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Am J Physiol Endocrinol Metab 273: E46-E51, 1997;
0193-1849/97 $5.00
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AJP - Endocrinology and Metabolism, Vol 273, Issue 1 E46-E51, Copyright © 1997 by American Physiological Society


ARTICLES

Poor fetal nutrition causes long-term changes in expression of insulin signaling components in adipocytes

S. E. Ozanne, B. T. Nave, C. L. Wang, P. R. Shepherd, J. Prins and G. D. Smith
Department of Clinical Biochemistry, Addenbrooke's Hospital, Cambridge, United Kingdom.

Insulin action on adipocytes was studied in the offspring of mothers who had been fed either a control (20% protein) or a low (8%)-protein diet during pregnancy and lactation. Adipocytes isolated from low-protein offspring had significantly higher basal and insulin-stimulated glucose uptakes than controls. This may be related to a threefold increase in insulin receptors in low-protein adipocytes. Consistent with these observed changes in glucose transport, adipocytes from low-protein animals had significantly higher basal and insulin-stimulated insulin receptor substrate (IRS)-1-associated phosphatidylinositol 3-kinase (PI 3-kinase) activities. There was also more p85-associated PI 3-kinase activity in these adipocytes. There was no difference in expression in the p85 regulatory subunit or the p110-alpha catalytic subunit of PI 3-kinase. In contrast, there was a sixfold reduction in the p110-beta catalytic subunit of PI 3-kinase in adipocytes from low-protein animals. These results suggest that poor fetal nutrition during pregnancy and lactation can have long-term effects on glucose transport and on the expression of key components of the insulin signaling pathway in adipocytes.


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