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High fat diet induced insulin resistance and glucose intolerance are gender-specific in IGF-1R heterozygous mice.

Abstract：

:Interactions between genes and environment play a critical role in the pathogenesis of type 2 diabetes. Low birth weight, due to genetic and environmental variables affecting fetal growth, is associated with increased susceptibility to the development of type 2 diabetes and metabolic disorders in adulthood. Clinical studies have shown that polymorphisms in the Insulin-like growth factor 1 (IGF-1) gene or heterozygous mutations in IGF-1 and IGF-1 receptor (IGF-1R) genes, resulting in reduced IGF-1 action, are associated with low birth weight and post-natal growth. Mice lacking one of the IGF-1R alleles (Igf1r(+/-)) exhibit a 10% reduction in post-natal growth, and develop glucose intolerance (males) and insulin resistance (males and females) as they age. To investigate whether adverse environmental factors could accelerate the onset of the metabolic syndrome, we conducted a short duration intervention of high fat diet (HFD) feeding in male and female Igf1r(+/-) and wild-type (WT) control mice. The HFD resulted in insulin resistance, hyperglycemia, and impaired glucose tolerance in males of both genotypes whereas in females exacerbated diabetes was observed only in the Igf1r(+/-) genotype, thus suggesting a sexual dimorphism in the influence of obesity on the genetic predisposition to diabetes caused by reduced IGF-1 action.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Garg N,Thakur S,McMahan CA,Adamo ML

doi

10.1016/j.bbrc.2011.08.123

subject

Has Abstract

pub_date

2011-09-30 00:00:00

pages

476-80

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(11)01542-7

journal_volume

413

pub_type

杂志文章

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