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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.
About
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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Journal ArticleDOI

Role of Brain Insulin Receptor in Control of Body Weight and Reproduction

TL;DR: Mice created with a neuron-specific disruption of the IR gene showed increased food intake, and both male and female mice developed diet-sensitive obesity with increases in body fat and plasma leptin levels, mild insulin resistance, elevated plasma insulin levels, and hypertriglyceridemia.
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Changes in Energy Expenditure Resulting from Altered Body Weight

TL;DR: Maintenance of a reduced or elevated body weight is associated with compensatory changes in energy expenditure, which oppose the maintenance of a body weight that is different from the usual weight, which may account for the poor long-term efficacy of treatments for obesity.
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Effects of recombinant leptin therapy in a child with congenital leptin deficiency.

TL;DR: The administration of leptin corrects their obesity by reducing their food intake and increasing their energy expenditure and these mice also have hyperinsulinemia, corticosterone excess, and infertility, which also are reversed by treatment with leptin.
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Severe early-onset obesity, adrenal insufficiency and red hair pigmentation caused by POMC mutations in humans

TL;DR: These findings represent the first examples of a genetic defect within the POMC gene and define a new monogenic endocrine disorder resulting in early–onset obesity, adrenal insufficiency and red hair pigmentation.
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The role of neuropeptide Y in the antiobesity action of the obese gene product.

TL;DR: In this paper, a truncated inactive protein was found to suppress food intake and decrease body weight in normal and ob/ob mice but not db/db (diabetic) mice, which are thought to lack the appropriate receptor.
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