Diet-induced obesity in female mice leads to offspring hyperphagia, adiposity, hypertension, and insulin resistance: a novel murine model of developmental programming

Samuelsson, A.-M., Matthews, P. A., Argenton, M. , Christie, M. R., McConnell, J. M., Jansen, E. H. J. M., Piersma, A. H., Ozanne, S. E., Twinn, D. F., Remacle, C., Rowlerson, A., Poston, L. and Taylor, P. D. (2008) Diet-induced obesity in female mice leads to offspring hyperphagia, adiposity, hypertension, and insulin resistance: a novel murine model of developmental programming. Hypertension, 51 (2). pp. 383-392. ISSN 0194-911X

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Maternal obesity is increasingly prevalent and may affect the long-term health of the child. We investigated the effects of maternal diet-induced obesity in mice on offspring metabolic and cardiovascular function. Female C57BL/6J mice were fed either a standard chow (3 fat, 7 sugar) or a palatable obesogenic diet (16 fat, 33 sugar) for 6 weeks before mating and throughout pregnancy and lactation. Offspring of control (OC) and obese dams (OO) were weaned onto standard chow and studied at 3 and 6 months of age. OO were hyperphagic from 4 to 6 weeks of age compared with OC and at 3 months locomotor activity was reduced and adiposity increased (abdominal fat pad mass; P<0.01). OO were heavier than OC at 6 months (body weight, P<0.05). OO abdominal obesity was associated with adipocyte hypertrophy and altered mRNA expression of β-adrenoceptor 2 and 3, 11βHSD-1, and PPAR-γ 2. OO showed resistance artery endothelial dysfunction at 3 months, and were hypertensive, as assessed by radiotelemetry (nighttime systolic blood pressure at 6 months mm Hg mean±SEM, male OO, 134±1 versus OC, 124±2, n=8, P<0.05; female OO, 137±2 versus OC, 122±4, n=8, P<0.01). OO skeletal muscle mass (tibialis anterior) was significantly reduced (P<0.01) OO fasting insulin was raised at 3 months and by 6 months fasting plasma glucose was elevated. Exposure to the influences of maternal obesity in the developing mouse led to adult offspring adiposity and cardiovascular and metabolic dysfunction. Developmentally programmed hyperphagia, physical inactivity, and altered adipocyte metabolism may play a mechanistic role. © 2008 American Heart Association, Inc.

Keywords:11beta hydroxysteroid dehydrogenase, beta adrenergic receptor, glucose, insulin, messenger RNA, peroxisome proliferator activated receptor gamma 2, abdominal fat, abdominal obesity, adipocyte, animal cell, animal experiment, animal model, animal tissue, artery resistance, article, body weight, cardiovascular function, controlled study, disease association, endothelial dysfunction, female, fetus, gene expression, glucose blood level, hyperphagia, hypertension, insulin blood level, insulin resistance, lactation, lipid diet, locomotion, maternal nutrition, mating, metabolic syndrome X, mouse, muscle mass, nonhuman, obesity, pregnancy, prevalence, priority journal, progeny, skeletal muscle, statistical significance, sugar intake, systolic blood pressure, telemetry, tibialis anterior muscle, weaning, Adipocytes, Adiposity, Animals, Arteries, Blood Pressure, Capillaries, Cell Size, Diet, Glucose Tolerance Test, Heart Rate, Male, Mice, Mice, Inbred C57BL, Pancreas, Pregnancy Complications, Prenatal Exposure Delayed Effects, Vascular Resistance
Subjects:B Subjects allied to Medicine > B100 Anatomy, Physiology and Pathology
Divisions:College of Science > School of Life Sciences
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ID Code:18118
Deposited On:31 Jul 2015 09:15

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