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Int J Obes (Lond). 2014 Feb;38(2):224-30. doi: 10.1038/ijo.2013.106. Epub 2013 Jun 10.

Fetal baboon sex-specific outcomes in adipocyte differentiation at 0.9 gestation in response to moderate maternal nutrient reduction.

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Department of Biology of Adipose Tissue Depots, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA, USA.
Division of Health Economics, Louisiana State Department of Health and Hospitals, Baton Rouge, LA, USA.
Center for Pregnancy and Newborn Research, University of Texas Health Science Center, San Antonio, TX, USA.



To investigate in vitro adipocyte differentiation in baboon fetuses in response to reduced maternal nutrition.


Cross-sectional comparison of adipocyte differentiation in normally grown fetuses and fetuses of pregnant baboons fed 70% of the control global diet from 30 days of pregnancy to term.


The subjects comprised control (CTR) fetuses (five female and five male) of mothers fed ad libitum and fetuses of mothers fed 70% of the global diet consumed by CTR (maternal nutrient reduction (MNR), five female and five male fetuses). The expression of genes/proteins involved in adipogenesis (PPARγ, FABP4 and adiponectin) and brown adipose tissue development (UCP1, TBX15 and COXIV) were determined in in vitro-differentiated stromal-vascular cultures from subcutaneous abdominal, subcutaneous femoral and omental adipose tissue depots. Adipocyte number per area (mm(2)) was determined histologically to assist in the evaluation of adipocyte size.


Maternal suboptimal nutrition suppressed growth of male but not female fetuses and led to adipocyte hypertrophy accompanied by increased markers of white- and, particularly, brown-type adipogenesis in male but not female fetuses.


Adipose tissue responses to fetal nonhuman primate undernutrition are sexually dimorphic. While female fetuses adapt adequately, the male ones enhance pathways involved in white and brown adipose tissue development but are unable to compensate for a delayed development of adipose tissue associated with intrauterine growth restriction. These differences need to be considered when assessing developmental programming of adiposity in response to suboptimal maternal nutrition.

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