Effect of Pregnancy for Females Born Small on Later Life Metabolic Disease Risk

Tran, Melanie, Gallo, Linda A., Wadley, Glenn D., Jefferies, Andrew J., Moritz, Karen M. and Wlodek, Mary E. (2012) Effect of Pregnancy for Females Born Small on Later Life Metabolic Disease Risk. PLoS One, 7 9 Article No. e45188: . doi:10.1371/journal.pone.0045188


Author Tran, Melanie
Gallo, Linda A.
Wadley, Glenn D.
Jefferies, Andrew J.
Moritz, Karen M.
Wlodek, Mary E.
Title Effect of Pregnancy for Females Born Small on Later Life Metabolic Disease Risk
Journal name PLoS One   Check publisher's open access policy
ISSN 1932-6203
Publication date 2012-09-01
Sub-type Article (original research)
DOI 10.1371/journal.pone.0045188
Open Access Status DOI
Volume 7
Issue 9 Article No. e45188
Total pages 8
Place of publication San Francisco, CA United States
Publisher Public Library of Science
Collection year 2013
Language eng
Formatted abstract
There is a strong inverse relationship between a females own birth weight and her subsequent risk for gestational diabetes with increased risk of developing diabetes later in life. We have shown that growth restricted females develop loss of glucose tolerance during late pregnancy with normal pancreatic function. The aim of this study was to determine whether growth restricted females develop long-term impairment of metabolic control after an adverse pregnancy adaptation. Uteroplacental insufficiency was induced by bilateral uterine vessel ligation (Restricted) or sham surgery (Control) in late pregnancy (E18) in F0 female rats. F1 Control and Restricted female offspring were mated with normal males and allowed to deliver (termed Ex-Pregnant). Age-matched Control and Restricted Virgins were also studied and glucose tolerance and insulin secretion were determined. Pancreatic morphology and hepatic glycogen and triacylglycerol content were quantified respectively. Restricted females were born lighter than Control and remained lighter at all time points studied (p<0.05). Glucose tolerance, first phase insulin secretion and liver glycogen and triacylglycerol content were not different across groups, with no changes in β-cell mass. Second phase insulin secretion was reduced in Restricted Virgins (-34%, p<0.05) compared to Control Virgins, suggestive of enhanced peripheral insulin sensitivity but this was lost after pregnancy. Growth restriction was associated with enhanced basal hepatic insulin sensitivity, which may provide compensatory benefits to prevent adverse metabolic outcomes often associated with being born small. A prior pregnancy was associated with reduced hepatic insulin sensitivity with effects more pronounced in Controls than Restricted. Our data suggests that pregnancy ameliorates the enhanced peripheral insulin sensitivity in growth restricted females and has deleterious effects for hepatic insulin sensitivity, regardless of maternal birth weight
Keyword Beta cell mass
Intrauterine growth retardation
Gestational Diabetes Mellitus
Protein Malnourished Rats
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2013 Collection
School of Biomedical Sciences Publications
 
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