ARS | Publication request: Persistence of an adverse metabolic phenotype in parenterally fed neonatal pigs

Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only
Publication Acceptance Date: March 23, 2012
Publication Date: April 21, 2012
Citation: Burrin, D.G., Stoll, B., El-Kadi, S., Genovese, K., Davis, T.A., Fiorotto, M.L., Thymann, T., Sangild, P. 2012. Persistence of an adverse metabolic phenotype in parenterally fed neonatal pigs [abstract]. Federation of American Societies for Experimental Biology Conference. 26:34.4.

Technical Abstract: The nutritional environment during fetal and neonatal life is a key determinant affecting the risk for adult-onset diseases, such as diabetes and obesity. We previously showed that chronic parenteral (PN) compared to enteral (EN) nutrition in neonatal pigs for two weeks leads to increased glucose intolerance, insulin resistance, and fat deposition. Our aim was to test whether glucose intolerance, insulin resistance, and fat deposition in the liver and body persist into late infancy and adolescence. Term newborn pigs were fed PN or EN (N=12/group) for 2 wk, followed by ad lib feeding of a high-fat (30%) and sucrose (20%) diet for 5 mon. Body composition was measured by dual-emission X-ray absorptiometry at 2 wk, 8 wk, and 5 mon, and serum chemistry and fasting intravenous glucose tolerance test (IVGTT; 1 g glucose/kg x sample 90 min) were obtained at 5 mon. At 2 and 8 wk of age, body weight was similar, but % fat was higher and % lean was lower in PN vs EN pigs. At 5 mon, there were no differences in serum markers of liver injury or lipidemia; however, the 90-min area-under-curve (AUC) for both glucose and insulin were lower (p<0.05) in PN than EN pigs, but the ratio of AUC insulin:glucose was not different between groups. We conclude that PN during the neonatal period increased adiposity transiently into early infancy but PN-induced glucose intolerance was not sustained into adolescence even when challenged with an obesogenic diet.