Adipose Tissue Plasticity During Catch-Up Fat Driven by Thrifty Metabolism
Relevance for Muscle-Adipose Glucose Redistribution During Catch-Up Growth
- Serge Summermatter1,
- Helena Marcelino1,
- Denis Arsenijevic1,
- Antony Buchala2,
- Olivier Aprikian3,
- Françoise Assimacopoulos-Jeannet4,
- Josiane Seydoux5,
- Jean-Pierre Montani1,
- Giovanni Solinas1 and
- Abdul G. Dulloo1
- 1Department of Medicine/Physiology, University of Fribourg, Fribourg, Switzerland;
- 2Department of Biology, University of Fribourg, Fribourg, Switzerland;
- 3Nestlé Research Center, Lausanne, Switzerland;
- 4Department of Cellular Physiology and Metabolism, Faculty of Medicine, University of Geneva, Geneva, Switzerland;
- 5Department of Basic Neurosciences, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
- Corresponding author: A.G. Dulloo, abdul.dulloo{at}unifr.ch.
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S.S. and H.M. contributed equally to this article.
Abstract
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.
Footnotes
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The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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- Received December 24, 2008.
- Accepted July 6, 2009.
- © 2009 by the American Diabetes Association.
