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.
Highlights
Obesity is currently one of the most common and severe complex disorders worldwide
Given that glucose-dependent insulinotropic polypeptide receptor (GIPR) are expressed in various tissues, including pancreatic islets, adipocytes, brain and stomach, Glucose-dependent insulinotropic polypeptide (GIP) signaling has been implicated in various activities, which may link overnutrition to obesity, insulin resistance and type 2 diabetes mellitus (T2DM)
We investigated the association of six tag single-nucleotide polymorphism (SNP) of GIP and four tag SNPs of GIPR with fat distribution and glucose-related traits in 2884 Han Chinese individuals. rs4794008 of GIP was associated with visceral fat accumulation, whereas other GIP and GIPR variants were related to both fat distribution and glucose-related traits
Summary
Obesity is currently one of the most common and severe complex disorders worldwide. It causes a great economic burden on public health due to the large number of individuals with obesity, and the associated consequences.[1] Visceral fat accumulation is the culprit in a variety of obesity-related disorders, including type 2 diabetes mellitus (T2DM), metabolic syndrome and cardiovascular diseases.[2] Effective management and intervention for obesity, especially for visceral adiposity, should be implemented to decrease the prevalence of T2DM and other metabolic diseases. Given that GIPRs are expressed in various tissues, including pancreatic islets, adipocytes, brain and stomach, GIP signaling has been implicated in various activities, which may link overnutrition to obesity, insulin resistance and T2DM. The blockade of GIPR signaling by GIPR knockout mice or GIP antagonist could decrease fat deposition under overnutrition.[7,8,9]
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