FTO: the first gene contributing to common forms of human obesity
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FTO : the first gene contributing to common forms of human obesity. / Loos, R J F; Bouchard, C.
I: Obesity reviews : an official journal of the International Association for the Study of Obesity, Bind 9, Nr. 3, 05.2008, s. 246-50.Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt
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TY - JOUR
T1 - FTO
T2 - the first gene contributing to common forms of human obesity
AU - Loos, R J F
AU - Bouchard, C
PY - 2008/5
Y1 - 2008/5
N2 - Genome-wide association, the latest gene-finding strategy, has led to the first major success in the field of obesity genetics with the discovery of FTO (fat mass and obesity associated gene) as an obesity-susceptibility gene. A cluster of variants in the first intron of FTO showed a strong and highly significant association with obesity-related traits in three independent genome-wide association studies, a finding that has been replicated in several other studies including adults and children of European descent. Homozygotes for the risk allele weigh on average 3-4 kg more and have a 1.67-fold increased risk of obesity compared with those who did not inherit a risk allele. We are still at an early stage in our understanding of the pathways through which FTO confers to increased obesity risk. Studies in humans and rodents have suggested a central role for FTO through regulation of food intake, whereas others have proposed a peripheral role through an effect on lipolytic activity in adipose tissue. There is no doubt that many more obesity-susceptibility loci remain to be discovered. Progress on this front will therefore require major collaborative efforts and pooling of compatible datasets. We stand to learn a lot about the genetic architecture of human obesity in the coming years. The expectations are high but many challenges remain. Among the latter, translating new advances into useful guidelines for prevention and treatment of obesity will be the most demanding.
AB - Genome-wide association, the latest gene-finding strategy, has led to the first major success in the field of obesity genetics with the discovery of FTO (fat mass and obesity associated gene) as an obesity-susceptibility gene. A cluster of variants in the first intron of FTO showed a strong and highly significant association with obesity-related traits in three independent genome-wide association studies, a finding that has been replicated in several other studies including adults and children of European descent. Homozygotes for the risk allele weigh on average 3-4 kg more and have a 1.67-fold increased risk of obesity compared with those who did not inherit a risk allele. We are still at an early stage in our understanding of the pathways through which FTO confers to increased obesity risk. Studies in humans and rodents have suggested a central role for FTO through regulation of food intake, whereas others have proposed a peripheral role through an effect on lipolytic activity in adipose tissue. There is no doubt that many more obesity-susceptibility loci remain to be discovered. Progress on this front will therefore require major collaborative efforts and pooling of compatible datasets. We stand to learn a lot about the genetic architecture of human obesity in the coming years. The expectations are high but many challenges remain. Among the latter, translating new advances into useful guidelines for prevention and treatment of obesity will be the most demanding.
KW - Alpha-Ketoglutarate-Dependent Dioxygenase FTO
KW - Animals
KW - Genetic Predisposition to Disease
KW - Homozygote
KW - Humans
KW - Obesity/genetics
KW - Proteins/genetics
KW - Rats
KW - Risk Factors
U2 - 10.1111/j.1467-789X.2008.00481.x
DO - 10.1111/j.1467-789X.2008.00481.x
M3 - Review
C2 - 18373508
VL - 9
SP - 246
EP - 250
JO - Obesity Reviews
JF - Obesity Reviews
SN - 1467-7881
IS - 3
ER -
ID: 258452225