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Nutrition‐/diet‐induced changes in gene expression in pancreatic β‐cells
Author(s) -
Chadt A.,
Yeo G. S. H.,
AlHasani H.
Publication year - 2012
Publication title -
diabetes, obesity and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.445
H-Index - 128
eISSN - 1463-1326
pISSN - 1462-8902
DOI - 10.1111/j.1463-1326.2012.01640.x
Subject(s) - biology , gene , type 2 diabetes , diabetes mellitus , pancreatic islets , disease , candidate gene , islet , phenotype , gene expression profiling , gene expression , mechanism (biology) , function (biology) , genetics , endocrinology , medicine , philosophy , epistemology
β‐Cell dysfunction is a critical component in the development of type 2 diabetes. Whilst both genetic and environmental factors contribute to the development of the disease, relatively little is known about the molecular network that is responsible for diet‐induced functional changes in pancreatic β‐cells. Recent genome‐wide association studies for diabetes‐related traits have generated a large number of candidate genes that constitute possible links between dietary factors and the genetic susceptibility for β‐cell failure. Here, we summarize recent approaches for identifying nutritionally regulated transcripts in islets on a genome‐wide scale. Polygenic mouse models for type 2 diabetes have been instrumental for investigating the mechanism of diet‐induced β‐cell dysfunction. Enhanced oxidative metabolism, triggered by a combination of dietary carbohydrates and fat, appears to play a critical role in the pathophysiology of diet‐induced impairment of islets. More systematic studies of gene–diet interactions in β‐cells of rodent models in combination with genetic profiling might reveal the regulatory circuits fundamental for the understanding of diet‐induced impairments of β‐cell function in humans.