Table of Contents
ISRN Endocrinology
Volume 2012 (2012), Article ID 627270, 8 pages
http://dx.doi.org/10.5402/2012/627270
Research Article

High-Fat Programming of Hyperglycemia, Hyperinsulinemia, Insulin Resistance, Hyperleptinemia, and Altered Islet Architecture in 3-Month-Old Wistar Rats

Diabetes Discovery Platform, South African Medical Research Council, P.O. Box 7505, Tygerberg, Cape Town 7505, South Africa

Received 20 June 2012; Accepted 10 July 2012

Academic Editors: W. B. Chan, R. P. Kauffman, and A. Saxe

Copyright © 2012 Marlon E. Cerf et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

High-fat programming, by exposure to a high-saturated-fat diet in utero and/or during lactation, compromises beta-cell development and function in neonatal and weanling offspring. Therefore, high-fat programming effects were investigated on metabolism and islet architecture in young adult rats. Three-month-old male and female Wistar rat offspring were studied: HFG (maintained on a high-fat diet throughout fetal life), HFP (high-fat diet maintenance from birth to 3 months), and HFGP (high-fat diet maintenance throughout fetal and postnatal life). Control rats were maintained on a standard laboratory diet. Pancreata were double immunolabeled for insulin and glucagon to assess islet morphology and with Ki-67 to determine islet and acinar cell proliferation. HFP and HFGP males were heavier, hyperleptinemic, and hyperinsulinemic. Hyperglycemia presented in HFP males, HFP females, and HFGP males. HFGP males and HFP females were insulin resistant. HFP males displayed beta- and alpha-cell hyperplasia with alpha-cell hypertrophy evident in HFP females. Acinar cell proliferation rates were increased in HFP males. Postnatal high-fat programming induced the most diabetogenic phenotype with high-fat maintenance throughout fetal and postnatal life resulting in a severely obese phenotype. Fetal and postnatal nutrition shapes offspring health outcomes.