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Laboratoire des dysfonctions Métabolique, Département de Nutrition, Faculté de Médicine, Université de Montréal, 2405 Chemin Côte Ste-Catherine, Montréal, Québec, Canada H3T 1A8
¹ Inserm U449/INRA U1235, IFR 62, René Laennec Faculty of Medicine, Lyon, France
² Institut Cochin, Département d’Endocrinologie, Métabolisme et Cancer, Paris, F-75014 France
³ Inserm, U567, Paris, F-75014 France
⁴ CNRS, UMR 8104, Paris, F-75014 France
⁵ Faculté de Médecine René Descartes, Université Paris Descartes, UMR-S 8104, Paris, F-75014 France
⁶ Nutrition Department, Inserm ‘Avenir’ Paris 6 University, EA 3502, AP/HP, Hôtel-Dieu, Paris, France
⁷ Mike Rosenbloom Laboratory for Cardiovascular Research, McGill University Health Center, 687 Pine Ave West, Montréal, Québec, Canada
⁸ Centre de Recherche Hôpital Laval, Université Laval, Québec, Canada

(Requests for offprints should be addressed to M Faraj; Email: may.faraj{at}umontreal.ca)

Adiponutrin is a newly described white adipose tissue (WAT)-derived protein whose function and regulation remain widely unclear in humans though it is suggested to be related to insulin sensitivity. Recently, we found that adiponutrin expression is reduced in type 2 diabetic subjects in basal and insulin-stimulated states. To examine adiponutrin regulation by the insulin pathway in relation to other WAT-related proteins with well-known relation to insulin signaling and action, we examined in healthy young men (1) the association of adiponutrin with p85 PI3K and HKII, leptin, adiponectin, and acylation-stimulating protein (ASP) and (2) the regulation of adiponutrin and WAT-derived proteins by 3-h hyperinsulinemic euglycemic clamp (HIEG). At baseline (N = 20), adiponutrin expressions were positively correlated with those of p85 PI3K (R = 0.54, P = 0.017), HKII (R = 0.58, P = 0.010), and serum leptin (R = 0.51, P = 0.036), but not with any other parameter measured including insulin sensitivity. Hyperinsulinemia (N = 10, +2365% above baseline) significantly increased the expression of adiponutrin (+770%, P = 0.002), p85 PI3K (+150%, P = 0.033), HKII (+147%, P = 0.007), and serum leptin (+11%, P = 0.031), while it decreased serum adiponectin (–15%, P = 0.001). In the insulin-stimulated state, adiponutrin mRNA expression levels correlated with basal p85 PI3K (R = 0.76, P = 0.018) and HKII (R = 0.86, P = 0.003) expression levels, with percentage increase in insulin (R = 0.73, P = 0.040), and with insulin-stimulated state HKII (R = 0.82, P = 0.007), leptin (R = 0.84, P = 0.005), and adiponectin (R = 0.85, P = 0.004) mRNA levels. In healthy young men, adiponutrin expression is unregulated by hyperinsulinemia and is related to basal and/or insulin-stimulated p85 PI3K, HKII, adiponectin, and leptin expression levels. We hypothesize that insulin-mediated regulation of adiponutrin expression is under the PI3K pathway. The relevance of the present findings to reduced adiponutrin expression in type 2 diabetes is discussed.