A metabolic defect promotes obesity in mice lacking melanocortin-4 receptors. - Wikidata - awgldk - TriplyDB

A metabolic defect promotes obesity in mice lacking melanocortin-4 receptors.

A metabolic defect promotes obesity in mice lacking melanocortin-4 receptors.

http://www.wikidata.org/entity/Q35431515

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Neither agouti-related protein nor neuropeptide Y is critically required for the regulation of energy homeostasis in mice Direct insulin and leptin action on pro-opiomelanocortin neurons is required for normal glucose homeostasis and fertility Kv1.3 gene-targeted deletion alters longevity and reduces adiposity by increasing locomotion and metabolism in melanocortin-4 receptor-null mice The melanocortin system and energy balance Neural Control of Energy Expenditure Central nervous control of energy and glucose balance: focus on the central melanocortin system A Deletion in the Canine POMC Gene Is Associated with Weight and Appetite in Obesity-Prone Labrador Retriever Dogs Severe Atherosclerosis and Hypercholesterolemia in Mice Lacking Both the Melanocortin Type 4 Receptor and Low Density Lipoprotein Receptor A pharmacologically active monoclonal antibody against the human melanocortin-4 receptor: effectiveness after peripheral and central administration Melanocortin receptor 4 deficiency affects body weight regulation, grooming behavior, and substrate preference in the rat Variation at the melanocortin 4 receptor gene and response to weight-loss interventions in the diabetes prevention program Effects of a novel MC4R agonist on maintenance of reduced body weight in diet-induced obese mice.Central neural regulation of brown adipose tissue thermogenesis and energy expenditure Melanocortin-3 receptors and metabolic homeostasis.Hypothalamic circuits regulating appetite and energy homeostasis: pathways to obesity.Mouse models of the metabolic syndrome.Leptin in human physiology and therapeutics Heritability of physical activity traits in Brazilian families: the Baependi Heart Study.Postnatal changes in the expression pattern of the imprinted signalling protein XLαs underlie the changing phenotype of deficient mice.Approach to assessing determinants of glucose homeostasis in the conscious mouse Recent advances in clinical practice challenges and opportunities in the management of obesity.Surfactant protein d deficiency in mice is associated with hyperphagia, altered fat deposition, insulin resistance, and increased basal endotoxemia.Anorexia nervosa: a unified neurological perspective Glucocorticoids exacerbate obesity and insulin resistance in neuron-specific proopiomelanocortin-deficient mice.Associations of fatty acids in cerebrospinal fluid with peripheral glucose concentrations and energy metabolism.The role of leptin in the regulation of energy balance and adiposity.Characterization of the hyperphagic response to dietary fat in the MC4R knockout mouse.Lack of cAMP-response element-binding protein 1 in the hypothalamus causes obesity.Assessment of voluntary ethanol consumption and the effects of a melanocortin (MC) receptor agonist on ethanol intake in mutant C57BL/6J mice lacking the MC-4 receptor Chronic HO-1 induction with cobalt protoporphyrin (CoPP) treatment increases oxygen consumption, activity, heat production and lowers body weight in obese melanocortin-4 receptor-deficient mice.Homeostastic and non-homeostatic functions of melanocortin-3 receptors in the control of energy balance and metabolism.The role of the central melanocortin system in the regulation of food intake and energy homeostasis: lessons from mouse models.Mice lacking dipeptidyl peptidase IV are protected against obesity and insulin resistance Peripheral mechanisms in appetite regulation.The orally active melanocortin-4 receptor antagonist BL-6020/979: a promising candidate for the treatment of cancer cachexia Hypothalamic inflammation: a double-edged sword to nutritional diseases.Emerging antiobesity drugs.Vagal control of satiety and hormonal regulation of appetite Recent developments in our understanding of melanocortin system in the regulation of food intake.Energy expenditure, physical activity and body-weight control.

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P2860

A metabolic defect promotes obesity in mice lacking melanocortin-4 receptors.

http://www.wikidata.org/entity/Q35431515

description

2000 nî lūn-bûn

@nan

2000 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2000 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2000年の論文

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2000年論文

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2000年論文

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2000年論文

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2000年論文

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2000年論文

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2000年论文

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name

A metabolic defect promotes obesity in mice lacking melanocortin-4 receptors.

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A metabolic defect promotes obesity in mice lacking melanocortin-4 receptors.

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type

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A metabolic defect promotes obesity in mice lacking melanocortin-4 receptors.

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A metabolic defect promotes obesity in mice lacking melanocortin-4 receptors.

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prefLabel

A metabolic defect promotes obesity in mice lacking melanocortin-4 receptors.

@ast

A metabolic defect promotes obesity in mice lacking melanocortin-4 receptors.

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Proceedings of the National Academy of Sciences of the United States of America

P1476

A metabolic defect promotes obesity in mice lacking melanocortin-4 receptors.

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P2093

D J Marsh

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G I Miura

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K Yagaloff

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L Ste Marie

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R D Palmiter

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P2860

A frameshift mutation in MC4R associated with dominantly inherited human obesity

Molecular cloning, expression, and gene localization of a fourth melanocortin receptor

Agouti protein is an antagonist of the melanocyte-stimulating-hormone receptor

A frameshift mutation in human MC4R is associated with a dominant form of obesity

Targeted disruption of the melanocortin-4 receptor results in obesity in mice

Localization of the melanocortin-4 receptor (MC4-R) in neuroendocrine and autonomic control circuits in the brain

Thermoregulatory and metabolic phenotypes of mice lacking noradrenaline and adrenaline

From lesions to leptin: hypothalamic control of food intake and body weight.

The Central Melanocortin System and Energy Homeostasis.

Pigmentation phenotypes of variant extension locus alleles result from point mutations that alter MSH receptor function.

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