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The neuroendocrinology of obesity

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TLDR
As the nosology of obesity improves, diagnostic efficiency and therapeutic success should increase, leading to a decrease in associated morbidity, mortality, and socioeconomic ramifications.
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This article is published in Endocrinology and Metabolism Clinics of North America.The article was published on 2001-09-01. It has received 59 citations till now. The article focuses on the topics: Birth weight & Weight loss.

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Citations
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Inhibition of PTP1B by trodusquemine (MSI-1436) causes fat-specific weight loss in diet-induced obese mice.

TL;DR: The data establish trodusquemine as an effective central and peripheral PTP1B inhibitor with the potential to elicit noncachectic fat‐specific weight loss and improve insulin and leptin levels.
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Obesity and endocrine disease

TL;DR: The fat cell has been found to be an endocrine organ that produces several peptides that are bioactive and participate in the regulation of adipocyte function that contributes to the development of obesity.
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The Hypothalamic - Pituitary -Adrenal Axis in the Neuroendocrine Regulation of Food Intake and Obesity: The Role of Corticotropin Releasing Hormone

TL;DR: The role of the hypothalamic-pituitary-adrenal axis in the control of food intake and the pathogenesis of obesity is reviewed and the interactions between other neurosystems and this hormonal axis are discussed.
References
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Chronic Central Leptin Infusion Enhances Insulin-Stimulated Glucose Metabolism and Favors the Expression of Uncoupling Proteins

TL;DR: While leptin maintains or favors energy-dissipating mechanisms (UCP1, UCP2, and UCP3), the latter are markedly depressed in pair-fed rats, which may prevent subsequent excessive storage processes, thereby maintaining normal body homeostasis.
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The ciliary neurotrophic factor and its receptor, CNTFRα

TL;DR: The neuroprotective effects of CNTF have been demonstrated in a number of in vitro cell models as well as in vivo in mutant mouse strains which exhibit motor neuron degeneration.
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The effects of subdiaphragmatic vagotomy in rats with ventromedial hypothalamic obesity.

TL;DR: There was a positive correlation between the level of serum insulin and basal gastric acid in VMH lesioned rats which remained significant when the effects of food intake were held constant and supports the possibility that ventromedial hypothalamic injury is followed by enhanced vagal activity and that the vagus may play an important part in the hyperinsulinemia of VMH obesity.
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Leptin increases serotonin turnover by inhibition of brain nitric oxide synthesis

TL;DR: The results indicate that the L-arginine/NO pathway is involved in mediating leptin effects on feeding behavior, and demonstrate that nNOS activity is required for the effects of leptin on brain 5-HT turnover.
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Hypothalamic obesity : The autonomic hypothesis and the lateral hypothalamus.

TL;DR: Several lines of evidence support the hypothesis that derangements in the function of the autonomic nervous system play an important role in the development of hypothalamic obesity, and implicate the VMH in the control of the sympathetic nervous system.
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