Metabolic Imprinting: Critical Impact of the Perinatal Environment on the Regulation of Energy Homeostasis
Epidemiological studies in humans suggest that maternal undernutrition, obesity and diabetes during gestation and lactation can all produce obesity in offspring. Animal models have allowed us to investigate the independent consequences of altering the pre- versus post-natal environments on a variety of metabolic, physiological and neuroendocrine functions as they effect the development in the offspring of obesity, diabetes, hypertension and hyperlipidemia (the 'metabolic syndrome'). During gestation, maternal malnutrition, obesity, type 1 and type 2 diabetes and psychological, immunological and pharmacological stressors can all promote offspring obesity. Normal post-natal nutrition can reduce the adverse impact of some of these pre-natal factors but maternal high-fat diets, diabetes and increased neonatal access to food all enhance the development of obesity and the metabolic syndrome in offspring. The outcome of these perturbations of the perinatal environmental is also highly dependent upon the genetic background of the individual. Those with an obesity-prone genotype are more likely to be affected by factors such as maternal obesity and high-fat diets than are obesity-resistant individuals. Many perinatal manipulations appear to promote offspring obesity by permanently altering the development of central neural pathways, which regulate food intake, energy expenditure and storage. Given their strong neurotrophic properties, either excess or an absence of insulin and leptin during the perinatal period are likely to be effectors of these developmental changes. Because obesity is associated with an increased morbidity and mortality and because of its resistance to treatment, prevention is likely to be the best strategy for stemming the tide of the obesity epidemic. Such prevention should begin in the perinatal period with the identification and avoidance of factors which produce permanent, adverse alterations in neural pathways which control energy homeostasis..
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E-Artikel |
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Erscheinungsjahr: |
2006 |
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Erschienen: |
2006 |
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Zur Gesamtaufnahme - volume:361 |
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Sprache: |
Englisch |
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Beteiligte Personen: |
Levin, Barry E. [VerfasserIn] |
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Biological sciences |
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PPN (Katalog-ID): |
JST065927915 |
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245 | 1 | 0 | |a Metabolic Imprinting: Critical Impact of the Perinatal Environment on the Regulation of Energy Homeostasis |
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520 | |a Epidemiological studies in humans suggest that maternal undernutrition, obesity and diabetes during gestation and lactation can all produce obesity in offspring. Animal models have allowed us to investigate the independent consequences of altering the pre- versus post-natal environments on a variety of metabolic, physiological and neuroendocrine functions as they effect the development in the offspring of obesity, diabetes, hypertension and hyperlipidemia (the 'metabolic syndrome'). During gestation, maternal malnutrition, obesity, type 1 and type 2 diabetes and psychological, immunological and pharmacological stressors can all promote offspring obesity. Normal post-natal nutrition can reduce the adverse impact of some of these pre-natal factors but maternal high-fat diets, diabetes and increased neonatal access to food all enhance the development of obesity and the metabolic syndrome in offspring. The outcome of these perturbations of the perinatal environmental is also highly dependent upon the genetic background of the individual. Those with an obesity-prone genotype are more likely to be affected by factors such as maternal obesity and high-fat diets than are obesity-resistant individuals. Many perinatal manipulations appear to promote offspring obesity by permanently altering the development of central neural pathways, which regulate food intake, energy expenditure and storage. Given their strong neurotrophic properties, either excess or an absence of insulin and leptin during the perinatal period are likely to be effectors of these developmental changes. Because obesity is associated with an increased morbidity and mortality and because of its resistance to treatment, prevention is likely to be the best strategy for stemming the tide of the obesity epidemic. Such prevention should begin in the perinatal period with the identification and avoidance of factors which produce permanent, adverse alterations in neural pathways which control energy homeostasis. | ||
540 | |a Copyright 2006 The Royal Society | ||
650 | 4 | |a development | |
650 | 4 | |a obesity | |
650 | 4 | |a diabetes | |
650 | 4 | |a genetics | |
650 | 4 | |a hypothalamus | |
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650 | 4 | |a Biological sciences |x Biology |x Zoology |x Animals |x Mammals |x Rodents |x Rats | |
650 | 4 | |a Biological sciences |x Biology |x Cytology |x Cell biology |x Cells |x Neurons | |
650 | 4 | |a Biological sciences |x Biology |x Developmental biology |x Reproduction |x Pregnancy | |
650 | 4 | |a Biological sciences |x Biochemistry |x Biomolecules |x Hormones |x Peptide hormones |x Pancreatic hormones |x Insulin | |
650 | 4 | |a Biological sciences |x Biology |x Physiology |x Body composition |x Body weight | |
650 | 4 | |a Health sciences |x Medical conditions |x Diseases |x Metabolic diseases |x Diabetes | |
650 | 4 | |a Biological sciences |x Biology |x Physiology |x Physiological regulation |x Homeostasis | |
650 | 4 | |a Health sciences |x Medical conditions |x Diseases |x Metabolic diseases |x Diabetes |x Diabetes mellitus |x Type 2 diabetes mellitus | |
650 | 4 | |a Health sciences |x Medical sciences |x Nutritional science |x Nutritional status |x Nutritional deficiencies |x Malnutrition | |
650 | 4 | |a Biological sciences |x Biology |x Physiology |x Body composition |x Body weight |x Obesity | |
650 | 4 | |a Biological sciences |x Biology |x Zoology |x Animals |x Mammals |x Rodents |x Rats | |
650 | 4 | |a Biological sciences |x Biology |x Cytology |x Cell biology |x Cells |x Neurons | |
650 | 4 | |a Biological sciences |x Biology |x Developmental biology |x Reproduction |x Pregnancy | |
650 | 4 | |a Biological sciences |x Biochemistry |x Biomolecules |x Hormones |x Peptide hormones |x Pancreatic hormones |x Insulin | |
650 | 4 | |a Biological sciences |x Biology |x Physiology |x Body composition |x Body weight | |
650 | 4 | |a Health sciences |x Medical conditions |x Diseases |x Metabolic diseases |x Diabetes | |
650 | 4 | |a Biological sciences |x Biology |x Physiology |x Physiological regulation |x Homeostasis | |
650 | 4 | |a Health sciences |x Medical conditions |x Diseases |x Metabolic diseases |x Diabetes |x Diabetes mellitus |x Type 2 diabetes mellitus | |
650 | 4 | |a Health sciences |x Medical sciences |x Nutritional science |x Nutritional status |x Nutritional deficiencies |x Malnutrition | |
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