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Prasad GVR, Bhamidi V. Managing cardiovascular disease risk in South Asian kidney transplant recipients. World J Transplant 2021; 11:147-160. [PMID: 34164291 PMCID: PMC8218347 DOI: 10.5500/wjt.v11.i6.147] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/26/2021] [Revised: 04/12/2021] [Accepted: 05/22/2021] [Indexed: 02/06/2023] Open
Abstract
South Asians (SA) are at higher cardiovascular risk than other ethnic groups, and SA kidney transplant recipients (SA KTR) are no exception. SA KTR experience increased major adverse cardiovascular events both early and late post-transplantation. Cardiovascular risk management should therefore begin well before transplantation. SA candidates may require aggressive screening for pre-transplant cardiovascular disease (CVD) due to their ethnicity and comorbidities. Recording SA ethnicity during the pre-transplant evaluation may enable programs to better assess cardiovascular risk, thus allowing for earlier targeted peri- and post-transplant intervention to improve cardiovascular outcomes. Diabetes remains the most prominent post-transplant cardiovascular risk factor in SA KTR. Diabetes also clusters with other metabolic syndrome components including lower high-density lipoprotein cholesterol, higher triglycerides, hypertension, and central obesity in this population. Dyslipidemia, metabolic syndrome, and obesity are all significant CVD risk factors in SA KTR, and contribute to increased insulin resistance. Novel biomarkers such as adiponectin, apolipoprotein B, and lipoprotein (a) may be especially important to study in SA KTR. Focused interventions to improve health behaviors involving diet and exercise may especially benefit SA KTR. However, there are few interventional clinical trials specific to the SA population, and none are specific to SA KTR. In all cases, understanding the nuances of managing SA KTR as a distinct post-transplant group, while still screening for and managing each CVD risk factor individually in all patients may help improve the long-term success of all kidney transplant programs catering to multi-ethnic populations.
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Affiliation(s)
- G V Ramesh Prasad
- Kidney Transplant Program, St. Michael's Hospital, Toronto M5C 2T2, ON, Canada
| | - Vaishnavi Bhamidi
- Kidney Transplant Program, St. Michael's Hospital, Toronto M5C 2T2, ON, Canada
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Roy A, Kamalanathan S, Sahoo J, Kar SS, Naik D, Narayanan N, Merugu C, Patel D. Comparison of islet cell function, insulin sensitivity, and incretin axis between Asian-Indians with either impaired fasting glucose or impaired glucose tolerance, and normal healthy controls. Diabetes Res Clin Pract 2021; 176:108846. [PMID: 33951481 DOI: 10.1016/j.diabres.2021.108846] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/07/2021] [Revised: 04/24/2021] [Accepted: 04/28/2021] [Indexed: 01/06/2023]
Abstract
AIMS The objective of this study was to compare the islet cell function, insulin sensitivity, and incretin axis between Asian-Indian subjects with either impaired fasting glucose (IFG), or impaired glucose tolerance (IGT), and normal glucose tolerance (NGT). MATERIALS AND METHODS Prediabetes subjects underwent a mixed meal tolerance test(MMTT) after overnight fasting. Samples for glucose, insulin, glucagon, and glucagon-like peptide-1 (GLP-1) were collected at 0, 30, 60, and 120 min. Insulin secretion sensitivity index -2 (ISSI-2) for beta-cell function and Matsuda index for insulin sensitivity were assessed. Alpha cell function was assessed by measuring the area under the curve (AUC) 0-120 glucagon/AUC0-120 glucose. RESULTS A total of sixty subjects were recruited with 20 in each group. The beta-cell function represented by ISSI-2 was impaired in prediabetes subjects as compared to NGT group (IFG: 2.09 ± 0.44 vs. NGT: 3.04 ± 0.80, P < 0.0001, and IGT: 2.33 ± 0.59 vs. NGT: 3.04 ± 0.80, P = 0.002). Similarly, AUC0-120 glucagon/AUC0-120 glucose was also lower in prediabetes group as compared to healthy controls (IFG: 0.41(0.54) vs. NGT: 1.07(0.39), P = 0.003 and IGT: 0.57(0.38) vs. NGT: 1.07(0.39), P = 0.001). CONCLUSION Asian-Indian prediabetes subjects have reduced beta-cell function with lesser glucagon secretion during MMTT as compared to normal healthy controls.
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Affiliation(s)
- Ayan Roy
- Department of Endocrinology, Jawaharlal Institute of Post Graduate Medical Education and Research (JIPMER), Puducherry, India; Department of Endocrinology and Metabolism, All India Institute of Medical Sciences, Jodhpur, Rajasthan, 342005, India
| | - Sadishkumar Kamalanathan
- Department of Endocrinology, Jawaharlal Institute of Post Graduate Medical Education and Research (JIPMER), Puducherry, India
| | - Jayaprakash Sahoo
- Department of Endocrinology, Jawaharlal Institute of Post Graduate Medical Education and Research (JIPMER), Puducherry, India.
| | - Sitanshu Sekhar Kar
- Department of Preventive and Social Medicine, Jawaharlal Institute of Post Graduate Medical Education and Research (JIPMER), Puducherry, India
| | - Dukhabandhu Naik
- Department of Endocrinology, Jawaharlal Institute of Post Graduate Medical Education and Research (JIPMER), Puducherry, India
| | - Niya Narayanan
- Department of Endocrinology, Jawaharlal Institute of Post Graduate Medical Education and Research (JIPMER), Puducherry, India
| | - Chandhana Merugu
- Department of Endocrinology, Jawaharlal Institute of Post Graduate Medical Education and Research (JIPMER), Puducherry, India
| | - Deepika Patel
- Department of Endocrinology, Jawaharlal Institute of Post Graduate Medical Education and Research (JIPMER), Puducherry, India
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PrayGod G, Filteau S, Range N, Kitilya B, Kavishe BB, Ramaiya K, Jeremiah K, Rehman AM, Changalucha J, Olsen MF, Andersen AB, Friis H, Krogh-Madsen R, Faurholt-Jepsen D. β-cell dysfunction and insulin resistance in relation to pre-diabetes and diabetes among adults in north-western Tanzania: a cross-sectional study. Trop Med Int Health 2021; 26:435-443. [PMID: 33406288 DOI: 10.1111/tmi.13545] [Citation(s) in RCA: 11] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/26/2022]
Abstract
OBJECTIVE Studies on phenotypes of diabetes in Africa are inconsistent. We assessed the role of β-cell dysfunction and insulin resistance on pre-diabetes and diabetes. METHODS We included 1890 participants with mean age of 40.6 (SD11.9) years in a cross-sectional study among male and female adults in Tanzania during 2016 to 2017. Data on C-reactive protein (CRP), alpha-acid glycoprotein (AGP), HIV, oral glucose tolerance test (OGTT), body composition and insulin were collected. Insulinogenic index and HOMA-IR were used to derive an overall marker of β-cell dysfunction and insulin resistance which was categorised as follows: normal β-cell function and insulin sensitivity, isolated β-cell dysfunction, isolated insulin resistance, and combined β-cell dysfunction and insulin resistance. Pre-diabetes and diabetes were defined as 2-hour OGTT glucose between 7.8-11.0 and ≥ 11.1 mmol/L, respectively. Multinomial regression assessed the association of β-cell dysfunction and insulin resistance with outcome measures. RESULTS β-cell dysfunction, insulin resistance, and combined β-cell dysfunction and insulin resistance were associated with higher pre-diabetes risk. Similarly, isolated β-cell dysfunction (adjusted relative risk ratio (aRRR) 4.8 (95% confidence interval (CI) 2.5, 9.0), isolated insulin resistance (aRRR 3.2 (95% CI 1.5, 6.9), and combined β-cell dysfunction and insulin resistance (aRRR 35.9 (95% CI 17.2, 75.2) were associated with higher diabetes risk. CRP, AGP and HIV were associated with higher diabetes risk, but fat mass was not. 31%, 10% and 33% of diabetes cases were attributed to β-cell dysfunction, insulin resistance, and combined β-cell dysfunction and insulin resistance, respectively. CONCLUSIONS β-cell dysfunction seemed to explain most of diabetes cases compared to insulin resistance in this population. Cohort studies on evolution of diabetes in Africa are needed to confirm these results.
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Affiliation(s)
- George PrayGod
- Mwanza Research Centre, National Institute for Medical Research, Mwanza, Tanzania
| | - Suzanne Filteau
- Faculty of Epidemiology and Population Health, London School of Hygiene & Tropical Medicine, London, UK
| | - Nyagosya Range
- Muhimbili Research Centre, National Institute for Medical Research, Dar es Saalam, Tanzania
| | - Brenda Kitilya
- Mwanza Research Centre, National Institute for Medical Research, Mwanza, Tanzania
| | - Bazil B Kavishe
- Mwanza Research Centre, National Institute for Medical Research, Mwanza, Tanzania
| | | | - Kidola Jeremiah
- Mwanza Research Centre, National Institute for Medical Research, Mwanza, Tanzania
| | - Andrea M Rehman
- Faculty of Epidemiology and Population Health, London School of Hygiene & Tropical Medicine, London, UK
| | - John Changalucha
- Mwanza Research Centre, National Institute for Medical Research, Mwanza, Tanzania
| | - Mette Frahm Olsen
- Department of Nutrition, Exercise and Sports, University of Copenhagen, Copenhagen, Denmark
| | | | - Henrik Friis
- Department of Nutrition, Exercise and Sports, University of Copenhagen, Copenhagen, Denmark
| | - Rikke Krogh-Madsen
- Centre of Inflammation and Metabolism and Centre for Physical Activity Research, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
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Mehta A, Singh S, Saeed A, Mahtta D, Bittner VA, Sperling LS, Virani SS. Pathophysiological Mechanisms Underlying Excess Risk for Diabetes and Cardiovascular Disease in South Asians: The Perfect Storm. Curr Diabetes Rev 2021; 17:e070320183447. [PMID: 32619174 DOI: 10.2174/1573399816666200703182458] [Citation(s) in RCA: 7] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/24/2020] [Revised: 05/14/2020] [Accepted: 05/15/2020] [Indexed: 01/09/2023]
Abstract
BACKGROUND South Asians are at a significantly increased risk of type 2 diabetes (T2D) and cardiovascular disease (CVD), are diagnosed at relatively younger ages, and exhibit more severe disease phenotypes as compared with other ethnic groups. The pathophysiological mechanisms underlying T2D and CVD risk in South Asians are multifactorial and intricately related. METHODS A narrative review of the pathophysiology of excess risk of T2D and CVD in South Asians. RESULTS T2D and CVD have shared risk factors that encompass biological factors (early life influences, impaired glucose metabolism, and adverse body composition) as well as behavioral and environmental risk factors (diet, sedentary behavior, tobacco use, and social determinants of health). Genetics and epigenetics also play a role in explaining the increased risk of T2D and CVD among South Asians. Additionally, South Asians harbor several lipid abnormalities including high concentration of small-dense low-density lipoprotein (LDL) particles, elevated triglycerides, low high-density lipoprotein (HDL)- cholesterol levels, dysfunctional HDL particles, and elevated lipoprotein(a) that predispose them to CVD. CONCLUSION In this comprehensive review, we have discussed risk factors that provide insights into the pathophysiology of excess risk of T2D and CVD in South Asians.
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Affiliation(s)
- Anurag Mehta
- Division of Cardiology, Department of Medicine, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine, Atlanta, GA, Georgia
| | - Sumitabh Singh
- Division of Endocrinology, Department of Medicine, Mayo Clinic, Rochester, Minnesota, United States
| | - Anum Saeed
- Division of Cardiology, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, PA, United States
| | - Dhruv Mahtta
- Health Policy, Quality & Informatics Program, Michael E. DeBakey Veterans Affairs Medical Center Health Services Research and Development Center for Innovations, Section of Cardiovascular Research, Department of Medicine, Baylor College of Medicine, Houston, Texas, TX, United States
| | - Vera A Bittner
- Division of Cardiovascular Medicine, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, United States
| | - Laurence S Sperling
- Division of Cardiology, Department of Medicine, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine, Atlanta, GA, Georgia
| | - Salim S Virani
- Health Policy, Quality & Informatics Program, Michael E. DeBakey Veterans Affairs Medical Center Health Services Research and Development Center for Innovations, Section of Cardiovascular Research, Department of Medicine, Baylor College of Medicine, Houston, Texas, TX, United States
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Bainey KR, Gupta M, Ali I, Bangalore S, Chiu M, Kaila K, Kaul P, Khan N, King-Shier KM, Palaniappan L, Pare G, Ramanathan K, Ross S, Shah BR. The Burden of Atherosclerotic Cardiovascular Disease in South Asians Residing in Canada: A Reflection From the South Asian Heart Alliance. CJC Open 2019; 1:271-281. [PMID: 32159121 PMCID: PMC7063609 DOI: 10.1016/j.cjco.2019.09.004] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/12/2019] [Accepted: 09/25/2019] [Indexed: 12/15/2022] Open
Abstract
South Asians (SAs), originating from the Indian subcontinent (India, Pakistan, Sri Lanka, Bangladesh, Nepal, and Bhutan), represent one quarter of the global population and are the largest visible minority in Canada. SAs experience the highest rates of coronary artery disease in Canada. Although conventional cardiovascular risk factors remain predictive in SA, the excess risk is not fully explained by these risk factors alone. Abdominal obesity, metabolic syndrome, and insulin resistance likely contribute a greater risk in SAs than in other populations. The South Asian Heart Alliance has been recently formed to investigate and recommend the best strategies for the prevention of cardiometabolic disease in SAs in Canada. This topic review represents a comprehensive overview of the magnitude of cardiovascular disease in SAs in Canada, with a review of conventional and novel risk markers in the SA population. Both primary and secondary prevention strategies are suggested and when possible, adapted specifically for the SA population. The need for SAs and their healthcare professionals to be more aware of the problem and potential solutions, along with the need for population-specific research, is highlighted.
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Affiliation(s)
- Kevin R. Bainey
- Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada
- Corresponding author: Dr Kevin R. Bainey, Mazankowski Alberta Heart Institute, University of Alberta, 2C2.12 WMC, 8440 112 St, Edmonton, Alberta T6G 2B7, Canada. Tel.: +1-780-407-2176; fax: +1-780-4076452.
| | - Milan Gupta
- Department of Medicine, McMaster University, Hamilton, and Canadian Collaborative Research Network, Brampton, Ontario, Canada
| | - Imtiaz Ali
- Department of Cardiac Sciences, Division of Cardiac Surgery, University of Calgary, Calgary, Alberta, Canada
| | - Sripal Bangalore
- Division of Cardiology, Department of Medicine, New York University School of Medicine, New York, New York, USA
| | - Maria Chiu
- Institute of Health Policy, Management and Evaluation, University of Toronto, Toronto, Ontario
| | - Kendeep Kaila
- Division of Cardiology, Department of Medicine, University of British Columbia, Vancouver, British Columbia, Canada
| | - Padma Kaul
- Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada
| | - Nadia Khan
- Nursing and Community Health Sciences, University of Calgary, Calgary, Canada
| | | | - Latha Palaniappan
- Division of Primary Care and Population Health, Department of Medicine, Stanford University School of Medicine, Stanford, California, USA
| | - Guillaume Pare
- Department of Pathology and Molecular Medicine, Department of Clinical Epidemiology and Biostatistics, Population Health Research Institute and Thrombosis and Atherosclerosis Research Institute, Hamilton Health Sciences, McMaster University, Hamilton, Ontario, Canada
| | - Krish Ramanathan
- Division of Cardiology, Department of Medicine, University of British Columbia, Vancouver, British Columbia, Canada
| | - Stephanie Ross
- Department of Health Research Methods, Evidence, and Impact, McMaster University, Hamilton, Ontario, Canada
| | - Baiju R. Shah
- Division of Endocrinology, University of Toronto, Toronto, Ontario, Canada
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Palaniappan L, Garg A, Enas E, Lewis H, Bari S, Gulati M, Flores C, Mathur A, Molina C, Narula J, Rahman S, Leng J, Gany F. South Asian Cardiovascular Disease & Cancer Risk: Genetics & Pathophysiology. J Community Health 2018; 43:1100-1114. [PMID: 29948525 PMCID: PMC6777562 DOI: 10.1007/s10900-018-0527-8] [Citation(s) in RCA: 20] [Impact Index Per Article: 2.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]
Abstract
South Asians (SAs) are at heightened risk for cardiovascular disease as compared to other ethnic groups, facing premature and more severe coronary artery disease, and decreased insulin sensitivity. This disease burden can only be partially explained by conventional risk factors, suggesting the need for a specific cardiovascular risk profile for SAs. Current research, as explored through a comprehensive literature review, suggests the existence of population specific genetic risk factors such as lipoprotein(a), as well as population specific gene modulating factors. This review catalogues the available research on cardiovascular disease and genetics, anthropometry, and pathophysiology, and cancer genetics among SAs, with a geographical focus on the U.S. A tailored risk profile will hinge upon population customized classification and treatment guidelines, informed by continued research.
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Affiliation(s)
| | - Arun Garg
- Laboratory Medicine and Pathology, Fraser Health Authority, New Westminster, BC, Canada
| | - Enas Enas
- Coronary Artery Disease among Asian Indians (CADI) Research Foundation, Lisle, IL, USA
| | - Henrietta Lewis
- Rollins School of Public Health, Global Epidemiology, Emory University, Atlanta, GA, USA
| | | | - Martha Gulati
- Division of Cardiology, University of Arizona College of Medicine, Phoenix, AZ, USA
| | - Cristina Flores
- The Warren Alpert Medical School, The Brown Human Rights Asylum Clinic (BHRAC), Brown University, Providence, RI, USA
| | - Ashish Mathur
- South Asian Heart Center, El Camino Hospital, Mountain View, CA, USA
| | - Cesar Molina
- South Asian Heart Center, El Camino Hospital, Mountain View, CA, USA
| | | | - Shahid Rahman
- I-Say, Bangladeshi American Youth Association, Teach & Travel, New York, NY, USA
| | - Jennifer Leng
- Immigrant Health and Cancer Disparities Center, Department of Psychiatry and Behavioral Sciences, Memorial Sloan Kettering Cancer Center, New York, NY, USA
- Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA
- Department of Healthcare Policy and Research, Weill Cornell Medical College, New York, NY, USA
| | - Francesca Gany
- Immigrant Health and Cancer Disparities Center, Department of Psychiatry and Behavioral Sciences, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
- Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
- Department of Healthcare Policy and Research, Weill Cornell Medical College, New York, NY, USA.
- Department of Medicine, Weill Cornell Medical College, New York, NY, USA.
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Richter B, Hemmingsen B, Metzendorf M, Takwoingi Y, Cochrane Metabolic and Endocrine Disorders Group. Development of type 2 diabetes mellitus in people with intermediate hyperglycaemia. Cochrane Database Syst Rev 2018; 10:CD012661. [PMID: 30371961 PMCID: PMC6516891 DOI: 10.1002/14651858.cd012661.pub2] [Citation(s) in RCA: 91] [Impact Index Per Article: 13.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
BACKGROUND Intermediate hyperglycaemia (IH) is characterised by one or more measurements of elevated blood glucose concentrations, such as impaired fasting glucose (IFG), impaired glucose tolerance (IGT) and elevated glycosylated haemoglobin A1c (HbA1c). These levels are higher than normal but below the diagnostic threshold for type 2 diabetes mellitus (T2DM). The reduced threshold of 5.6 mmol/L (100 mg/dL) fasting plasma glucose (FPG) for defining IFG, introduced by the American Diabetes Association (ADA) in 2003, substantially increased the prevalence of IFG. Likewise, the lowering of the HbA1c threshold from 6.0% to 5.7% by the ADA in 2010 could potentially have significant medical, public health and socioeconomic impacts. OBJECTIVES To assess the overall prognosis of people with IH for developing T2DM, regression from IH to normoglycaemia and the difference in T2DM incidence in people with IH versus people with normoglycaemia. SEARCH METHODS We searched MEDLINE, Embase, ClincialTrials.gov and the International Clinical Trials Registry Platform (ICTRP) Search Portal up to December 2016 and updated the MEDLINE search in February 2018. We used several complementary search methods in addition to a Boolean search based on analytical text mining. SELECTION CRITERIA We included prospective cohort studies investigating the development of T2DM in people with IH. We used standard definitions of IH as described by the ADA or World Health Organization (WHO). We excluded intervention trials and studies on cohorts with additional comorbidities at baseline, studies with missing data on the transition from IH to T2DM, and studies where T2DM incidence was evaluated by documents or self-report only. DATA COLLECTION AND ANALYSIS One review author extracted study characteristics, and a second author checked the extracted data. We used a tailored version of the Quality In Prognosis Studies (QUIPS) tool for assessing risk of bias. We pooled incidence and incidence rate ratios (IRR) using a random-effects model to account for between-study heterogeneity. To meta-analyse incidence data, we used a method for pooling proportions. For hazard ratios (HR) and odds ratios (OR) of IH versus normoglycaemia, reported with 95% confidence intervals (CI), we obtained standard errors from these CIs and performed random-effects meta-analyses using the generic inverse-variance method. We used multivariable HRs and the model with the greatest number of covariates. We evaluated the certainty of the evidence with an adapted version of the GRADE framework. MAIN RESULTS We included 103 prospective cohort studies. The studies mainly defined IH by IFG5.6 (FPG mmol/L 5.6 to 6.9 mmol/L or 100 mg/dL to 125 mg/dL), IFG6.1 (FPG 6.1 mmol/L to 6.9 mmol/L or 110 mg/dL to 125 mg/dL), IGT (plasma glucose 7.8 mmol/L to 11.1 mmol/L or 140 mg/dL to 199 mg/dL two hours after a 75 g glucose load on the oral glucose tolerance test, combined IFG and IGT (IFG/IGT), and elevated HbA1c (HbA1c5.7: HbA1c 5.7% to 6.4% or 39 mmol/mol to 46 mmol/mol; HbA1c6.0: HbA1c 6.0% to 6.4% or 42 mmol/mol to 46 mmol/mol). The follow-up period ranged from 1 to 24 years. Ninety-three studies evaluated the overall prognosis of people with IH measured by cumulative T2DM incidence, and 52 studies evaluated glycaemic status as a prognostic factor for T2DM by comparing a cohort with IH to a cohort with normoglycaemia. Participants were of Australian, European or North American origin in 41 studies; Latin American in 7; Asian or Middle Eastern in 50; and Islanders or American Indians in 5. Six studies included children and/or adolescents.Cumulative incidence of T2DM associated with IFG5.6, IFG6.1, IGT and the combination of IFG/IGT increased with length of follow-up. Cumulative incidence was highest with IFG/IGT, followed by IGT, IFG6.1 and IFG5.6. Limited data showed a higher T2DM incidence associated with HbA1c6.0 compared to HbA1c5.7. We rated the evidence for overall prognosis as of moderate certainty because of imprecision (wide CIs in most studies). In the 47 studies reporting restitution of normoglycaemia, regression ranged from 33% to 59% within one to five years follow-up, and from 17% to 42% for 6 to 11 years of follow-up (moderate-certainty evidence).Studies evaluating the prognostic effect of IH versus normoglycaemia reported different effect measures (HRs, IRRs and ORs). Overall, the effect measures all indicated an elevated risk of T2DM at 1 to 24 years of follow-up. Taking into account the long-term follow-up of cohort studies, estimation of HRs for time-dependent events like T2DM incidence appeared most reliable. The pooled HR and the number of studies and participants for different IH definitions as compared to normoglycaemia were: IFG5.6: HR 4.32 (95% CI 2.61 to 7.12), 8 studies, 9017 participants; IFG6.1: HR 5.47 (95% CI 3.50 to 8.54), 9 studies, 2818 participants; IGT: HR 3.61 (95% CI 2.31 to 5.64), 5 studies, 4010 participants; IFG and IGT: HR 6.90 (95% CI 4.15 to 11.45), 5 studies, 1038 participants; HbA1c5.7: HR 5.55 (95% CI 2.77 to 11.12), 4 studies, 5223 participants; HbA1c6.0: HR 10.10 (95% CI 3.59 to 28.43), 6 studies, 4532 participants. In subgroup analyses, there was no clear pattern of differences between geographic regions. We downgraded the evidence for the prognostic effect of IH versus normoglycaemia to low-certainty evidence due to study limitations because many studies did not adequately adjust for confounders. Imprecision and inconsistency required further downgrading due to wide 95% CIs and wide 95% prediction intervals (sometimes ranging from negative to positive prognostic factor to outcome associations), respectively.This evidence is up to date as of 26 February 2018. AUTHORS' CONCLUSIONS Overall prognosis of people with IH worsened over time. T2DM cumulative incidence generally increased over the course of follow-up but varied with IH definition. Regression from IH to normoglycaemia decreased over time but was observed even after 11 years of follow-up. The risk of developing T2DM when comparing IH with normoglycaemia at baseline varied by IH definition. Taking into consideration the uncertainty of the available evidence, as well as the fluctuating stages of normoglycaemia, IH and T2DM, which may transition from one stage to another in both directions even after years of follow-up, practitioners should be careful about the potential implications of any active intervention for people 'diagnosed' with IH.
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Affiliation(s)
- Bernd Richter
- Institute of General Practice, Medical Faculty of the Heinrich‐Heine‐University DüsseldorfCochrane Metabolic and Endocrine Disorders GroupPO Box 101007DüsseldorfGermany40001
| | - Bianca Hemmingsen
- Institute of General Practice, Medical Faculty of the Heinrich‐Heine‐University DüsseldorfCochrane Metabolic and Endocrine Disorders GroupPO Box 101007DüsseldorfGermany40001
| | - Maria‐Inti Metzendorf
- Institute of General Practice, Medical Faculty of the Heinrich‐Heine‐University DüsseldorfCochrane Metabolic and Endocrine Disorders GroupPO Box 101007DüsseldorfGermany40001
| | - Yemisi Takwoingi
- University of BirminghamInstitute of Applied Health ResearchEdgbastonBirminghamUKB15 2TT
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Abstract
PURPOSE OF REVIEW The purpose of this study was to review the epidemiology and pathogenesis of diabetes in Asian Indians with a particular focus on 'Asian Indian type 2 diabetes phenotype'. RECENT FINDINGS The prevalence of diabetes is rapidly increasing among Asian Indians, particularly in the past two decades. The diabetes rates in urban India now exceed that seen in Indians migrated to developed nations. Urbanization, changes from traditional healthier diets to high-refined carbohydrate intake, and sedentary lifestyle have contributed to this steep increase in the prevalence of diabetes in India. Type 2 diabetes among Asian Indians is characterized by onset at a younger age, greater abdominal obesity despite relatively lower BMI, greater insulin resistance, and early decline in beta cell function. Asian Indians are also at a higher risk for premature coronary artery disease. SUMMARY The clinical profile of type 2 diabetes in Asian Indians differs from Caucasians with higher central obesity, increased inflammatory markers such as high sensitive C-reactive protein, greater insulin resistance, early loss of beta cell function, and a higher risk of coronary artery disease. Mechanistic studies are needed to characterize the pathophysiology of the Asian Indian phenotype.
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Affiliation(s)
- Viral N Shah
- aBarbara Davis Center for Diabetes, University of Colorado Anschutz Campus, Aurora, Colorado, USA bMadras Diabetes Research Foundation and Dr Mohan's Diabetes Specialties Centre, Chennai, India *Viral N. Shah and Viswanathan Mohan contributed equally to the writing of this article
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Abstract
The rising prevalence of diabetes in South Asians has significant health and economic implications. South Asians are predisposed to the development of diabetes due to biologic causes which are exacerbated by lifestyle and environmental factors. Furthermore, they experience significant morbidity and mortality from complications of diabetes, most notably coronary artery disease, cerebrovascular disease, and chronic kidney disease. Therefore, understanding the pathophysiology and genetics of diabetes risk factors and its associated complications in South Asians is paramount to curbing the diabetes epidemic. With this understanding, the appropriate screening, preventative and therapeutic strategies can be implemented and further developed. In this review, we discuss in detail the biologic and lifestyle factors that predispose South Asians to diabetes and review the epidemiology and pathophysiology of microvascular and macrovascular complications of diabetes in South Asians. We also review the ongoing and completed diabetes prevention and management studies in South Asians.
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Gujral UP, Pradeepa R, Weber MB, Narayan KV, Mohan V. Type 2 diabetes in South Asians: similarities and differences with white Caucasian and other populations. Ann N Y Acad Sci 2013. [DOI: 10.1111/j.1749-6632.2012.06838.x
http:/www.ncbi.nlm.nih.gov/pubmed/23317344] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 03/30/2023]
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Gujral UP, Pradeepa R, Weber MB, Narayan KMV, Mohan V. Type 2 diabetes in South Asians: similarities and differences with white Caucasian and other populations. Ann N Y Acad Sci 2013; 1281:51-63. [PMID: 23317344 PMCID: PMC3715105 DOI: 10.1111/j.1749-6632.2012.06838.x] [Citation(s) in RCA: 266] [Impact Index Per Article: 22.2] [Reference Citation Analysis] [Abstract] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/23/2022]
Abstract
Type 2 diabetes mellitus (T2DM) is one of the leading causes of morbidity and mortality. While all ethnic groups are affected, the prevalence of T2DM in South Asians, both in their home countries and abroad, is extremely high and is continuing to rise rapidly. Innate biological susceptibilities coupled with rapid changes in physical activity, diet, and other lifestyle behaviors are contributing factors propelling the increased burden of disease in this population. The large scope of this problem calls for investigations into the cause of increased susceptibility and preventative efforts at both the individual and population level that are aggressive, culturally sensitive, and start early. In this review, we outline the biological and environmental factors that place South Asians at elevated risk for T2DM, compared with Caucasian and other ethnic groups.
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Affiliation(s)
- Unjali P Gujral
- Graduate Division of Biological and Biomedical Sciences, Nutrition and Health Sciences Program, Laney Graduate School, Emory University, Atlanta, GA 30322, USA.
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Walker M, Berrish TS, Stewart MW, Humphriss DB, Barriocanal L, Alberti KG. Metabolic heterogeneity in impaired glucose tolerance. Metabolism 1997; 46:914-7. [PMID: 9258274 DOI: 10.1016/s0026-0495(97)90079-2] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
Type II (non-insulin-dependent) diabetes mellitus is a metabolically heterogeneous condition, and is invariably preceded by impaired glucose tolerance (IGT). We examined whether metabolic heterogeneity is a feature of IGT. Three subject groups were studied: IGT subjects with two or more living non-insulin-dependent diabetic relatives (IGTWF, n = 17), and IGT subjects (IGTWOF, n = 17) and subjects with normal glucose tolerance (NGT, n = 25) without a family history of diabetes. Glucose tolerance, glucose (KITTG) and nonesterified fatty acid (KITTNEF) insulin sensitivity, and first-phase insulin secretion (FPIS) were assessed by oral glucose tolerance (OGTT), insulin tolerance (ITT), and intravenous glucose tolerance (IVGTT) tests, respectively. Comparison of groups was made by ANOVA and t test. The three groups were matched for age, gender, body mass index (BMI), and waist to hip ratio (WHR). IGTWOF and IGTWF subjects had comparable 2-hour plasma glucose levels on OGTT, and insulin secretion and KITTG were decreased to comparable degrees. However, in comparison to IGTWF subjects, IGTWOF subjects had increased fasting serum triglyceride (geometric mean, 1.8 [range, 0.8 to 4.5] v 1.1 [0.4 to 2.5] mmol. L-1, P = .02) and 2-hour plasma nonesterified fatty acid ([NEFA] mean +/- SD, 0.12 +/- 0.07 v 0.08 +/- 0.03 mmol.L-1, P < .02) levels and decreased KITTNEF values (4.0 [1.7 to 8.9] v 6.2 [2.8 to 12.1]%.min-1, P < .02). Thus, the two IGT groups had comparable changes in glucose metabolism, but IGTWOF subjects had additional abnormalities of lipid metabolism. In conclusion, metabolic heterogeneity is a feature of IGT, and this may reflect underlying etiological heterogeneity.
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Affiliation(s)
- M Walker
- Human Diabetes and Metabolism Research Centre, University of Newcastle upon Tyne, UK
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Osei K, Schuster DP. Decreased insulin-mediated but not non-insulin-dependent glucose disposal rates in glucose intolerance and type II diabetes in African (Ghanaian) immigrants. Am J Med Sci 1996; 311:113-21. [PMID: 8615385 DOI: 10.1097/00000441-199603000-00002] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/31/2023]
Abstract
The authors evaluated the significance of beta cell function, non-insulin-dependent glucose disposal (glucose effectiveness [Sg]), and insulin-dependent glucose disposal (insulin sensitivity) in African immigrants with varying degrees of glucose tolerance. Thirty-two African immigrants residing in Franklin County, Ohio, were studied. There were 16 subjects with normal glucose tolerance (NGT), 11 with intermediate glucose tolerance (IGT), and 5 with type II diabetes mellitus (DM). Insulin sensitivity index and Sg were measured by an insulin-modified, frequently sampled intravenous glucose tolerance test. The mean fasting and post-glucose serum glucose levels were lowest in the NGT, intermediate in the IGT group, and highest in the DM group. Mean serum insulin and c-peptide responses rose briskly by threefold to a peak in the NGT and the IGT groups. In the DM group, mean serum insulin and c-peptide responses were severely blunted to glucose stimulation. The sensitivity index was highest in the NGT (3.09 +/- 0.27), intermediate in the IGT (1.81 +/- 0.47), and lowest in the DM (0.48 +/- 0.28 x 10(-2).mins-1 (microU/ml)-1). The Sg was identical in the NGT (2.78 +/- 0.22) and IGT (2.78 +/- 0.27) groups but was slightly but not significantly lower in the DM (2.20 +/- 0.35 x 10(-2).mins-1). In addition, the glucose decay constant was not statistically different in the NGT (3.00 +/- 0.38) and IGT (2.25 +/- 0.19) group, but the mean values were significantly greater than in the patients with diabetes (0.78 +/- 0.15 percent/mins). The mean disposition index (sensitivity index X beta cell function as assessed by both insulin and c-peptide) was significantly greater in NGT than in the IGT (P<0.05) and in the diabetic group (P<0.001). In summary, the authors demonstrate that, in native African immigrants, type II diabetes is associated with significant reduction in beta cell function, insulin sensitivity, and glucose decay constant, but not in Sg. In patients with intermediate or impaired glucose tolerance, there is moderate insulin resistance and evidence of inadequate compensation by beta cell, but the Sg, the Sg at theoretical insulin concentration, and glucose decay constant remain normal. They conclude that, unlike other ethnic and racial groups, in glucose intolerant native African patients, alterations in Sg or non-insulin dependent glucose disposal (ie, tissue glucose sensitivity) do not appear to play a significant role in the impairment of glucose tolerance and type II diabetes in African immigrants.
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Affiliation(s)
- K Osei
- Department of Medicine, The Ohio State University Hospitals, Columbus, USA
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Osei K, Schuster DP. Decreased Insulin-Mediated but Not Non-Insulin-Dependent Glucose Disposal Rates in Glucose Intolerance and Type II Diabetes in African (Ghanaian) Immigrants. Am J Med Sci 1996. [DOI: 10.1016/s0002-9629(15)41658-1] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/29/2022]
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Berrish TS, Hetherington CS, Alberti KG, Walker M. Peripheral and hepatic insulin sensitivity in subjects with impaired glucose tolerance. Diabetologia 1995; 38:699-704. [PMID: 7672492 DOI: 10.1007/bf00401842] [Citation(s) in RCA: 20] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/26/2023]
Abstract
Recent evidence suggests that the postprandial hyperglycaemia in impaired glucose tolerance is primarily due to impaired suppression of basal hepatic glucose output. This in turn appears to be secondary to decreased first phase insulin secretion, although decreased hepatic insulin sensitivity, which is a feature of non-insulin-dependent diabetes mellitus, might also play a role. Eight mildly overweight subjects with impaired glucose tolerance and eight closely matched control subjects with normal glucose tolerance underwent an intravenous glucose tolerance test to assess first phase insulin secretion. Insulin sensitivity was examined by a 150-min hyperinsulinaemic-euglycaemic clamp. Somatostatin was infused from 150 min to suppress endogenous insulin secretion, and glucagon and insulin were replaced by constant infusion. Glucose with added dideuterated glucose (labelled infusion technique) was infused to maintain euglycaemia. First phase insulin secretion (delta 0-10 min insulin area divided by delta 0-10 min glucose area) was significantly decreased in the subjects with impaired glucose tolerance (median [range]: 1.2 [0.2-19.4] vs 9.1 [2.6-14.5] mU.mmol-1; p < 0.01). During the clamp, circulating insulin (93 +/- 8 [mean +/- SEM] and 81 +/- 10 mU.l-1) and glucagon (54 +/- 4 and 44 +/- 6 ng.l-1) levels were comparable. Total glucose disposal was decreased in subjects with impaired glucose tolerance (2.78 +/- 0.27 vs 4.47 +/- 0.53 mg.kg-1.min-1; p < 0.02), and was primarily due to decreased non-oxidative glucose disposal. However, hepatic glucose output rates were comparable during the clamp (0.38 +/- 0.10 and 0.30 +/- 0.18 mg.kg-1.min-1).(ABSTRACT TRUNCATED AT 250 WORDS)
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Affiliation(s)
- T S Berrish
- Human Diabetes and Metabolism Research Centre, University of Newcastle upon Tyne, UK
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