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A role for adipose tissue de-novo lipogenesis in glucose homeostasis during catch-up growth: A Randle cycle favouring fat storage.

Journal article
Authors Helena Marcelino
Christelle Veyrat-Durebex
Serge Summermatter
Delphine Sarafian
Jennifer Miles-Chan
Denis Arsenijevic
Fabio Zani
Jean-Pierre Montani
Josiane Seydoux
Giovanni Solinas
Abdul G. Dulloo
Published in Diabetes
Issue 2013 Feb
Pages 362-372
ISSN 0012-1797
Publication year 2013
Published at
Pages 362-372
Language en
Keywords adipose tissue, diabetes, insulin resistance, lipogenesis, growth
Subject categories Basic Medicine

Abstract

Catch-up growth, a risk factor for type 2 diabetes, is characterized by hyperinsulinemia and accelerated body fat recovery. Using a rat model of semistarvation-refeeding that exhibits catch-up fat, we previously reported that during refeeding on a low-fat diet, glucose tolerance is normal but insulin-dependent glucose utilization is decreased in skeletal muscle and increased in adipose tissue, where de novo lipogenic capacity is concomitantly enhanced. Here we report that isocaloric refeeding on a high-fat (HF) diet blunts the enhanced in vivo insulin-dependent glucose utilization for de novo lipogenesis (DNL) in adipose tissue. These are shown to be early events of catch-up growth that are independent of hyperphagia and precede the development of overt adipocyte hypertrophy, adipose tissue inflammation, or defective insulin signaling. These results suggest a role for enhanced DNL as a glucose sink in regulating glycemia during catch-up growth, which is blunted by exposure to an HF diet, thereby contributing, together with skeletal muscle insulin resistance, to the development of glucose intolerance. Our findings are presented as an extension of the Randle cycle hypothesis, whereby the suppression of DNL constitutes a mechanism by which dietary lipids antagonize glucose utilization for storage as triglycerides in adipose tissue, thereby impairing glucose homeostasis during catch-up growth.

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