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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.
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

Genetic variation in the beta 3-adrenergic receptor and an increased capacity to gain weight in patients with morbid obesity.

TL;DR: A mutation resulting in the replacement of tryptophan by arginine at position 64 (Trp64Arg) was detected by an analysis of restriction-fragment–length polymorphisms with the use of the endonuclease Bst NI, which discriminates between the normal and mutant sequences.
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Association of a polymorphism in the β3-adrenergic receptor gene with features of the insulin resistance syndrome in Finns

TL;DR: The Trp64Arg allele of the beta 3-adrenergic receptor is associated with abdominal obesity and resistance to insulin and may contribute to the early onset of NIDDM.
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Co-localization of growth hormone secretagogue receptor and NPY mRNA in the arcuate nucleus of the rat.

TL;DR: The results indicate that GHS have other effects on neuroendocrine regulation than GH release via GHRH neurons, and Stimulation of the arcuate NPY neurons via GHS-R may explain the increased appetite and the cortisol release seen after administration of some GHS compounds.
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