Abstract

Objective To investigate the effects of adult catch-up growth on insulin sensitivity and stress in rats, as well as the probable mechanism of insulin resistance. Methods Male Sprague-Dawley rats were divided into 6 groups:caloric restriction group ( R4, caloric restriction for 4 weeks) and normal controls for 4 weeks ( NC4 ) ; catchup growth group refed with normal chow( RN4, refeeding for 4 weeks after caloric restriction for 4 weeks), catch-up growth group refed with high-fat diet( RH4, refeeding for 4 weeks after caloric restriction for 4 weeks ), normal chow (NC8) or high-fat diet( HF8 ) controls for 8 weeks. The animal model of catch-up growth was devoloped by way of refeeding after caloric restriction as scheduled. The glucose infusion rate( GIR ), 2-deoxyglucose uptake and insulinsitmulated insulin signaling in skeletal muscle during hyperinsulinemic-euglycemic clamp, plasma corticosterone, and 11β-hydroxysteroid dehydrogenase type 1 ( 11β-HSD1 ) mRNA expression level in skeletal muscle were determined.Results After caloric restriction for 4 weeks, plasma corticosterone and 1 1 β-HSD1 mRNA expression in skeletal muscle were significantly higher in R4 group compared with NC4 group( both P<0. 05 ), but there were no differences in 2-deoxyglucose uptake and Ser473 phosphorylation of Akt in skeletal muscle between two groups. The plasma corticosterone and 11β-HSD1 mRNA expression in skeletal muscle in RN4 group were significantly higher than those in NC8 group, and were higher in RH4 group than those in NC8 and HF8 groups; while the 2-deoxyglucose uptake and insulin-stimulated Ser473 phosphorylation of Akt in skeletal muscle during the clamp in RN4 were remarkably lower than those in NC8 group, and were lower in RH4 than those in NC8, HF8, and RN4 groups (all P < 0. 05 ).Conctusions Catch-up growth rats refed with normal chow or high-fat diet are characterized by significant insulin resistance and stress in the whole body and skeletal muscle. These changes are more evident in catch-up growth rats refed with high-fat diet. The interaction of increased stress and diet might be of utmost importance in the etiology of insulin resistance in catch-up growth animals. Key words: Catch-up growth; Insulin resistance; Stress; Rats

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