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Maternal Nutrient Restriction between Early and Midgestation and Its Impact Upon Appetite Regulation after Juvenile Obesity

Centre for Reproduction and Early Life (S.P.S., M.A.H., L.L.Y.C., N.P., T.S., H.B., M.E.S., D.S.G.), Institute for Clinical Research, University Hospital, Nottingham NG7 2UH, United Kingdom; Alberta Institute of Human Nutrition (R.C.B.), University of Alberta, Edmonton, AB, Canada T6G 0H3; Department of Animal Sciences (D.K.), University of Missouri, Columbia, Missouri 65201; and School of Veterinary Medicine and Science (D.S.G.), University of Nottingham, Sutton Bonington LE12 5RD, United Kingdom

Address all correspondence and requests for reprints to: Professor Michael E. Symonds or Dr. David S. Gardner, Academic Division of Child Health, School of Human Development, University Hospital, Nottingham NG7 2UH, United Kingdom. E-mail: michael.symonds{at}nottingham.ac.uk or david.gardner{at}nottingham.ac.uk, respectively.

The impact of maternal nutrient restriction during early-to-midgestation, a period coinciding with early fetal brain development, on appetite regulation and energy balance in the offspring after juvenile obesity was examined. Pregnant sheep were either fed to meet fully their nutritional requirements throughout gestation or 50% of this amount between 30 and 80 d gestation. After weaning, offspring were either made obese through exposure to a sedentary obesogenic environment or remained lean. Maternal nutrient restriction had no effect on birth weight or subsequent growth. At 1 wk of age, only, gene expression for neuropeptide Y in the hypothalamus was reduced in nutrient-restricted offspring. By 1 yr of age, all O animals had increased plasma leptin, nonesterified fatty acids, and insulin, with the latter effect amplified in NR offspring. Fasting plasma glucose, triglycerides, and cortisol were unaffected by obesity. The entrained reduction in physical activity that led to obesity persisted when all animals were maintained within individual pens. However, NRO offspring exhibited reduced daily food intake and were, therefore, no longer in positive "energy balance." This adaptation was accompanied by elevated hypothalamic gene expression for the melanocortin-4 and insulin receptors, AMP-activated kinase, and acetyl coenzyme A carboxylase . In conclusion, nutrient restriction specifically targeted over the period of early fetal brain development contributes to a profoundly different adaptation in energy balance after juvenile obesity. The extent to which this adaptive response may benefit the offspring or result in an exacerbated risk of type 2 diabetes remains to be established.

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