Obesity and Genetics, the Obesity Gene

[nadinbrzezinski]

The links to the etiology of obesity and chemicals can be found here

http://www.democraticunderground.com/discuss/duboard.php?az=view_all&address=389x7045342

Now on to the Obesity gene

The Human Obesity Gene Map: The 2002 Update

Yvon C. Chagnon*, Tuomo Rankinen†, Eric E. Snyder†, S. John Weisnagel‡, Louis Pérusse‡ and Claude Bouchard†

1. *Psychiatric Genetic Unit, Laval University Robert-Giffard Research Center, Québec, Canada
2. †Human Genomics Laboratory, Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana
3. ‡Division of Kinesiology, Department of Social and Preventive Medicine, Faculty of Medicine, Laval University, Sainte-Foy, Québec, Canada

Correspondence: Yvon C. Chagnon, Psychiatric Genetic Unit, Laval University Robert-Giffard Research Center, 2601, chemin de la Canardière, room F-6459, Beauport (Québec), G1J 2G3 Canada. E-mail: [email protected]

Received 16 December 2002; Accepted 17 December 2002.
Top of page
Abstract

This is the ninth update of the human obesity gene map, incorporating published results through October 2002 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 various animal crossbreeding experiments, and association and linkage studies with candidate genes and other markers is reviewed. For the first time, transgenic and knockout murine models exhibiting obesity as a phenotype are incorporated (N = 38). As of October 2002, 33 Mendelian syndromes relevant to human obesity have been mapped to a genomic region, and the causal genes or strong candidates have been identified for 23 of these syndromes. QTLs reported from animal models currently number 168; there are 68 human QTLs for obesity phenotypes from genome-wide scans. Additionally, significant linkage peaks with candidate genes have been identified in targeted studies. Seven 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 222 studies reporting positive associations with 71 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. More than 300 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.

http://www.nature.com/oby/journal/v11/n3/abs/oby200347a.html

A mutation in the human leptin receptor gene causes obesity and pituitary dysfunction

Karine Clément1,2,3, Christian Vaisse1,2,3, Najiba Lahlou4, Sylvie Cabrol5, Veronique Pelloux1, Dominique Cassuto1, Micheline Gourmelen5, Christian Dina2, Jean Chambaz6, Jean-Marc Lacorte6, Arnaud Basdevant1,2, Pierre Bougnères6, Yves Lebouc5, Philippe Froguel1,2 & Bernard Guy-Grand1,2

1. Laboratoire de Nutrition et Service de Médecine et Nutrition, Hôtel-Dieu place du Parvis Notre Dame, 75004 Paris, France
2. Institut de Biologie-CNRS EP10, Institut Pasteur de Lille, rue Calmette, 59000 Lille, France
3. Inserm U342, Hôpital Saint Vincent de Paul et service d'Endocrinologie-Diabéte de l'Enfant, avenue Denfert Rochereau, 75014 Paris, France
4. Explorations fonctionnelles endocriniennes, Hôpital d'enfant Armand Trousseau, avenue du Dr Arnold Netter, 75012 Paris, France
5. CJF INSERM 9508, 15 rue de l'Ecole de Médecine, 75005 Paris, France
6. These authors contributed equally to this work.

Correspondence to: Philippe Froguel1,2 Correspondence and request for materials should be addressed to P.F. (e-mail: Email: [email protected])

Top of page
Abstract

The adipocyte-specific hormone leptin, the product of the obese (ob) gene,regulates adipose-tissue mass through hypothalamic effects on satiety and energy expenditure1, 2, 3, 4. Leptin acts through the leptin receptor, a single-transmembrane-domain receptor of the cytokine-receptor family5, 6, 7. In rodents, homozygous mutations ingenes encoding leptin1 or the leptin receptor6 cause early-onsetmorbid obesity, hyperphagia and reduced energy expenditure.

http://www.nature.com/nature/journal/v392/n6674/full/392398a0.html

Obesity Gene: Mice Lacking FTO Gene Burn More Energy And Do Not Become Overweight

ScienceDaily (Mar. 2, 2009) — Obesity has become an epidemic in many parts of the western hemisphere; over 30% of the population of Germany are overweight.
See Also:
Health & Medicine


Scientists from the University of Cologne, in cooperation with scientists from the University of Düsseldorf, have been able to verify the relevance of a certain gene with regard to obesity for the first time.

In 2006, scientists discovered increased amounts of variations of the FTO genes were in overweight people. However, the relevance of this gene and its regular function remained unclear for a long time.

http://www.sciencedaily.com/releases/2009/02/090227072

New Insight Into The Link Between Genetics And Obesity

Researchers from the University of Cambridge, Oxford University and Cancer Research UK, London, have found that the FTO gene, codes for an enzyme that can act directly on DNA to modify it -- suggesting that it might have a role in controlling the turning on and off of other genes.

They also found that FTO is highly expressed in a region of the brain, called the hypothalamus, which has important roles in the control of hunger and satiety and that, in certain parts of the hypothalamus, the levels of FTO are influenced by feeding and fasting.

http://www.sciencedaily.com/releases/2007/11/071108141509.htm

Childhood Obesity Risk Increased By Newly-Discovered Genetic Mutations, Says Study

ScienceDaily (Jan. 19, 2009) — Three new genetic variations that increase the risk of obesity are revealed in a new study, published January 18 in the journal Nature Genetics. The authors suggest that if each acted independently, these variants could be responsible for up to 50% of cases of severe obesity.
See Also:
Health & Medicine





Together with existing research, the new findings should ultimately provide the tools to predict which young children are at risk of becoming obese. Health professionals could then intervene to help such children before they develop weight problems, say the researchers from Imperial College London, the French National Research Institute CNRS and other international institutions.

In the UK, one in ten children under the age of six is obese, according to the Department of Health's National Child Measurement Programme 2007/08.

For today's ten-year study, scientists looked at the genetic makeup of obese children under six and morbidly obese adults, most of whom had been obese since childhood or adolescence, and compared this with age matched people of normal weight. The study reveals three previously unidentified genetic variations that increase the risk of severe obesity significantly, giving new insight into the reasons why some people become obese and others do not.

http://www.sciencedaily.com/releases/2009/01/090118200638.htm