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Am J Physiol Regul Integr Comp Physiol (February 10, 2005). doi:10.1152/ajpregu.00335.2004
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Submitted on May 25, 2004
Accepted on February 4, 2005

Islet cell response in the neonatal rat after exposure to a high fat diet during pregnancy

Marlon E Cerf1*, K. Williams2, X. I Nkomo3, C. J Muller4, D. F Du Toit4, J. Louw2, and S. A Wolfe-Coote2

1 Diabetes Research Group, Medical Research Council, Tygerberg, South Africa; Anatomy and Histology, University of Stellenbosch, Tygerberg, South Africa
2 Diabetes Research Group, Medical Research Council, Tygerberg, South Africa
3 Biochemistry and Microbiology, University of Port Elizabeth, Port Elizabeth, South Africa
4 Anatomy and Histology, University of Stellenbosch, Tygerberg, South Africa

* To whom correspondence should be addressed. E-mail: marlon.cerf{at}mrc.ac.za.

Although pancreatic beta-cells are capable of adapting their mass in response to insulin requirements, there is evidence that a dietary insult could compromise this ability. Fetal malnutrition has been linked to low birth weight and the development of Type 2 diabetes later in life, while reduced beta-cell mass has been reported in adult rats fed a high fat diet (HFD). Reported here are the effects of exposure to a HFD, during different periods of gestation, on neonatal rat weight and beta- and alpha-cell development. The experimental groups comprised of neonatal offspring obtained from Wistar rats fed a high fat (40% as energy) diet for either the first (HF1), second (HF2) or third (HF3) week, or all three (HF1-3) weeks of gestation. Neonatal weights, circulating glucose and insulin concentrations were measured on postnatal day one after which the pancreata were excised and processed for histological immunocytochemical examination and image analysis. HF1 and HF2 neonates were hypoglycemic, while HF1-3 neonates were hyperglycemic. Low birth weights were observed only in HF1 neonates. No significant differences were detected in the circulating insulin concentrations in the neonates, although beta-cell volume and numbers were reduced in HF1-3 neonates. Beta-cell numbers also declined in HF1 and HF3 neonates. Alpha-cell volume, number and size were, however, increased in HF1-3 neonates. Alphacell size was also increased in HF1 and HF3 neonates. In neonates, exposure to a maternal HFD throughout gestation was found to have the most adverse effect on beta-cell development and resulted in hyperglycemia.




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