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Am J Physiol Endocrinol Metab (September 6, 2005). doi:10.1152/ajpendo.00248.2005
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Submitted on June 2, 2005
Accepted on August 23, 2005

Maternal hyperinsulinemia predisposes rat fetuses for hyperinsulinemia and adult--onset obesity and maternal mild food restriction reverses this phenotype

Malathi Srinivasan1, Ravikumar Aalinkeel1, Fei Song1, Paul Mitrani1, Jignesh D Pandya1, Brenda Strutt2, David J Hill2, and Mulchand S Patel1*

1 Department of Biochemistry, State University of New York at Buffalo, Buffalo, NY, USA
2 Department of Physiology, Medicine and Pediatrics, University of Western Ontario, London, Ontario, Canada

* To whom correspondence should be addressed. E-mail: mspatel{at}buffalo.edu.

We have previously shown that artificial rearing of newborn female rat pups on a high carbohydrate (HC) milk formula resulted in chronic hyperinsulinemia and adult-onset obesity (HC phenotype) and that the maternal HC phenotype was transmitted to their progeny (2-HC rats) due to fetal development in the HC female rat. The aims of this study were to investigate (i) the fetal adaptations that predisposed them for the expression of the HC phenotype in adulthood and (ii) if the transfer of the HC phenotype to the progeny could be reversed by maternal food restriction. Fetal parameters such as plasma insulin and glucose levels, mRNA level of preproinsulin gene, pancreatic insulin content and islet insulin secretory response in vitro were determined. On gestational day 21, 2-HC fetuses were hyperinsulinemic, had increased insulin content and mRNA level of the preproinsulin gene in their pancreata and demonstrated an altered glucose-stimulated insulin secretory response by isolated islets. Modification of the intrauterine environment in HC female rats was achieved by pair-feeding them to the amount of diet consumed by age-matched control rats from the time of their weaning. This mild dietary restriction reversed their HC phenotype and also prevented the development of the HC phenotype in their progeny. These findings show that malprogramming of the progeny of the hyperinsulinemic/obese HC female for the expression of the HC phenotype is initiated in utero and that normalization of the maternal environment in HC female rats by mild food restriction resulted in the normal phenotype in their progeny.




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