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Maternal Endocrine Adaptation throughout Pregnancy to Nutritional Manipulation: Consequences for Maternal Plasma Leptin and Cortisol and the Programming of Fetal Adipose Tissue Development

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TLDR
At term, irrespective of maternal nutrition in late gestation, fetuses sampled from ewes NR in early gestation possessed more adipose tissue, whereas when eWes were fed to appetite throughout gestation, fetal adipose tissues deposition and leptin mRNA abundance were both reduced, which may result in the offspring of NR mothers being at increased risk of obesity in later life.
Abstract
Maternal nutrient restriction at specific stages of gestation has differential effects on fetal development such that the offspring are programmed to be at increased risk of adult disease. We investigated the effect of gestational age and maternal nutrition on the maternal plasma concentration of leptin and cortisol together with effects on fetal adipose tissue deposition plus leptin, IGF-I, IGF-II ligand, and receptor mRNA abundance near to term. Singleton bearing ewes were either nutrient restricted (NR; consuming 3.2-3.8 MJ/d of metabolizable energy) or fed to appetite (consuming 8.7-9.9 MJ/d) over the period of maximal placental growth, i.e. between 28 and 80 d gestation. After 80 d gestation, ewes were either fed to calculated requirements, consuming 6.7-7.5 MJ/d, or were fed to appetite and consumed 8.0-10.9 MJ/d. Pregnancy resulted in a rise in plasma leptin concentration by 28 d gestation, which continued up to 80 d gestation when fed to appetite but not with nutrient restriction. Plasma cortisol was also lower in NR ewes up to 80 d gestation, a difference no longer apparent when food intake was increased. At term, irrespective of maternal nutrition in late gestation, fetuses sampled from ewes NR in early gestation possessed more adipose tissue, whereas when ewes were fed to appetite throughout gestation, fetal adipose tissue deposition and leptin mRNA abundance were both reduced. These changes may result in the offspring of NR mothers being at increased risk of obesity in later life.

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References
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Leptin and the regulation of body weight in mammals

TL;DR: The role of leptin in the control of body weight and its relevance to the pathogenesis of obesity are reviewed.
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A Transgenic Model of Visceral Obesity and the Metabolic Syndrome

TL;DR: Increased adipocyte 11β HSD-1 activity may be a common molecular etiology for visceral obesity and the metabolic syndrome.
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In utero programming of chronic disease

TL;DR: This review examines the evidence linking these diseases to fetal undernutrition and provides an overview of previous studies in this area.
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Subjective assessment of body fat in live sheep

TL;DR: The results show that body condition scores can provide an acceptable and useful estimate of the proportion of fat in the live animal, and that the level of prediction is superior to that afforded by live weight.
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Birth Weight and Adult Hypertension, Diabetes Mellitus, and Obesity in US Men

TL;DR: Findings support the hypothesis that early life exposures, for which birth weight is a marker, are associated with several chronic diseases in adulthood.
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