Poor fetal nutrition causes long term changes in expression of
insulin signalling components in adipocytes .
Ozanne, S. E., B. T. Nave, C. L. Wang, P. R. Shepherd, J. Prins, and
G. D. Smith.
Dept. of Clinical Biochemistry, Addenbrooke's Hospital, Hills Road,
Cambridge, CB2 2QR, U.K.
APStracts 4:0072E, 1997.
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
three-fold 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 IRS-1 associated 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 six fold 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
signalling pathway in adipocytes.
Received 10 January 1997; accepted in final form 18 March 1997.
APS Manuscript Number E16-7.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 3 April 1997