obese children (89.7 ± 54.8 min vs 72.5 ± 26.0 min, P = 0.05). Daily calorie intake was significantly higher in obese children than that in dyspeptic children (2325 ± 469 vs 1503 ± 272 cal, P < 0.0001). The endpoint of the satiety drinking test was significantly correlated with body weight or BMI (both R = 0.41, P = 0.04), but not with daily calorie intake, gastric emptying rate or age. CONCLUSIONS & INFERENCES The satiety drinking test is a potentially useful non-invasive tool in the investigation of children with FD and obesity.
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Affiliation(s)
- I Hoffman
- Department of Paediatric Gastroenterology, University Hospitals Leuven, Leuven, Belgium.
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Borg J, Melander O, Johansson L, Uvnäs-Moberg K, Rehfeld JF, Ohlsson B. Gastroparesis is associated with oxytocin deficiency, oesophageal dysmotility with hyperCCKemia, and autonomic neuropathy with hypergastrinemia. BMC Gastroenterol 2009; 9:17. [PMID: 19243587 PMCID: PMC2650701 DOI: 10.1186/1471-230x-9-17] [Citation(s) in RCA: 25] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/17/2008] [Accepted: 02/25/2009] [Indexed: 11/23/2022] Open
Abstract
Background Gastrointestinal (GI) dysmotility and autonomic neuropathy are common problems among diabetics with largely unknown aetiology. Many peptides are involved in the autonomic nervous system regulating the GI tract. The aim of this study was to examine if concentrations of oxytocin, cholecystokinin (CCK), gastrin and vasopressin in plasma differ between diabetics with normal function and dysfunction in GI motility. Methods Nineteen patients with symptoms from the GI tract who had been examined with gastric emptying scintigraphy, oesophageal manometry, and deep-breathing test were included. They further received a fat-rich meal, after which blood samples were collected and plasma frozen until analysed for hormonal concentrations. Results There was an increase in postprandial oxytocin plasma concentration in the group with normal gastric emptying (p = 0.015) whereas subjects with delayed gastric emptying had no increased oxytocin secretion (p = 0.114). Both CCK and gastrin levels increased after the meal, with no differences between subjects with normal respective delayed gastric emptying. The concentration of vasopressin did not increase after the meal. In patients with oesophageal dysmotility the basal level of CCK tended to be higher (p = 0.051) and those with autonomic neuropathy had a higher area under the curve (AUC) of gastrin compared to normal subjects (p = 0.007). Conclusion Reduced postprandial secretion of oxytocin was found in patients with delayed gastric emptying, CCK secretion was increased in patients with oesophageal dysmotility, and gastrin secretion was increased in patients with autonomic neuropathy. The findings suggest that disturbed peptide secretion may be part of the pathophysiology of digestive complications in diabetics.
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Affiliation(s)
- Julia Borg
- Department of Clinical Sciences, Gastroenterology Division, Malmö University Hospital, Lund University, Lund, Sweden.
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Hasler WL, Coleski R, Chey WD, Koch KL, McCallum RW, Wo JM, Kuo B, Sitrin MD, Katz LA, Hwang J, Semler JR, Parkman HP. Differences in intragastric pH in diabetic vs. idiopathic gastroparesis: relation to degree of gastric retention. Am J Physiol Gastrointest Liver Physiol 2008; 294:G1384-91. [PMID: 18403619 DOI: 10.1152/ajpgi.00023.2008] [Citation(s) in RCA: 30] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/31/2023]
Abstract
Evidence suggests that distinct mechanisms underlie diabetic and idiopathic gastroparesis. Differences in gastric acid in gastroparesis of different etiologies and varying degrees of gastric stasis are uninvestigated. We tested the hypotheses that 1) gastric pH profiles show differential alteration in diabetic vs. idiopathic gastroparesis and 2) abnormal pH profiles relate to the severity of gastric stasis. Sixty-four healthy control subjects and 44 gastroparesis patients (20 diabetic, 24 idiopathic) swallowed wireless transmitting capsules and then consumed (99m)Tc-sulfur colloid-labeled meals for gastric scintigraphy. Gastric pH from the capsule was recorded every 5 s. Basal pH was higher in diabetic (3.64 +/- 0.41) vs. control subjects (1.90 +/- 0.18) and idiopathic subjects (2.41 +/- 0.42; P < 0.05). Meals evoked initial pH increases that were greater in diabetic (4.98 +/- 0.32) than idiopathic patients (3.89 +/- 0.39; P = 0.03) but not control subjects (4.48 +/- 0.14). pH nadirs prior to gastric capsule evacuation were higher in diabetic patients (1.50 +/- 0.23) than control subjects (0.58 +/- 0.11; P = 0.003). Four-hour gastric retention was similar in diabetic (18.3 +/- 0.5%) and idiopathic (19.4 +/- 0.5%) patients but higher than control subjects (2.2 +/- 0.5%; P < 0.001). Compared with control subjects, those with moderate-severe stasis (>20% retention at 4 h) had higher basal (3.91 +/- 0.55) and nadir pH (2.23 +/- 0.42) values (P < 0.05). In subgroup analyses, both diabetic and idiopathic patients with moderate-severe gastroparesis exhibited increased pH parameters vs. those with mild gastroparesis. In conclusion, diabetic patients with gastroparesis exhibit reduced gastric acid, an effect more pronounced in those with severely delayed gastric emptying. Idiopathic gastroparetic subjects exhibit nearly normal acid profiles, although those with severely delayed emptying show reduced acid vs. those with mild delays. Thus both etiology and degree of gastric stasis determine gastric acidity in gastroparesis.
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Affiliation(s)
- William L Hasler
- Division of Gastroenterology, Univ. of Michigan Health System, Ann Arbor, MI 48109, USA.
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Intagliata N, Koch KL. Gastroparesis in type 2 diabetes mellitus: prevalence, etiology, diagnosis, and treatment. Curr Gastroenterol Rep 2007; 9:270-9. [PMID: 17883973 DOI: 10.1007/s11894-007-0030-3] [Citation(s) in RCA: 30] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/20/2022]
Abstract
The worldwide epidemic of type 2 diabetes mellitus (T2DM) is a substantial economic and social burden. Although gastroparesis associated with type 1 diabetes mellitus (T1DM) has been recognized for years, only recently have studies shown that patients with T2DM also have high rates of gastroparesis. Individuals with T2DM constitute 90% to 95% of the diabetic population. Unique characteristics that distinguish this population are obesity, insulin resistance, and associated comorbidities. These features highlight the importance of investigating gastric emptying in individuals with T2DM and upper gastrointestinal symptoms. The purpose of this review is to examine the literature pertaining to diabetes and the effect of diabetes on gastric neuromuscular function, with a focus on T2DM. An understanding of gastric motility in T2DM is important to diagnose gastroparesis, to treat upper gastrointestinal symptoms, and to restore normal gastric motility, which may lead, in turn, to improved glucose control.
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Affiliation(s)
- Nicolas Intagliata
- Section on Gastroenterology, Wake Forest University Medical Center, Nutrition Building, E-115, Medical Center Boulevard, Winston-Salem, NC 27157, USA
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Crowell MD, Decker GA, Levy R, Jeffrey R, Talley NJ. Gut-brain neuropeptides in the regulation of ingestive behaviors and obesity. Am J Gastroenterol 2006; 101:2848-56; quiz 2914. [PMID: 17026567 DOI: 10.1111/j.1572-0241.2006.00832.x] [Citation(s) in RCA: 14] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
Abstract
The prevalence of obesity has increased to epidemic proportions and has become an urgent public health problem. Obesity causes significant morbidity and mortality and its impact on health-care costs in the United States is growing dramatically. Apart from bariatric surgery treatment, options are limited. Future advances in treatment will rely on a better understanding of the pathogenesis and physiology of obesity. Alterations in gastrointestinal (GI) sensory-motor function and symptoms have been associated with obesity. GI neuroendocrine communications between the periphery and the brain regulate energy balance and ingestive behaviors. These interactions are largely mediated by the gut-brain peptides through negative and positive feedback loops that maintain energy homeostasis. Bariatric surgery has been shown effective, but the mechanisms of weight loss following these procedures clearly require further studies and a better understanding of the affects of bariatric surgery on the gut-brain neuropeptide homeostasis. Gut-brain peptides may provide attractive therapeutic targets in the fight against this very morbid disease. We review alterations in GI function and some of the more important gut-brain neuropeptides that occur in obesity.
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Meier JJ, Nauck MA, Kask B, Holst JJ, Deacon CF, Schmidt WE, Gallwitz B. Influence of gastric inhibitory polypeptide on pentagastrin-stimulated gastric acid secretion in patients with type 2 diabetes and healthy controls. World J Gastroenterol 2006; 12:1874-80. [PMID: 16609993 PMCID: PMC4087512 DOI: 10.3748/wjg.v12.i12.1874] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/09/2005] [Revised: 07/02/2005] [Accepted: 08/26/2005] [Indexed: 02/06/2023] Open
Abstract
AIM Gastric inhibitory polypeptide is secreted from intestinal K-cells in response to nutrient ingestion and acts as an incretin hormone in human physiology. While animal experiments suggested a role for GIP as an inhibitor of gastric secretion, the GIP effects on gastric acid output in humans are still controversial. METHODS Pentagastrin was administered at an infusion rate of 1 microg . kg(-1) . h(-1) over 300 min in 8 patients with type 2 diabetes (2 female, 6 male, 54+/- 10 years, BMI 30.5+/- 2.2 kg/m(2); no history of autonomic neuropathy) and 8 healthy subjects (2/6, 46+/- 6 years., 28.9+/- 5.3 kg/m(2)). A hyperglycaemic clamp (140 mg/dl) was performed over 240 min. Placebo, GIP at a physiological dose (1 pmol . kg(-1) . min(-1)), and GIP at a pharmacological dose (4 pmol . kg(-1) . min(-1)) were administered over 60 min each. Boluses of placebo, 20 pmol GIP/kg, and 80 pmol GIP/kg were injected intravenously at the beginning of each infusion period, respectively. Gastric volume, acid and chloride output were analysed in 15-min intervals. Capillary and venous blood samples were drawn for the determination of glucose and total GIP. Statistics were carried out by repeated-measures ANOVA and one-way ANOVA. RESULTS Plasma glucose concentrations during the hyperglycaemic clamp experiments were not different between patients with type 2 diabetes and controls. Steady-state GIP plasma levels were 61+/- 8 and 79+/- 12 pmol/l during the low-dose and 327+/- 35 and 327+/- 17 pmol/l during the high-dose infusion of GIP, in healthy control subjects and in patients with type 2 diabetes, respectively (P=0.23 and P=0.99). Pentagastrin markedly increased gastric acid and chloride secretion (P< 0.001). There were no significant differences in the rates of gastric acid or chloride output between the experimental periods with placebo or any dose of GIP. The temporal patterns of gastric acid and chloride secretion were similar in patients with type 2 diabetes and healthy controls (P=0.86 and P=0.61, respectively). CONCLUSION Pentagastrin-stimulated gastric acid secretion is similar in patients with type 2 diabetes and healthy controls. GIP administration does not influence gastric acid secretion at physiological or pharmacological plasma levels. Therefore, GIP appears to act as an incretin rather than as an enterogastrone in human physiology.
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Affiliation(s)
- Juris J Meier
- Department of Medicine I, St. Josef-Hospital, Ruhr-University of Bochum, Gudrunstrasse 56, 44791 Bochum, Germany.
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Yao SK, Ke MY, Wang ZF, Xu DB, Zhang YL. Visceral response to acute retrograde gastric electrical stimulation in healthy human. World J Gastroenterol 2005; 11:4541-4546. [PMID: 16052685 PMCID: PMC4398705 DOI: 10.3748/wjg.v11.i29.4541] [Citation(s) in RCA: 14] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/19/2004] [Revised: 12/01/2004] [Accepted: 12/03/2004] [Indexed: 02/06/2023] Open
Abstract
AIM To investigate the visceral response to acute retrograde gastric electrical stimulation (RGES) in healthy humans and to derive optimal parameters for treatment of patients with obesity. METHODS RGES with a series of effective parameters were performed via a bipolar mucosal electrode implanted along the great curvature 5 cm above pylorus of stomach in 12 healthy human subjects. Symptoms associated with dyspepsia and other discomfort were observed and graded during RGES at different settings, including long pulse and pulse train. Gastric myoelectrical activity at baseline and during different settings of stimulation was recorded by a multi-channel electrogastrography. RESULTS The gastric slow wave was entrained in all the subjects at the pacing parameter of 9 cpm in frequency, 500 ms in pulse width, and 5 mA in amplitude. The frequently appeared symptoms during stimulation were satiety, bloating, discomfort, pain, sting, and nausea. The total symptom score for each subject significantly increased as the amplitude or pulse width was adjusted to a higher scale in both long pulse and pulse train. There was a wide diversity of visceral responses to RGES among individuals. CONCLUSION Acute RGES can result in a series of symptoms associated with dyspepsia, which is beneficial to the treatment of obesity. Optimal parameter should be determined according to the individual sensitivity to electrical stimulation.
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Affiliation(s)
- Shu-Kun Yao
- Department of Gastroenterology, Peking Union Medical College Hospital, Beijing 100730, China
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12
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Abstract
In the vast majority of affected individuals, obesity involves overconsumption of food relative to calorie requirements. The sensory function of the stomach may play a key role in the cessation of food ingestion. This sensation of the stomach is, in part, determined by its motor functions, such as tone and compliance and the rate of emptying. However, studies of gastric emptying in normal-weight and obese persons have shown inconsistent results. Gastric capacity was larger in obese persons when tested with an intragastric latex balloon filled with water. In contrast, other studies using the barostat or imaging (single-photon emission computed tomography) techniques reported no differences in gastric volume or compliance between obese and lean subjects. On the other hand, increased body mass and fasting gastric volume are independently associated with delayed satiation under standard laboratory conditions of food ingestion. These data suggest that changes in gastric motor and sensory functions in obesity may present useful targets to prevent and treat obesity. Further well-controlled, validated studies are needed to clarify the potential role of altering the stomach's function as a means of controlling food intake in obesity.
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Affiliation(s)
- Moo-In Park
- Clinical Enteric Neuroscience Translational and Epidemiological Research Program, Gastroenterology Research Unit, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
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Decker GA, Crowell MD. Obesity and gastrointestinal sensory-motor function. CURRENT TREATMENT OPTIONS IN GASTROENTEROLOGY 2005; 8:347-52. [PMID: 16009036 DOI: 10.1007/s11938-005-0028-6] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 05/03/2023]
Abstract
Obesity has become a significant public health problem in the United States and has been associated with significant morbidity and mortality. Alterations in gastrointestinal sensory-motor function are now recognized to be associated with obesity and may be the cause of functional gastrointestinal symptoms commonly seen in these patients. The gut peptides are intimately involved in this process and may provide attractive therapeutic targets in the fight against this very morbid disease.
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Affiliation(s)
- G Anton Decker
- Division of Gastroenterology & Hepatology, Mayo Clinic Scottsdale, 13400 East Shea Boulevard, Scottsdale, AZ 85259, USA
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Kim DY, Camilleri M, Murray JA, Stephens DA, Levine JA, Burton DD. Is there a role for gastric accommodation and satiety in asymptomatic obese people? OBESITY RESEARCH 2001; 9:655-61. [PMID: 11707531 DOI: 10.1038/oby.2001.89] [Citation(s) in RCA: 60] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/11/2023]
Abstract
OBJECTIVE The relationships of gastric accommodation and satiety in moderately obese individuals are unclear. We hypothesized that obese people had increased gastric accommodation and reduced postprandial satiety. The objective of this study was to compare gastric accommodation and satiety between obese and non-obese asymptomatic subjects. RESEARCH METHODS AND PROCEDURES In 13 obese (body mass index [BMI] > or = 30 kg/m(2); mean BMI, 37.0 +/- 4.9 kg/m(2)) and 19 non-obese control subjects (BMI < 30 kg/m(2); mean BMI, 26.2 +/- 2.9 kg/m(2)), we used single photon emission computed tomography to measure fasting and postprandial gastric volumes and expressed the accommodation response as the ratio of postprandial/fasting volumes. The satiety test measured maximum tolerable volume of ingestion of liquid nutrient meal (Ensure) and symptoms 30 minutes after cessation of ingestion. RESULTS Total fasting and postprandial gastric volumes and the ratio of postprandial/fasting gastric volume were not different between asymptomatic obese and control subjects. However, the fasting volume of the distal stomach was greater in obese than in control subjects. Maximum tolerable volume of ingested Ensure and aggregate symptom score 30 minutes later were also not different between obese and control subjects. DISCUSSION Asymptomatic obese individuals (within the BMI range of 32.6 to 48 kg/m(2)) did not show either increased postprandial gastric accommodation or reduced satiety. These data suggest that gastric accommodation is unlikely to provide an important contribution to development of moderate obesity.
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Affiliation(s)
- D Y Kim
- Enteric Neuroscience Program, Gastroenterology Research Unit, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905, USA
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15
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Carantoni M, Avogaro A, Tiengo A, Fellin R. Extreme but asymptomatic hypergastrinemia with gastroparesis in a young woman with insulin dependent diabetes mellitus. J Endocrinol Invest 1998; 21:323-8. [PMID: 9648055 DOI: 10.1007/bf03350336] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/08/2023]
Abstract
Overt diabetic gastroparesis is a rare long-term complication of diabetes, probably resulting from autonomic neuropathy of vagus nerve. It is now clear that neural damage plays a pivotal role in the pathogenesis of the disease. Some studies showed high basal gastrin levels in patients with diabetic gastroparesis, but the clinical meaning of this observation is still unclear. We report the case of a young woman with Insulin Dependent Diabetes Mellitus (IDDM) who was referred to evaluate nausea and vomiting associated to ketoacidosis. Our hypothesis of autonomic neuropathy with gastroparesis was confirmed. We observed a progressive increase in fasting gastrin concentration (20-fold normal values) in the absence of any clinical and laboratory signs of Zollinger-Ellison (ZE) syndrome. The increasing vomiting induced a severe state of cachexia, which required total parenteral nutrition for a long period. All therapeutic approaches were unsuccessful, and the patient rapidly died, suggesting a possible link between the severity of the clinical picture and the gastrin plasma levels.
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Affiliation(s)
- M Carantoni
- Dipartimento di Medicina Clinical e Sperimentale, Università degli Studi di Ferrara, Italy
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16
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Baydoun R, Dunbar JC. Impaired insulin but normal pentagastrin effect on gastric acid secretion in diabetic rats: a role for nitric oxide. Diabetes Res Clin Pract 1997; 38:1-8. [PMID: 9347240 DOI: 10.1016/s0168-8227(97)00087-9] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
Significant changes in gastrointestinal function, decreased gastric secretion and motility in particular, are often observed in patients with chronic diabetes. The mechanisms leading to those remain unclear. In these studies we evaluated the gastric acid secretory response to insulin and pentagastrin in normal Wistar and streptozotocin diabetic rats. We also sought to determine the role of nitric oxide (NO) in this process. The animals were anesthetized with sodium pentobarbital. Warm saline was perfused through a polyethylene tube placed in the oesophagus and collected from the duodenum at 10 min intervals. Following a 50 min equilibration period, a bolus intra-jugular infusion of insulin (4.0 U/kg), 2-deoxyglucose (200 mg/kg) or pentagastrin 4.0 (ug/kg) was started and samples of the gastrointestinal perfusate were collected for an additional 80 min. Insulin-stimulated acid secretion peaked 60 min after bolus infusion in normal animals; a response that was significantly decreased in the diabetic rats. Similarly, 2-deoxyglucose-induced glucopenia increased gastric acid secretion to a lower extent in diabetic versus normal rats. The stimulatory response to pentagastrin was prompt and essentially equal in normal and diabetic animals. However, when hypoglycemia was prevented by glucose infusion, insulin did not stimulate gastric acid secretion in normal rats. Further, glucose infusion in these animals actually enhanced the secretory response to pentagastrin. Nitro-L-arginine methyl ester (L-NAME 20 mg/kg i.v.), an inhibitor of NO synthetase, also prevented the secretory response to insulin but not to pentagastrin. Preinfusion of arginine (100 mg/kg i.v.) in diabetic rats restored the gastric secretory response to insulin toward that of normal animals. We conclude that the gastric acid secretory response to insulin, but not to pentagastrin, is decreased in diabetic animals, that this response may operate through a NO mediated mechanism possibly set in motion by central nervous system glucopenia and that this NO-mediated mechanism is attenuated in diabetes.
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Affiliation(s)
- R Baydoun
- Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201, USA
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17
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Abstract
Gastrointestinal motility is closely linked to the rate at which nutrients become systemically available. Regulation of gastric emptying represents the most important brake against delivery of nutrients to the intestine in excess of digestive and absorptive capacity. In man, gastric emptying is slowed in proportion to the energy density of the meal, which will level out the rate of energy delivery to the duodenum. Studies suggest a more rapid gastric emptying in obesity, although the opposite has been reported in some experimental settings. Moreover, gastric volume is larger in obese individuals and appropriate satiety signals are not triggered in response to gastric distension. Postprandial intestinal transit time in obesity is similar to that in normal-weight subjects, however, despite this fact, intestinal absorption of nutrients is more efficient in obesity. Several regulatory mechanisms for gastrointestinal motility, such as the autonomous and enteric nervous systems and gastrointestinal regulatory peptides, are also of importance for feeding behaviour and metabolism. Dysfunction of the autonomous nervous system has been observed, the sensitivity to cholecystokinin is decreased in obesity, and plasma concentrations of somatostatin and neurotensin are lower than in normal-weight subjects. These changes in regulatory mechanisms favour rapid gastrointestinal transit of ingested nutrients and promote rapid intestinal absorption in obesity and decreased satiety in response to ingested food. It is presently not known whether the observed changes in gastrointestinal motility in obesity represent a primary feature linked to the pathogenesis of such disease.
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Affiliation(s)
- O Wisén
- Department of Internal Medicine, Karolinska Hospital, Stockholm, Sweden
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18
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Kinsley BT, Gramm HF, Rolla AR. Diabetic gastroparesis: a review. THE JOURNAL OF DIABETIC COMPLICATIONS 1991; 5:207-17. [PMID: 1779016 DOI: 10.1016/0891-6632(91)90078-4] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/28/2022]
Affiliation(s)
- B T Kinsley
- Department of Medicine, New England Deaconess Hospital, Boston, Massachussetts 02215
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19
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Abstract
Orocecal transit time was assessed with lactulose hydrogen breath test in 12 obese patients during intravenous infusion of placebo or naloxone 40 micrograms/kg/hr given in randomized order and in double-blind conditions. Transit time was also evaluated in 22 healthy controls. Orocecal transit was significantly (P less than 0.01) longer in the obese patients, during placebo treatment (median 130, range 100-200 min) than in the healthy controls (median 75, range 40-170 min). Compared with placebo, transit time in the obese subjects was delayed (P less than 0.05) during naloxone treatment (median 150, range 100-230 min).
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Affiliation(s)
- G Basilisco
- Cattedra di Patologia Medica III, Istituto di Scienze Mediche, Milano, Italy
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20
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Horowitz M, Harding PE, Maddox AF, Wishart JM, Akkermans LM, Chatterton BE, Shearman DJ. Gastric and oesophageal emptying in patients with type 2 (non-insulin-dependent) diabetes mellitus. Diabetologia 1989; 32:151-159. [PMID: 2753246 DOI: 10.1007/bf00265086] [Citation(s) in RCA: 273] [Impact Index Per Article: 7.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
Gastric emptying of a digestible solid and liquid meal and oesophageal emptying of a solid bolus were measured with scintigraphic techniques in 20 randomly selected Type 2 (non-insulin-dependent) diabetic patients receiving oral hypoglycaemic therapy and 20 control subjects. In the diabetic patients, the relationships between oesophageal emptying, gastric emptying, gastrointestinal symptoms, autonomic nerve function and glycaemic control were examined. The percentage of the solid meal remaining in the stomach at 100 min (p less than 0.001), the 50% gastric emptying time for the liquid meal (p less than 0.05) and oesophageal emptying (p less than 0.05) were slower in the diabetic patients compared to the control subjects. Scores for upper gastrointestinal symptoms and autonomic nerve dysfunction did not correlate significantly (p greater than 0.05) with oesophageal, or gastric emptying. The 50% gastric emptying time for the liquid meal was positively related (r = 0.58, p less than 0.01) to the plasma glucose concentration at the time of the performance of the gastric emptying test and the lag period, before any solid food emptied from the stomach, was longer (p less than 0.05) in subjects with plasma glucose concentrations during the gastric emptying measurement greater than the median, compared to those with glucose concentrations below the median. These results indicate that delayed gastric and oesophageal emptying occur frequently in Type 2 diabetes mellitus and that delayed gastric emptying relates, at least in part, to plasma glucose concentrations.
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Affiliation(s)
- M Horowitz
- Department of Medicine, University of Adelaide, South Australia
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21
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Pederson RA, Campos RV, Chan CB, Buchan AM, Wheeler MB, Brown JC. Gastrin release in obese Zucker rats. REGULATORY PEPTIDES 1989; 24:131-42. [PMID: 2564209 DOI: 10.1016/0167-0115(89)90232-2] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/01/2023]
Abstract
In this study, gastrin release in the obese Zucker rat was investigated by in vivo and in vitro experiments. Obese rats exhibited normal plasma gastrin levels at 3 weeks (preobese), were moderately hypergastrinemic at 3 months and severely hypergastrinemic at 5 months, compared to lean littermates. Following oral peptone, plasma gastrin levels doubled in both lean and obese rats. Basal and vagally stimulated gastrin release from perfused stomachs was greater in obese compared to lean rats and atropine had no effect on basal gastrin release in either group. Basal somatostatin release from the perfused stomach was found not to differ in both groups of animals. Morphological studies revealed an increase in the number of gastrin-containing G-cells in adult obese rats compared to lean littermates, but not in 3-week-old pups compared to lean littermates, indicating a strong correlation between cell number and plasma gastrin levels. These data indicate that the obese Zucker rat exhibits fasting hypergastrinemia in vivo, a condition which appears after weaning and increases in severity with age. Gastrin hypersecretion persists from the vascularly perfused stomach preparation. The basal hypergastrinemia of the obese Zucker rat is independent of a hyperactive postganglionic cholinergic drive but is associated with and probably causally related to an increase in antral G-cell numbers.
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Affiliation(s)
- R A Pederson
- Department of Physiology, University of British Columbia, Vancouver, Canada
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22
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Gulliford MC, Bicknell EJ, Scarpello JH. Evaluation of gastrin secretion in diabetic subjects with normal or abnormal cardiovascular autonomic function tests. ACTA DIABETOLOGICA LATINA 1988; 25:275-82. [PMID: 3245389 DOI: 10.1007/bf02581125] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/04/2023]
Abstract
The serum gastrin response to a meat extract drink was measured in 16 non-diabetic subjects, in 40 diabetic subjects and 9 patients with positive tests for gastric parietal cell antibodies. Standard cardiovascular autonomic function tests were also performed in diabetic subjects. The test drink produced a highly significant rise in the serum gastrin concentration (p less than 0.001). Diabetic subjects with normal cardiovascular autonomic function tests had slightly lower stimulated gastrin concentrations than non-diabetic subjects. In diabetic subjects with abnormal cardiovascular autonomic function tests the distribution of gastrin concentrations after the test drink was bimodal. Eleven out of 20 had 45-min gastrin concentrations greater than 120 pg/ml, compared with 2 out of 20 diabetics with normal cardiovascular autonomic function tests and 1 out of 16 non-diabetic subjects (p less than 0.001). Much higher gastrin responses were found in 5 out of 9 patients with positive tests for gastric parietal cell antibodies. An increased gastrin response may be found in patients with abnormal autonomic function but its value as a marker is limited by the small amplitude of the change and by the significant prevalence of atrophic gastritis, in which much higher gastrin responses may be found.
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Affiliation(s)
- M C Gulliford
- Department of Endocrinology and Diabetes Mellitus, North Staffordshire Royal Infirmary, Stoke-on-Trent, U.K
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Abstract
Diabetic neuropathy is a common complication of diabetes that may be associated both with considerable morbidity (painful polyneuropathy, neuropathic ulceration) and mortality (autonomic neuropathy). The epidemiology and natural history of diabetic neuropathy is clouded with uncertainty, largely due to confusion in the definition and measurement of this disorder. We have reviewed a variety of the clinical manifestations associated with somatic and autonomic neuropathy and discussed current views related to the management of the different abnormalities. Although unproven, the best evidence suggests that near normal control of blood glucose in the early years following onset of diabetes may help delay the development of clinically significant nerve impairment. Intensive therapy to achieve normalization of blood glucose may also lead to reversibility of early diabetic neuropathy, but again this is unproven. Our ability to manage successfully the many different manifestations of diabetic neuropathy depends ultimately on our success in uncovering the pathogenic processes underlying this disorder. The recent resurgence of interest in the vascular hypothesis, for example, has opened up new avenues of investigation for therapeutic intervention. Paralleling our increased understanding of the pathogenesis of diabetic neuropathy, there must be refinements in our ability to measure quantitatively the different types of defects that occur in this disorder. These tests must be validated and standardized to allow comparability between studies and more meaningful interpretation of study results.
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Affiliation(s)
- A Vinik
- Department of Internal Medicine, School of Public Health, University of Michigan, Ann Arbor 48109
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Ewing DJ, Clarke BF. Autonomic neuropathy: its diagnosis and prognosis. CLINICS IN ENDOCRINOLOGY AND METABOLISM 1986; 15:855-88. [PMID: 3536203 DOI: 10.1016/s0300-595x(86)80078-0] [Citation(s) in RCA: 150] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/06/2023]
Abstract
Autonomic neuropathy is now well established as a relatively common and significant complication of diabetes mellitus. Its importance has been clarified in recent years during which the extent of autonomic control over all areas of body function has been defined. Using simple cardiovascular reflex tests, autonomic abnormalities can be demonstrated without any corresponding symptoms. The often stated concept of 'patchy' involvement in diabetic autonomic neuropathy should now be rejected as too should the view that autonomic neuropathy is either 'present' or 'absent' based on a single test result. When generalized and predominantly metabolic disturbances, as in diabetes, give rise to impaired nerve function, autonomic as well as somatic components of the nerve are affected. Where damage is severe this leads to the characteristic florid picture of symptomatic autonomic neuropathy with its particularly poor prognosis. For the physician in a busy clinic, much of the theoretical and experimental basis for autonomic neuropathy may not appear of direct relevance. However, he has now to be aware of the clinical implications of autonomic damage in the diabetic. This may have particular relevance in the care of the diabetic foot (see Chapter 10), the recognition of many of the vague symptoms associated with autonomic damage, the treatment of disabling features such as postural dizziness and nocturnal diarrhoea, and an awareness of the poor prognosis associated with symptomatic autonomic neuropathy. He will also need to be alert to the dangers of general anaesthesia in such patients, and the possibility of sudden unexpected deaths. Diabetic autonomic neuropathy causes widespread abnormalities, some of which are clinically apparent, some of which can be detected by sensitive tests, and others which have yet to be discovered. Inclusion of the neuropeptides and other hormones within the compass of autonomic control has opened up a whole new area of investigative interest, with many complex interrelationships which still need to be unravelled. This should lead to better understanding of the pathophysiological processes that cause damage to diabetic nerves. With so much research effort directed towards better glycaemic control and aldose reductase inhibitors (see Chapter 8), it may eventually be possible to reverse or prevent this potentially disabling and lethal complication of diabetes.
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Meryn S, Stein D, Straus EW. Fasting- and meal-stimulated peptide hormone concentrations before and after gastric surgery for morbid obesity. Metabolism 1986; 35:798-802. [PMID: 3528741 DOI: 10.1016/0026-0495(86)90218-0] [Citation(s) in RCA: 18] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/06/2023]
Abstract
The influence of morbid obesity and of gastric surgery operation in circulating peptide hormone concentrations was studied in 26 patients. Plasma hormone levels were determined in the fasting state and after a standardized test meal before and six to nine months after gastric surgery. Before surgery fasting and postprandial blood glucose and hormone levels did not significantly differ in morbidly obese subjects from those in obese or normal subjects, except that in morbidly obese subjects, postprandial gastrin concentration remained at peak levels and did not return to fasting levels 120 minutes after the test meal. An average weight loss of 92 lb following the gastric surgery operation was accompanied by a decrease of fasting glucose and insulin levels and a decreased postprandial insulin response. There were no significant differences in plasma levels of pancreatic glucagon, of pancreatic polypeptide in the basal state, or of pancreatic glucagon after the test meal between the preoperative and postoperative groups. As compared to preoperative values, fasting gastrin levels decreased after surgery, the postprandial release of gastrin was virtually absent, and that of pancreatic polypeptide reduced. The significance of altered postprandial pancreatic polypeptide response and of the reversal of prolonged postprandial hypergastrinemia to a state of low circulating gastrin levels following gastric surgery on gastrointestinal secretion and mucosa remain to be determined.
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Ikeda T, Mokuda O, Kuno S, Tokumori Y, Tominaga M, Mashiba H. Enhanced intestinal insulinotropic effect in streptozotocin-diabetic rats. THE AMERICAN JOURNAL OF PHYSIOLOGY 1985; 248:E304-8. [PMID: 3883801 DOI: 10.1152/ajpendo.1985.248.3.e304] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/07/2023]
Abstract
To study the intestinal insulinotropic effects in the diabetic state, an investigation was made into the release of insulin from isolated rat pancreas perfused with portal venous effluent (PVE) obtained from the isolated perfused intestine of streptozotocin-induced diabetic rats. Rat intestine was perfused with Krebs-Ringer bicarbonate medium for 1 h, and the PVE was collected from both untreated and glucose-treated intestines of control and diabetic rats. The PVE, after adjusting its glucose concentration to the desired level, was used as the perfusing medium for the pancreas of a different rat. Glucose concentration in the perfusion medium was maintained at 5.5 mM for 20 min and at 16.7 mM for the next 30 min. Insulin output from pancreas perfused with PVE from untreated intestine of diabetic rats (252 +/- 45 ng/30 min, mean +/- SD) was similar to that of controls (269 +/- 72 ng/30 min). Pancreatic insulin output with PVE from glucose-treated intestine of diabetic rats (579 +/- 100 ng/30 min) was significantly greater compared with either that using PVE from untreated intestine of diabetic rats (P less than 0.01) or that from glucose-treated intestine of control rats (368 +/- 57 ng/30 min) (P less than 0.02). These results indicate that the insulinotropic effect is markedly enhanced in streptozotocin-induced diabetic rats.
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