作者: Ying Zhao , Flora Ling , Timothy M. Griffin , Ting He , Rheal Towner
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摘要: Id1, a helix-loop-helix (HLH) protein that inhibits the function of basic HLH E transcription factors in lymphoid cells, has been implicated diet- and age-induced obesity by unknown mechanisms. Here we show Id1-deficient mice are resistant to high fat obesity, as revealed reduced weight gain body fat, increased lipid oxidation, attenuated hepatosteatosis, lower levels droplets brown adipose tissue, smaller white adipocytes after diet feeding or aged animals. Id1 deficiency improves glucose tolerance, lowers serum insulin levels, reduces TNFα gene expression tissue. also Sirtuin 1 peroxisome proliferator-activated receptor γ coactivator 1α, regulators mitochondrial biogenesis energy expenditure, This effect was accompanied elevation several genes encoding proteins involved oxidative phosphorylation fatty acid such cytochrome c, medium-chain acyl-CoA dehydrogenase, adipocyte 2. Moreover, phenotype for similar expressing an dominant-positive construct, ET2, suggesting balance between Id plays role regulating metabolism sensitivity.