Family studies have shown that in some populations up to 75% of the variation of body mass index can be explained by genetic factors. However, in @entity1 , no major @entity28 gene has been identified to date. In contrast, there are a number of genetically well defined animal models for @entity28 . In two of those models (ob/ob and db/db), defects in the same pathway are responsible for @entity28 . Recently, some evidence has been found for the OB gene also being involved in @entity1 @entity28 . In this study we investigated the potential role of the @entity13156 ( @entity13156 ) in the etiology of massive @entity28 in @entity1 using familial linkage analyses and case-control association studies. The typing of two microsatellite markers (D1S198 and D1S209), flanking the @entity13156 gene, in 256 sib pairs showed no evidence for linkage with @entity28 . In order to be able to detect small gene effects, association studies with a 3'-UTR insertion/deletion polymorphism were carried out. The results of these analyses remained non-significant (chi 2 = 3.442, P = 0.18). However, subjects heterozygous for the insertion/deletion polymorphism showed a slight trend towards lower insulin values 30 min after an oral @entity413 load compared to homozygous individuals (P = 0.02). In summary, our results do not support a major role of the @entity1 @entity13156 gene in the development of morbid @entity28 in our population.

Genetic studies of the XXXX gene in morbidly obese French Caucasian families.

@entity1 :: ('9606', 'Species') :: ['humans', 'human'] @entity13156 :: ('3953', 'Gene') :: ['OBR', 'OB receptor'] @entity413 :: ('MESH:D005947', 'Chemical') :: ['glucose'] @entity28 :: ('MESH:D009765', 'Disease') :: ['obesity']
@entity13156 :: (3953,Gene) :: ['leptin receptor']
