Location: Arkansas Children's Nutrition CenterTitle: Hyperinsulinemia and ectopic fat deposition develop in the face of hyperadiponectinemia in young obese rats) Author
Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only
Publication Acceptance Date: 3/15/2010
Publication Date: 4/12/2010
Citation: Ronis, M.J., Marecki, J.C., Shankar, K., Badger, T.M. 2010. Hyperinsulinemia and ectopic fat deposition develop in the face of hyperadiponectinemia in young obese rats. Federation of American Societies for Experimental Biology Conference. FASEB J. 24:105.6. Interpretive Summary:
Technical Abstract: The role of reduced adiponenctin signaling in childhood obesity is unclear. Weanling male Sprague-Dawley rats were overfed a high fat diet via total enteral nutrition. Excessive caloric intake led to increased weight and fat mass; dyslipidemia; ectopic fat deposition; and hyperinsulinemia (P less than 0.05). Expression of fatty acid transporter CD36 was elevated in both liver and muscle (P < 0.05). Akt phosphorylation was elevated in liver but not muscle, and hepatic nuclear FoxO1 protein reduced (P < 0.05). Overfeeding increased serum adiponectin from 24.6 +/- 1.9 micro g/ml to 46.3 +/- 5.9 micro g/ml (P < 0.05) correlating with increased fat mass. TNF-alpha expression in fat was unchanged. AMP kinase phosphorylation, PPAR-alpha expression, and fatty acid oxidation was elevated in both liver and muscle (P < 0.05). Thus excessive intake of high fat diet in young rats resulted in adiponectin-independent increases in serum insulin and elevated ectopic fat deposition. Fatty acid transport appears to be the major mechanism underlying ectopic fat deposition. These data suggest age-related differences in the role of adiponectin in pathological responses associated with obesity.