Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/101249
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Type: Journal article
Title: The effect of maternal and post-weaning low and high glycaemic index diets on glucose tolerance, fat deposition and hepatic function in rat offspring
Author: Gugusheff, J.
Sim, P.
Kheng, A.
Gentili, S.
Al-Nussairawi, M.
Brand-Miller, J.
Muhlhausler, B.
Citation: Journal of Developmental Origins of Health and Disease, 2016; 7(3):320-329
Publisher: Cambridge University Press
Issue Date: 2016
ISSN: 2040-1744
2040-1752
Statement of
Responsibility: 
J. Gugusheff, P. Sim, A. Kheng, S. Gentili, M. Al-Nussairawi, J. Brand-Miller and B. Muhlhausler
Abstract: Clinical studies have reported beneficial effects of a maternal low glycaemic index (GI) diet on pregnancy and neonatal outcomes, but the impact of the diet on the offspring in later life, and the mechanisms underlying these effects, remain unclear. In this study, Albino Wistar rats were fed either a low GI (n = 14) or high GI (n = 14) diet during pregnancy and lactation and their offspring weaned onto either the low or high GI diet. Low GI dams had better glucose tolerance (AUC[glucose], 1322 ± 55 v. 1523 ± 72 mmol min/l, P< 0.05) and a lower proportion of visceral fat (19.0 ± 2.9 v. 21.7 ± 3.8% of total body fat, P<0.05) compared to high GI dams. Female offspring of low GI dams had lower visceral adiposity (0.45 ± 0.03 v. 0.53 ± 0.03% body weight, P< 0.05) and higher glucose tolerance (AUC[glucose], 1243 ± 29 v. 1351 ± 39 mmol min/l, P<0.05) at weaning, as well as lower hepatic PI3K-p85 mRNA at 12 weeks of age. No differences in glucose tolerance or hepatic gene expression were observed in male offspring, but the male low GI offspring did have reduced hepatic lipid content at weaning. These findings suggest that consuming a low GI diet during pregnancy and lactation can improve glucose tolerance and reduce visceral adiposity in the female offspring at weaning, and may potentially produce long-term reductions in the hepatic lipogenic capacity of these offspring.
Keywords: fat mass; insulin resistance; programming
Description: First published online 10 December 2015
Rights: © Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2015
DOI: 10.1017/S2040174415007965
Grant ID: http://purl.org/au-research/grants/nhmrc/1004211
Published version: http://dx.doi.org/10.1017/s2040174415007965
Appears in Collections:Agriculture, Food and Wine publications
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