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      The effect of glucose-dependent insulinotropic polypeptide ( GIP) variants on visceral fat accumulation in Han Chinese populations

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          Abstract

          Objectives:

          We aim to validate the effects of glucose-dependent insulinotropic polypeptide (GIP) on fat distribution and glucose metabolism in Han Chinese populations.

          Methods:

          We genotyped six tag single-nucleotide polymorphisms (SNPs) of GIP and four tag SNPs of glucose-dependent insulinotropic polypeptide receptor ( GIPR) among 2884 community-based individuals from Han Chinese populations. Linear analysis was applied to test the associations of these variants with visceral fat area (VFA) and subcutaneous fat area (SFA) quantified by magnetic resonance imaging as well as glucose-related traits.

          Results:

          We found that the C allele of rs4794008 of GIP tended to increase the VFA and the VFA/SFA ratio in all subjects ( P=0.050 and P=0.054, respectively), and rs4794008 was associated with the VFA/SFA ratio in males ( P=0.041) after adjusting for the BMI. The VFA-increasing allele of rs4794008 was not related to any glucose metabolism traits. However, rs9904288 of GIP was associated with the SFA in males as well as glucose-related traits in all subjects ( P range, 0.004–0.049), and the GIPR variants displayed associations with both fat- and glucose-related traits.

          Conclusions:

          The results could provide the evidence that GIP might modulate visceral fat accumulation via incretin function or independent of incretin.

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          Most cited references18

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          Global, regional, and national prevalence of overweight and obesity in children and adults during 1980-2013: a systematic analysis for the Global Burden of Disease Study 2013.

          Marie Ng, Tom Fleming, Margaret W. Robinson … (2015)
          In 2010, overweight and obesity were estimated to cause 3·4 million deaths, 3·9% of years of life lost, and 3·8% of disability-adjusted life-years (DALYs) worldwide. The rise in obesity has led to widespread calls for regular monitoring of changes in overweight and obesity prevalence in all populations. Comparable, up-to-date information about levels and trends is essential to quantify population health effects and to prompt decision makers to prioritise action. We estimate the global, regional, and national prevalence of overweight and obesity in children and adults during 1980-2013. We systematically identified surveys, reports, and published studies (n=1769) that included data for height and weight, both through physical measurements and self-reports. We used mixed effects linear regression to correct for bias in self-reports. We obtained data for prevalence of obesity and overweight by age, sex, country, and year (n=19,244) with a spatiotemporal Gaussian process regression model to estimate prevalence with 95% uncertainty intervals (UIs). Worldwide, the proportion of adults with a body-mass index (BMI) of 25 kg/m(2) or greater increased between 1980 and 2013 from 28·8% (95% UI 28·4-29·3) to 36·9% (36·3-37·4) in men, and from 29·8% (29·3-30·2) to 38·0% (37·5-38·5) in women. Prevalence has increased substantially in children and adolescents in developed countries; 23·8% (22·9-24·7) of boys and 22·6% (21·7-23·6) of girls were overweight or obese in 2013. The prevalence of overweight and obesity has also increased in children and adolescents in developing countries, from 8·1% (7·7-8·6) to 12·9% (12·3-13·5) in 2013 for boys and from 8·4% (8·1-8·8) to 13·4% (13·0-13·9) in girls. In adults, estimated prevalence of obesity exceeded 50% in men in Tonga and in women in Kuwait, Kiribati, Federated States of Micronesia, Libya, Qatar, Tonga, and Samoa. Since 2006, the increase in adult obesity in developed countries has slowed down. Because of the established health risks and substantial increases in prevalence, obesity has become a major global health challenge. Not only is obesity increasing, but no national success stories have been reported in the past 33 years. Urgent global action and leadership is needed to help countries to more effectively intervene. Bill & Melinda Gates Foundation. Copyright © 2014 Elsevier Ltd. All rights reserved.
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            Body Fat Distribution and Insulin Resistance

            Pavankumar Patel, Nicola Abate (2013)
            The burden of obesity has increased globally over the last few decades and its association with insulin resistance and related cardio-metabolic problems have adversely affected our ability to reduce population morbidity and mortality. Traditionally, adipose tissue in the visceral fat depot has been considered a major culprit in the development of insulin resistance. However, there is a growing body of evidence supporting the role of subcutaneous truncal/abdominal adipose tissue in the development of insulin resistance. There are significant differences in the functional characteristics of subcutaneous abdominal/truncal vs. intraabdominal vs. gluteo-femoral fat depots. More recently, mounting evidence has been supporting the role of adipose tissue function in the development of metabolic complications independent of adipose tissue volume or distribution. Decreased capacity for adipocyte differentiation and angiogenesis along with adipocyte hypertrophy can trigger a vicious cycle of inflammation leading to subcutaneous adipose tissue dysfunction and ectopic fat deposition. Therapeutic lifestyle change continues to be the most important intervention in clinical practice to improve adipose tissue function and avoid development of insulin resistance and related cardio-metabolic complications.
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              Oral glucose tolerance test indexes for insulin sensitivity and secretion based on various availabilities of sampling times.

              Florian Gerich, Tina Van Havere, A Fritsche … (2001)
              Article 0 comments Cited 74 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Nutr Diabetes
                Journal ID (iso-abbrev): Nutr Diabetes
                Title: Nutrition & Diabetes
                Publisher: Nature Publishing Group
                ISSN (Electronic): 2044-4052
                Publication date (Print): May 2017
                Publication date (Electronic): 22 May 2017
                Publication date PMC-release: 1 May 2017
                Volume: 7
                Issue: 5
                Page: e278
                Affiliations
                [1 ]Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Center for Diabetes, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital , Shanghai, China
                [2 ]Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College of Huazhong University of Science and Technology , Wuhan, China
                [3 ]Kao (China) Research & Development Center Company Limited , Shanghai, China
                [4 ]Institute for Metabolic Diseases, Department of Endocrinology, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital South Campus , Shanghai, China
                Author notes
                [* ]Department of Endocrinology and Metabolism, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital , 600 Yishan Road, Shanghai 200233, China. E-mail: alfredhc@ 123456sjtu.edu.cn
                [5]

                These authors contributed equally to this work.

                Article
                Publisher Item ID: nutd201728
                DOI: 10.1038/nutd.2017.28
                PMC ID: 5518809
                PubMed ID: 28530680
                SO-VID: 91ac5b9a-87d5-4179-a703-cb2e49e836bb
                Copyright © Copyright © 2017 The Author(s)
                License:

                This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

                History
                Date received : 10 February 2017
                Date revision received : 05 April 2017
                Date accepted : 06 April 2017
                Categories
                Subject: Original Article

                ScienceOpen disciplines: Endocrinology & Diabetes
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes

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