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Adipose Tissue Plasticity During Catch-Up Fat Driven by Thrifty Metabolism Relevance for Muscle-Adipose Glucose Redistribution During Catch-Up Growth

Journal article
Authors Serge Summermatter
Helena Marcelino
Denis Arsenijevic
Antony Buchala
Olivier Aprikian
Françoise Assimacopoulos-Jeannet
Josiane Seydoux
Jean-Pierre Montani
Giovanni Solinas
Abdul G. Dulloo
Published in Diabetes
Volume 58
Issue 10
Pages 2228-2237
ISSN 0012-1797
Publication year 2009
Published at Institute of Medicine, Department of Molecular and Clinical Medicine
Pages 2228-2237
Language en
Keywords Obesity, adiposity, insulin sensitivity, lipogenesis, AMPK, PI3K
Subject categories Basic Medicine


OBJECTIVE Catch-up growth, a risk factor for later type 2 diabetes, is characterized by hyperinsulinemia, accelerated body-fat recovery (catch-up fat), and enhanced glucose utilization in adipose tissue. Our objective was to characterize the determinants of enhanced glucose utilization in adipose tissue during catch-up fat. RESEARCH DESIGN AND METHODS White adipose tissue morphometry, lipogenic capacity, fatty acid composition, insulin signaling, in vivo glucose homeostasis, and insulinemic response to glucose were assessed in a rat model of semistarvation-refeeding. This model is characterized by glucose redistribution from skeletal muscle to adipose tissue during catch-up fat that results solely from suppressed thermogenesis (i.e., without hyperphagia). RESULTS Adipose tissue recovery during the dynamic phase of catch-up fat is accompanied by increased adipocyte number with smaller diameter, increased expression of genes for adipogenesis and de novo lipogenesis, increased fatty acid synthase activity, increased proportion of saturated fatty acids in triglyceride (storage) fraction but not in phospholipid (membrane) fraction, and no impairment in insulin signaling. Furthermore, it is shown that hyperinsulinemia and enhanced adipose tissue de novo lipogenesis occur concomitantly and are very early events in catch-up fat. CONCLUSIONS These findings suggest that increased adipose tissue insulin stimulation and consequential increase in intracellular glucose flux play an important role in initiating catch-up fat. Once activated, the machinery for lipogenesis and adipogenesis contribute to sustain an increased insulin-stimulated glucose flux toward fat storage. Such adipose tissue plasticity could play an active role in the thrifty metabolism that underlies glucose redistribution from skeletal muscle to adipose tissue.

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