Maternal diabetes compromises the organization of hypothalamic feeding circuits and impairs leptin sensitivity in offspring. - Wikidata - awgldk - TriplyDB

Maternal diabetes compromises the organization of hypothalamic feeding circuits and impairs leptin sensitivity in offspring.

Maternal diabetes compromises the organization of hypothalamic feeding circuits and impairs leptin sensitivity in offspring.

http://www.wikidata.org/entity/Q35417339

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Regulation and Function of RFRP-3 (GnIH) Neurons during Postnatal Development Early Life Nutrition and Energy Balance Disorders in Offspring in Later Life Developmental programming of hypothalamic neuronal circuits: impact on energy balance control Embryonic development of the hypothalamic feeding circuitry: Transcriptional, nutritional, and hormonal influences The molecular mechanisms of offspring effects from obese pregnancy Effects of maternal obesity on placental function and fetal development Reduced melanocortin production causes sexual dysfunction in male mice with POMC neuronal insulin and leptin insensitivity.Examination of the influence of leptin and acute metabolic challenge on RFRP-3 neurons of mice in development and adulthood.Insulin and Leptin Signaling Interact in the Mouse Kiss1 Neuron during the Peripubertal Period.Implications of maternal conditions and pregnancy course on offspring's medical problems in adult life.Intrauterine growth restriction alters term fetal baboon hypothalamic appetitive peptide balance.Neonatal insulin action impairs hypothalamic neurocircuit formation in response to maternal high-fat feeding.InsR/FoxO1 signaling curtails hypothalamic POMC neuron number.Sexual dimorphism in offspring glucose-sensitive hypothalamic gene expression and physiological responses to maternal high-fat diet feeding.Leptin regulates glutamate and glucose transporters in hypothalamic astrocytes.Gene-environment interactions controlling energy and glucose homeostasis and the developmental origins of obesity SOCS3 deficiency in leptin receptor-expressing cells mitigates the development of pregnancy-induced metabolic changes.Maternal nutritional manipulations program adipose tissue dysfunction in offspring Feed your head: neurodevelopmental control of feeding and metabolism 5-HT2A and 5-HT2C receptors as hypothalamic targets of developmental programming in male rats Severe maternal hyperglycemia exacerbates the development of insulin resistance and fatty liver in the offspring on high fat diet.The cellularity of offspring's adipose tissue is programmed by maternal nutritional manipulations.Alterations in perivascular innervation function in mesenteric arteries from offspring of diabetic rats.PVN pathways controlling energy homeostasis.Development of the hypothalamic melanocortin system.Organizational actions of metabolic hormones.Development, brain plasticity and reward: early high-fat diet exposure confers vulnerability to obesity-view from the chair.Nutritional programming of hypothalamic development: critical periods and windows of opportunity High-fat diet alters the dopamine and opioid systems: effects across development.Differential associations of leptin with adiposity across early childhood.Towards a 'systems'-level understanding of the nervous system and its disorders.Developmental programming by maternal insulin resistance: hyperinsulinemia, glucose intolerance, and dysregulated lipid metabolism in male offspring of insulin-resistant mice.Metabolic programming of insulin action and secretion.Nutritional manipulations in the perinatal period program adipose tissue in offspring.Maternal diabetes mellitus and the origin of non-communicable diseases in offspring: the role of epigenetics.New perspectives on the origin of hypertension; the role of the hypothalamic melanocortin system.Influence of maternal overnutrition and gestational diabetes on the programming of metabolic health outcomes in the offspring: experimental evidence.Intranasal insulin reverts central pathology and cognitive impairment in diabetic mother offspring Long-term consequences of obesity on female fertility and the health of the offspring.The Cross-Link between Adipokines, Insulin Resistance and Obesity in Offspring of Diabetic Pregnancies.

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P2860

Maternal diabetes compromises the organization of hypothalamic feeding circuits and impairs leptin sensitivity in offspring.

http://www.wikidata.org/entity/Q35417339

description

2011 nî lūn-bûn

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2011 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի օգոստոսին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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Maternal diabetes compromises ...... eptin sensitivity in offspring

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Sebastien G Bouret

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Sophie M Steculorum

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P2860

Central nervous system control of food intake

Maternal obesity induced by diet in rats permanently influences central processes regulating food intake in offspring

Leptin deficiency causes insulin resistance induced by uncontrolled diabetes.

Prenatal stress, glucocorticoids and the programming of the brain.

Leptin therapy improves insulin-deficient type 1 diabetes by CNS-dependent mechanisms in mice

Formation of projection pathways from the arcuate nucleus of the hypothalamus to hypothalamic regions implicated in the neural control of feeding behavior in mice.

Trophic action of leptin on hypothalamic neurons that regulate feeding.

Wired on hormones: endocrine regulation of hypothalamic development.

Respective contributions of maternal insulin resistance and diet to metabolic and hypothalamic phenotypes of progeny

Leptin therapy reverses hyperglycemia in mice with streptozotocin-induced diabetes, independent of hepatic leptin signaling.

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4171-4179

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scholarly article

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10.1210/EN.2011-1279

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11

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152

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Sophie M Steculorum

Sebastien G Bouret

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2011-08-23T00:00:00Z

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21862611

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3199015

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