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: [e-mail]

Received 16 December 2002; Accepted 17 December 2002.
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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: [e-mail])

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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.
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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

[Sinti]

1. You know, back in the day it would have been called the 'survival' gene

and by back in the day I mean back in the ice age, or other times of famine :)

I guarantee there is a gene and/or other physical factors that causes some people to gain more weight than others. I've lived with someone who ate precisely what I ate daily - no more no less, the exact food. I know, I fixed it all. They would gain weight, I would stay the same. What the other individual ate had to change for them to lose the weight, apparently they needed more of some stuff and less of other stuff. :shrug: We try to do what works around here - forget the dogma.

There are other factors, also, I'm sure. Stress wold likely cause a person to keep weight on or even gain weight. Under stress the body would react as if it's under threat. The biggest threat to human existence is starvation. It makes sense that it would store more for later while stressed.

All the toxins in our environment I'm convinced also play a part. As food gets more fake and toxic people get heavier and heavier.

It's good to see real science looking into the many factors, and treating it like a medical problem, rather than just taking a bat to people's heads - as if that ever worked.

[nadinbrzezinski]

2. Oh absolutely and I am also almost betting something is

making it express itself more than it should just by available food.

And yes, it is nice to see that science is looking at this.

[imdjh]

4. I wish science would look into zero calorie food that looks and tastes like the real thing.

Ever notice on Star Trek that the only fat people are guest stars and a couple of somewhat dimwitted (though warp capable) species? I think that David Ogden Stiers is the fattest person to ever be on Star Trek, though Riker was headed for a record for a regular.

ANyway, it's the replicators. They can turn out extra cheese pizza with no calories. Not only that, but somehow they manage to starve Seven Of Nine while keeping her tits inflated. I have known some big chested girls, but if they got down to Seven's body fat percentage, those girls would be flat.

[nadinbrzezinski]

6. Actually replicator food has normal caloric loads

:-)

Yes, I know a few of the writers.

But Star Trek is supposed to be an ideal world... (and about the cold war, now about the war on terror, and social cometary) but the mostly thin and healthy crew is part of that utopia and of course Hollywood. Had lots of fun with some professors looking at that in college.

[imdjh]

8. Do you kick puppies?

I was kind of looking forward to replicators and zero calorie double cheese pizza.

[imdjh]

3. Oh, see, I saw it the other way. Evolution.

I always figured that we fatties had evolved to the point of needing very little food.

[nadinbrzezinski]

5. It is actually, but in a culture wiht a LOT of food

it is maladaptive. Which reminds for the exploding heads department... I need to look for the peer review on BMR of overweight and obese people... surprisingly it is less.

Yes I read that a few months ago... no hunt the article again...

[imdjh]

7. All I know is, that if I go on diets, I lose weight. Especially if I exercise.

But it's a lot of work, and I haven't been my optimum weight in a long long time. I lose weight quickly, especially on Medifast or Adkins. But keeping it off is hard and no one around you says, "Hey IM, you're getting chunky there." because they are too polite, so you kid yourself until it's time to start all over.

[nadinbrzezinski]

9. May I make a sugestion?

Don't go on a diet... start eating when you're hungry, and stopping when you are full. Eat slow, in smaller plates, and do not do this while reading, watching TV or any other distraction.

If you do that... and have absolutely no forbidden foods, your chances of success should go up.

Going on a diet has a lot of those components about forbidden foods and all that. Oh and of course keep the exercise, good for the heart and other things...

I like to tell people go read Ian McKenna's I can make you thin. It is intuitive eating brought down to the masses... but it is as old as well humans.

[librechik]

13. Paul McKenna

he is great....

[FarCenter]

10. The Mifflin equation is the more accurate of several BMR estimator

MEN: kcal/day = 5 + 10(wt) + 6.25 (ht) – 5 (age)
WOMEN: kcal/day = -161 + 10 (wt) + 6.25 (ht) – 5 (age)

See http://www.korr.com/products/predictive_eqns.htm for an online calculator of BMR using Mifflin, Harris-Benedict and Owen equations.

[FarCenter]

11. A review paper from the journal CELL on obesity and genetics

Obesity and the Regulation of Energy Balance
Bruce M. Spiegelman and Jeffrey S. Flier
Cell, Vol. 104, 531–543, February 23, 2001,

http://www.richardhill.com.au/obesityEnergyBalance.pdf

Conclusions
Obesity and its antithesis, starvation, have always been part of the human condition, and for most of human history have been seen as resulting simply from availability of food, or acts of will related to attainment of desired body shape. Although this view persists in some quarters to this day, the last 5 years of the millennium have witnessed a dramatic increase in our understand ing of the biology of regulated energy balance and body weight. Physiologic pathways whose existence was debated 10 years ago are now being characterized in molecule lecular detail, with immediate implications for understanding of pathogenesis of human obesity and other disorders of energy balance. The roadmap provided by these advances establishes a clear direction for future research, but critical details remain to be discovered, and therapeutic applications remain to be realized. In particular,
the mechanisms by which environmental factors, including diet and exercise, interact with molecular pathways in the common forms of obesity is largely unknown at present. Insights from the sequencing of the human genome and the coming advances in proteomics are likely to fuel the next wave of progress. It is likely that both new genes and new regulatory pathways will be identified. It may seem unlikely that the recent wave of progress can be matched in the early years of the current millennium, but we would not choose to make that bet.

[FarCenter]

12. The Human Obesity Gene Map is now the Obesity Gene Map Database

You can query it at http://obesitygene.pbrc.edu/

The 2005 version is available free from the journal NATURE at http://www.nature.com/oby/journal/v14/n4/pdf/oby200671a.pdf

[nadinbrzezinski]

14. for the evening crew