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Prenatal low protein and postnatal high fat diets induce rapid adipose tissue growth by inducing Igf2 expression in Sprague Dawley rat offspring

Kate J. Claycombe, Eric O. Uthus, James N. Roemmich, LuAnn K. Johnson, W. Thomas Johnson
Journal of nutrition 2013 v.143 no. pp. 1533-1539
adipocytes, adipose tissue, conception, dietary protein, energy, fat intake, genes, high fat diet, insulin resistance, insulin-like growth factor II, lactation, low protein diet, maternal nutrition, messenger RNA, mitochondrial DNA, obesity, pregnancy, prenatal development, progeny, protein intake, rats, weaning
Maternal low protein diets during prenatal development contribute to the development of obesity and insulin resistance in offspring. In this study, obese-prone Sprague -Dawley rats were fed diets having either 8% (low protein, LP) or 20% (normal protein, NP) protein for 3-wk prior to conception and throughout pregnancy and lactation. At weaning, their offspring were fed diets for 12 wk having normal protein and either 10% (normal fat, NF) or 45% (high fat, HF) fat. Adipose tissue growth rate was increased by HF postnatal diet, but the rate was greater in the offspring of LP-fed dams (26-fold increase) compared to NP-fed dams (13-fold increase). IGF2 mRNA was increased by HF postnatal diet in subcutaneous, but not in visceral, adipose tissue regardless of the dams’ prenatal diet. The HF postnatal diet increased the number of small adipocytes (20-80 µm, P<0.005) in visceral adipose tissue of offspring regardless of their dams’ prenatal diet, but the increase in smaller adipocytes did not occur in the subcutaneous adipose tissue of offspring fed HF diet whose dams were fed LP prenatal diet. Mitochondrial DNA copy number was lower in subcutaneous adipose tissue of offspring fed HF diet if their dams had been fed the LP diet. Neither prenatal protein intake nor postnatal fat intake influenced mitochondrial copy number in visceral adipose tissue. These findings suggest that prenatal dietary protein intake influences the rate of adipose tissue growth in offspring in response to high fat intake through alterations in adipocyte numbers and sizes. The mechanism may involve depot specific effects of prenatal protein intake on the expression of the epigenetically imprinted Igf2 gene and energy utilization during preadipocyte differentiation.