The role of mouse Akt2 in insulin-dependent suppression of adipocyte lipolysis in vivo

Diabetologia
Shlomit KorenM J Birnbaum

Abstract

The release of fatty acids from adipocytes, i.e. lipolysis, is maintained under tight control, primarily by the opposing actions of catecholamines and insulin. A widely accepted model is that insulin antagonises catecholamine-dependent lipolysis through phosphorylation and activation of cAMP phosphodiesterase 3B (PDE3B) by the serine-threonine protein kinase Akt (protein kinase B). Recently, this hypothesis has been challenged, as in cultured adipocytes insulin appears, under some conditions, to suppress lipolysis independently of Akt. To address the requirement for Akt2, the predominant isoform expressed in classic insulin target tissues, in the suppression of fatty acid release in vivo, we assessed lipolysis in mice lacking Akt2. In the fed state and following an oral glucose challenge, Akt2 null mice were glucose intolerant and hyperinsulinaemic, but nonetheless exhibited normal serum NEFA and glycerol levels, suggestive of normal suppression of lipolysis. Furthermore, insulin partially inhibited lipolysis in Akt2 null mice during an insulin tolerance test (ITT) and hyperinsulinaemic-euglycaemic clamp, respectively. In support of these in vivo observations, insulin antagonised catecholamine-induced lipolysis in primary brown...Continue Reading

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Citations

Feb 3, 2016·Frontiers in Endocrinology·Bronwen MartinStuart Maudsley
Jul 12, 2017·Nature Medicine·Michael P Czech
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Jun 5, 2020·Diabetes, Metabolic Syndrome and Obesity : Targets and Therapy·Jia ZhaoJiao Guo
Nov 4, 2020·Pharmacological Reports : PR·Tamhida Masi, Bhoomika M Patel

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