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Biology of Reproduction 67, 220-231 (2002)
© 2002 Society for the Study of Reproduction, Inc.

Regular Article

Altered Meiotic Regulation in Oocytes from Diabetic Mice

Shannondoah A. Coltona, Galen M. Pieperb, and Stephen M. Downs2,a

a Biology Department, Marquette University, Milwaukee, Wisconsin 53233 b Department of Surgery, Division of Transplant Surgery, Medical College of Wisconsin, Milwaukee, Wisconsin 53226

In the present study, we have utilized a streptozotocin-induced diabetic mouse model to examine how the diabetic condition and different glucose concentrations affect several parameters of reproductive physiology. We report that oocyte maturation is altered under all experimental conditions examined. In cumulus cell-enclosed oocytes (CEO) from diabetic mice, spontaneous maturation was accelerated but the FSH-mediated delay of spontaneous maturation was suppressed. Higher glucose levels in the culture medium suppressed spontaneous maturation but did not influence the transient arrest mediated by FSH. Meiotic arrest in CEO by hypoxanthine and dibutyryl cAMP (dbcAMP) was less effective at higher glucose concentrations. In addition, both FSH-induced maturation in vitro and hCG-induced maturation in vivo were reduced by the diabetic condition. The ovulation rate was lowered by about 50% in diabetic mice and fewer ovulated ova had reached metaphase II. Despite the decreased number of ova at metaphase II, in vitro cultures showed the oocytes were capable of completing meiotic maturation at control levels. Insulin treatment reversed the detrimental effects of diabetes on meiotic induction, ovulation, and completion of meiotic maturation. Cultures of pronuclear-staged embryos confirmed a negative effect of diabetes and hyperglycemia on development to the blastocyst stage. These data suggest that defects in meiotic regulation brought about by the diabetic condition are due to decreased communication between the somatic and germ cell compartments, and it is concluded that such conditions may contribute to postfertilization developmental abnormalities.

First decision: 10 October 2001.

1 This work was supported by funds from NIH (HD25291 and HD 39172 to S.M.D.).

2 Correspondence: Stephen M. Downs, Marquette University, Biology Department, P.O. Box 1881, Milwaukee, WI 53201-1881. FAX: 414 288 7357; stephen.downs{at}marquette.edu




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