作者: K. Du
关键词:
摘要: Insulin resistance is a major hallmark in the development of type II diabetes, which characterized by failure insulin to promote glucose uptake muscle and suppress production liver. The serine-threonine kinase Akt (PKB) principal target signaling that inhibits hepatic output when available from food. Here we show TRB3, mammalian homolog Drosophila tribbles, functions as negative modulator Akt. TRB3 expression induced liver under fasting conditions, disrupts binding directly blocking activation kinase. Amounts RNA protein were increased livers db/db diabetic mice compared with those wild-type mice. Hepatic overexpression amounts comparable promoted hyperglycemia intolerance. Our results suggest that, interfering activation, contributes individuals susceptibility diabetes.