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Open AccessJournal ArticleDOI

The human obesity gene map: the 2003 update.

TLDR
This is the tenth update of the human obesity gene map, incorporating published results up to the end of October 2003 and continuing the previous format.
Abstract
This is the tenth update of the human obesity gene map, incorporating published results up to the end of October 2003 and continuing the previous format. Evidence from single-gene mutation obesity cases, Mendelian disorders exhibiting obesity as a clinical feature, quantitative trait loci (QTLs) from human genome-wide scans and animal crossbreeding experiments, and association and linkage studies with candidate genes and other markers is reviewed. Transgenic and knockout murine models relevant to obesity are also incorporated (N = 55). As of October 2003, 41 Mendelian syndromes relevant to human obesity have been mapped to a genomic region, and causal genes or strong candidates have been identified for most of these syndromes. QTLs reported from animal models currently number 183. There are 208 human QTLs for obesity phenotypes from genome-wide scans and candidate regions in targeted studies. A total of 35 genomic regions harbor QTLs replicated among two to five studies. Attempts to relate DNA sequence variation in specific genes to obesity phenotypes continue to grow, with 272 studies reporting positive associations with 90 candidate genes. Fifteen such candidate genes are supported by at least five positive studies. The obesity gene map shows putative loci on all chromosomes except Y. Overall, more than 430 genes, markers, and chromosomal regions have been associated or linked with human obesity phenotypes. The electronic version of the map with links to useful sites can be found at http:obesitygene.pbrc.edu.

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Obesity and Cardiovascular Disease: Pathophysiology, Evaluation, and Effect of Weight Loss

TL;DR: The available evidence of the impact of obesity on CVD is reviewed with emphasis on the evaluation of cardiac structure and function in obese patients and the effect of weight loss on the cardiovascular system.
Journal ArticleDOI

The human obesity gene map: the 2005 update.

TL;DR: The 12th update of the human obesity gene map is presented, which incorporates published results up to the end of October 2005, and shows putative loci on all chromosomes except Y.
Journal ArticleDOI

The human obesity gene map: the 2004 update.

TL;DR: This paper presents the 12th update of the human obesity gene map, which incorporates published results up to the end of October 2005, and shows putative loci on all chromosomes except Y.
Journal ArticleDOI

Behavioral Treatment of Obesity

TL;DR: Behavioral treatment for obesity seeks to identify and modify eating, activity, and thinking habits that contribute to patients' weight problems as discussed by the authors, recognizing that body weight is affected by factors other than behavior, which include genetic, metabolic, and hormonal influences.
Journal ArticleDOI

The genetics of human obesity

TL;DR: In the future, dissection of the complex genetic architecture of obesity will provide new avenues for treatment and prevention, and will increase the understanding of the regulation of energy balance in humans.
References
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Journal ArticleDOI

Positional cloning of the mouse obese gene and its human homologue

TL;DR: The ob gene product may function as part of a signalling pathway from adipose tissue that acts to regulate the size of the body fat depot.
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Identification and expression cloning of a leptin receptor Ob-R

TL;DR: The ob gene product, leptin, is an important circulating signal for the regulation of body weight and a series of leptin-alkaline phosphatase (AP) fusion proteins as well as [125I]leptin fusion proteins were generated to identify high affinity leptin-binding sites in the mouse choroid plexus.
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A central role for JNK in obesity and insulin resistance

TL;DR: It is shown that JNK activity is abnormally elevated in obesity and an absence of JNK1 results in decreased adiposity, significantly improved insulin sensitivity and enhanced insulin receptor signalling capacity in two different models of mouse obesity.
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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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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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