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Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas, USA
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Waseda Research Institute for Science and Engineering, Waseda University, Tokyo, Japan
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Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas, USA
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Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas, USA
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Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas, USA
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Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas, USA
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Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas, USA
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Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas, USA
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Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas, USA
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Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas, USA
Department of Pediatrics, University of Kansas Medical Center, Kansas City, Kansas, USA
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cells regulates programming of the setpoint for testicular growth and function. In the absence of a functional Prl3c1 gene, the setpoint for testicular size and functional output was increased. The testicular homeostatic setpoint control system
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, the concept of the Developmental Origin of Health and Disease ( Gluckman & Hanson 2004 ) proposes that changes in the intrauterine environment modify the metabolic status of the foetus, and thereby prenatal programming, play a key role in juvenile
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their interactive effects likely program the adult phenotype. The foetus is normally protected from high maternal glucocorticoid levels by the ‘placental glucocorticoid barrier’, in which the enzyme 11β-hydroxysteroid dehydrogenase type 2 (HSD11B2
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nutritional or hormonal factors during critical periods of life (such as pregnancy and/or lactation) with the development of chronic diseases in adulthood, such as obesity and type 2 diabetes. This biological phenomenon is known as metabolic programming
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Department of Physiological Sciences, Department of Basic and Experimental Nutrition, Laboratory of Molecular Endocrinology, Department of Applied Nutrition, Roberto Alcântara Gomes Biology Institute
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Introduction Environmental, nutritional, or hormonal influences in early life (gestation and lactation) may change some physiological parameters in adulthood, a phenomenon known as programing ( Lucas 1994 , Barker 2007 , Moura & Passos 2005
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2004 ). This association is thought to reflect the impact of early developmental disturbances that program adverse outcomes in adult life ( Gluckman & Hanson 2004 ). The latter may manifest as a predisposition for disease states, such as that which
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Birth weight is a determinant of blood leptin concentrations in adults. Since nutrition during pregnancy can affect birth weight, the hypothesis that feed intake during pregnancy alters leptin expression in progeny was examined. Leptin mRNA was measured in subcutaneous adipose tissue and leptin protein was measuredin blood plasma from 59 day old female pigs whose mothers were fed at the same restricted rate except that half were permitted to consume 35% more feed during the second quarter of pregnancy. Leptin mRNA abundance in adipose tissue (P=0.015) and plasma leptin concentration (P=0.01) were higher in progeny from mothers provided with more feed. Body weight at birth was negatively correlated with the abundance of leptin mRNA in subcutaneous fat at 59 days of age (P=0.01). This study shows for the first time that maternal nutrition during pregnancy programs postnatal leptin expression in offspring.
Children’s Brain Tumour Research Centre,
School of Nursing, The University of Nottingham, Nottingham NG7 2UH, UK
Macaulay Institute, Craigiebuckler, Aberdeen AB15 8QH, UK
Astra Zeneca, Alderley Park, Cheshire, UK
Discipline of Physiology, University of Adelaide, Adelaide, South Australia 5005, Australia
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Children’s Brain Tumour Research Centre,
School of Nursing, The University of Nottingham, Nottingham NG7 2UH, UK
Macaulay Institute, Craigiebuckler, Aberdeen AB15 8QH, UK
Astra Zeneca, Alderley Park, Cheshire, UK
Discipline of Physiology, University of Adelaide, Adelaide, South Australia 5005, Australia
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Children’s Brain Tumour Research Centre,
School of Nursing, The University of Nottingham, Nottingham NG7 2UH, UK
Macaulay Institute, Craigiebuckler, Aberdeen AB15 8QH, UK
Astra Zeneca, Alderley Park, Cheshire, UK
Discipline of Physiology, University of Adelaide, Adelaide, South Australia 5005, Australia
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Children’s Brain Tumour Research Centre,
School of Nursing, The University of Nottingham, Nottingham NG7 2UH, UK
Macaulay Institute, Craigiebuckler, Aberdeen AB15 8QH, UK
Astra Zeneca, Alderley Park, Cheshire, UK
Discipline of Physiology, University of Adelaide, Adelaide, South Australia 5005, Australia
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Children’s Brain Tumour Research Centre,
School of Nursing, The University of Nottingham, Nottingham NG7 2UH, UK
Macaulay Institute, Craigiebuckler, Aberdeen AB15 8QH, UK
Astra Zeneca, Alderley Park, Cheshire, UK
Discipline of Physiology, University of Adelaide, Adelaide, South Australia 5005, Australia
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Children’s Brain Tumour Research Centre,
School of Nursing, The University of Nottingham, Nottingham NG7 2UH, UK
Macaulay Institute, Craigiebuckler, Aberdeen AB15 8QH, UK
Astra Zeneca, Alderley Park, Cheshire, UK
Discipline of Physiology, University of Adelaide, Adelaide, South Australia 5005, Australia
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Children’s Brain Tumour Research Centre,
School of Nursing, The University of Nottingham, Nottingham NG7 2UH, UK
Macaulay Institute, Craigiebuckler, Aberdeen AB15 8QH, UK
Astra Zeneca, Alderley Park, Cheshire, UK
Discipline of Physiology, University of Adelaide, Adelaide, South Australia 5005, Australia
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Children’s Brain Tumour Research Centre,
School of Nursing, The University of Nottingham, Nottingham NG7 2UH, UK
Macaulay Institute, Craigiebuckler, Aberdeen AB15 8QH, UK
Astra Zeneca, Alderley Park, Cheshire, UK
Discipline of Physiology, University of Adelaide, Adelaide, South Australia 5005, Australia
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Children’s Brain Tumour Research Centre,
School of Nursing, The University of Nottingham, Nottingham NG7 2UH, UK
Macaulay Institute, Craigiebuckler, Aberdeen AB15 8QH, UK
Astra Zeneca, Alderley Park, Cheshire, UK
Discipline of Physiology, University of Adelaide, Adelaide, South Australia 5005, Australia
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Children’s Brain Tumour Research Centre,
School of Nursing, The University of Nottingham, Nottingham NG7 2UH, UK
Macaulay Institute, Craigiebuckler, Aberdeen AB15 8QH, UK
Astra Zeneca, Alderley Park, Cheshire, UK
Discipline of Physiology, University of Adelaide, Adelaide, South Australia 5005, Australia
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Children’s Brain Tumour Research Centre,
School of Nursing, The University of Nottingham, Nottingham NG7 2UH, UK
Macaulay Institute, Craigiebuckler, Aberdeen AB15 8QH, UK
Astra Zeneca, Alderley Park, Cheshire, UK
Discipline of Physiology, University of Adelaide, Adelaide, South Australia 5005, Australia
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Children’s Brain Tumour Research Centre,
School of Nursing, The University of Nottingham, Nottingham NG7 2UH, UK
Macaulay Institute, Craigiebuckler, Aberdeen AB15 8QH, UK
Astra Zeneca, Alderley Park, Cheshire, UK
Discipline of Physiology, University of Adelaide, Adelaide, South Australia 5005, Australia
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Children’s Brain Tumour Research Centre,
School of Nursing, The University of Nottingham, Nottingham NG7 2UH, UK
Macaulay Institute, Craigiebuckler, Aberdeen AB15 8QH, UK
Astra Zeneca, Alderley Park, Cheshire, UK
Discipline of Physiology, University of Adelaide, Adelaide, South Australia 5005, Australia
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Children’s Brain Tumour Research Centre,
School of Nursing, The University of Nottingham, Nottingham NG7 2UH, UK
Macaulay Institute, Craigiebuckler, Aberdeen AB15 8QH, UK
Astra Zeneca, Alderley Park, Cheshire, UK
Discipline of Physiology, University of Adelaide, Adelaide, South Australia 5005, Australia
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, Zhang et al. 2001 ). It is currently not known whether these processes are susceptible to long-term nutritional programming. The abundance of mRNA for growth factor genes is established to be nutritionally regulated in those fetal tissues whose
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metabolic programming or metabolic imprinting. There are strong associations between metabolic programming and functional and structural changes in the brain. Hypothalamic neuron dense areas related to body weight (BW) control are changed in adult rats that
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substantiate the hypothesis that an early perturbation due to in utero androgen excess resets the reproductive and metabolic trajectory of the growing fetus and programs target tissue differentiation and development, supporting a potential role of epigenetics