The Human Obesity Gene Map: The 1996 Update

Pérusse, Louis; Chagnon, YC; Ft, Dionne; Bouchard, Claude

doi:10.1002/j.1550-8528.1997.tb00283.x

Cited by 53 publications

(38 citation statements)

References 57 publications

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“…dence on complex inheritance without a database (e.g., Duffy, 1997;Perusse et al, 1997). Internet gives a general asthma database (http://cooke.gsf.de).…”

Section: Methodsmentioning

confidence: 99%

Mapping oligogenes for atopy and asthma by meta-analysis

et al. 2000

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Meta-analysis is presented for published studies on linkage or allelic association that have in common only reported significance levels. Reporting is biassed, and nonsignificance is seldom quantified. Therefore meta-analysis cannot identify oligogenes within a candidate region nor establish their significance, but it defines candidate regions well. Applied to a database on atopy and asthma, candidate regions are identified on chromosomes 6, 5, 16, 11, 12, 13, 14, 7, 20, and 10, in rank order from strongest to weakest evidence. On the other hand, there is little support for chromosomes 9, 8, 18, 1, and 15 in the same rank order. The evidence from 156 publications is reviewed for each region. With reasonable type I and II errors several thousand affected sib pairs would be required to detect a locus accounting for 1/10 of the genetic effect on asthma. Identification of regions by a genome scan for linkage and allelic association requires international collaborative studies to reach the necessary sample size, using lod-based methods that specify a weakly parametric alternative hypothesis and can be combined over studies that differ in ascertainment, phenotypes, and markers. This has become the central problem in complex inheritance.

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“…dence on complex inheritance without a database (e.g., Duffy, 1997;Perusse et al, 1997). Internet gives a general asthma database (http://cooke.gsf.de).…”

Section: Methodsmentioning

confidence: 99%

Mapping oligogenes for atopy and asthma by meta-analysis

et al. 2000

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“…Hepatic complications in obese children have been reported, particularly hepatic steatosis characterized by raised serum transaminase levels (124). Abnormal liver enzymes may be associated with cholelithiasis, but this condition is rare in children and adolescents.…”

Section: Hepatic and Gastric Complicationsmentioning

confidence: 99%

“…Several types of research have been used to identify these genes and the specific DNA sequence variation responsible for the increase in risk of becoming obese. The evidence accumulated so far has recently been reviewed (124) and provides statistical or experimental support for a role for about 70 genes, loci or markers. Many more years of research will be needed before the important genes and critical mutations are finally identified for both excess body fat content and upper body and abdominal fat accumulation.…”

Section: Types Of Genetic Effectsmentioning

confidence: 99%

Global burden of obesity in 2005 and projections to 2030

et al. 2008

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“…Among the genetic factors, polymorphism or mutations in any of the following genes may be involved in the pathophysiology of obesity: badrenergic receptor, tumor necrosis factor (TNF), pro-opiomelanocortin (POMC), neuropeptide Y (NPY), NPY-receptor, melanocortin receptor (MC4R), leptin, and leptin receptor. 3 Severe obesity is associated with a higher likelihood of continued overweight. This risk is much higher in children with obese parents.…”

Section: Introductionmentioning

confidence: 99%

Role of obesity and leptin in the pubertal process and pubertal growth—a review

2003

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The prevalence of obesity is increasing alarmingly to epidemic proportions in children and adolescents, especially in industrialized countries. The finding that overweight children, especially girls, tend to mature earlier than lean children has led to the hypothesis that the degree of body fatness may trigger the neuroendocrine events that lead to the onset of puberty. Obese children have high leptin levels, and these may play a role in their earlier onset of puberty. Leptin receptors have been identified in the hypothalamus, gonadotrope cells of the anterior pituitary, and ovarian follicular cells, as well as Leydig cells. Leptin accelerates gonadotropin-releasing hormone (GnRH) pulsatility in hypothalamic neurons, and it has a direct effect on the anterior pituitary. Leptin administration at low doses may have a permissive, threshold effect on the central networks that regulate gonadotropin secretion. However, at high levels, such as those in obese people, it can have an inhibitory effect on the gonads. Children with obesity also have increased adrenal androgen levels, which may be involved in the accelerated growth of these children before puberty. Recent data indicate that leptin has a specific role in stimulating the activity of enzymes essential for the synthesis of adrenal androgens. Children with exogenous obesity frequently show an increase in height velocity with tall stature for age despite low growth hormone levels. Our group has shown that leptin acts as a skeletal growth factor, with a direct effect on skeletal growth centers, in the mice mandibular condyle, a model of endochondral ossification. In summary, obesity is associated with early puberty. Elevated leptin levels might have a permissive effect on the pubertal process and pubertal growth.

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The Human Obesity Gene Map: The 1996 Update

Cited by 53 publications

References 57 publications

Mapping oligogenes for atopy and asthma by meta-analysis

Mapping oligogenes for atopy and asthma by meta-analysis

Global burden of obesity in 2005 and projections to 2030

Role of obesity and leptin in the pubertal process and pubertal growth—a review

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