Horm Metab Res 2010; 42(7): 491-495
DOI: 10.1055/s-0030-1249058
Original Basic

© Georg Thieme Verlag KG Stuttgart · New York

Intrauterine Growth Retardation Leads to the Functional Change of Insulin Secretion in the Newborn Rats

Q. X. Yuan1 , J. Y. Zhou2 , 3 , L. P. Teng2 , C. P. Liu1 , J. Guo2 , L. J. Liu2 , W. De2 , K. F. Xu1 , X. D. Mao1 , C. Liu1
  • 1Department of Endocrinology, First Affiliated Hospital, Nanjing Medical University, Nanjing, P. R. China
  • 2Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, P. R. China
  • 3Current Address: Medical Laboratory Center, Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, P. R. China
Further Information

Publication History

received 30.06.2009

accepted after second revision 09.02.2010

Publication Date:
11 March 2010 (online)

Abstract

To investigate the observed variation in glucose tolerance and insulin secretion in intrauterine growth retarded newborn rats and to explore the mechanism of the variations, Sprague-Dawley pregnant rats were allocated into two groups: a control group and an intrauterine energy restricted group. The intrauterine growth retardation (IUGR) in the rats was induced by 50% calorie restriction in pregnant rats from gestational day 15 until term as compared to the control group. The pancreata of control and IUGR newborn rats were dissected respectively. RT-PCR was used to study the mRNA level related to insulin synthesis and exocytosis. Intraperitoneal glucose tolerance tests were done to study the function of the pancreatic islet. We found that birth weight and pancreas mass of IUGR newborn rats were significantly lower than those of controls. Although no significant differences were observed in mRNA level of insulin and PDX-1, the expression of genes related to insulin exocytosis such as munc13-1, vamp-2, syntaxin1a, rab3a were reduced significantly in IUGR newborn rats. IUGR animals were glucose-intolerant. The observed blood insulin level and insulin secretion response to glucose challenge were both found to be at reduced level in IUGR newborn rats as compared with the normal control group rats. With these findings, we hypothesize that IUGR can induce changes in glucose homeostasis due to, at least in part, a reduced function of insulin exocytosis in newborn rats.

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Correspondence

C. Liu

Department of Endocrinology

First Affiliated Hospital

Nanjing Medical University

Nanjing 210029

P. R. China

Phone: +86/25/83714511/6530

Fax: +86/25/86202571

Email: liuchao@nfmcn.com

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