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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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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.
Journal ArticleDOI

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

Congenital leptin deficiency is associated with severe early-onset obesity in humans

TL;DR: The severe obesity found in two severely obese children who are members of the same highly consanguineous pedigree provides the first genetic evidence that leptin is an important regulator of energy balance in humans.
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Abnormal splicing of the leptin receptor in diabetic mice

TL;DR: A leptin receptor was recently cloned from choroid plexus and shown to map to the same 6-cM interval on mouse chromosome 4 as db8, suggesting that the weight-reducing effects of leptin may be mediated by signal transduction through a leptin receptor in the hypothalamus.
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A mutation in the human leptin receptor gene causes obesity and pituitary dysfunction

TL;DR: A homozygous mutation in the human leptin receptor gene results in a truncated leptin receptor lacking both the transmembrane and the intracellular domains, which indicates that leptin is an important physiological regulator of several endocrine functions in humans.
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