Journal
DIABETES OBESITY & METABOLISM
Volume 14, Issue -, Pages 57-67Publisher
WILEY-BLACKWELL
DOI: 10.1111/j.1463-1326.2012.01640.x
Keywords
genome-wide expression profiling; laser capture microdissection
Categories
Funding
- European Union [EUGENE2, LSHM-CT-2004-512013, SysProt, LSHG-CT-2006-37457, EUFP7-HEALTH-2009-241592 EurOCHIP, EUFP7-HEALTH-266408 Full4Health]
- Medical Research Council [G0600717B] Funding Source: researchfish
Ask authors/readers for more resources
beta-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 beta-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 beta-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 beta-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 genediet interactions in beta-cells of rodent models in combination with genetic profiling might reveal the regulatory circuits fundamental for the understanding of diet-induced impairments of beta-cell function in humans.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available