Genetic studies of the leptin receptor gene in morbidly obese French Caucasian families |
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Authors: | Stephan Francke Karine Clement Christian Dina Hiroshi Inoue Philip Behn Vincent Vatin Arnaud Basdevant Bernard Guy-Grand M Alan Permutt Philippe Froguel J Hager |
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Institution: | CNRS EP10 Institut Pasteur de Lille, 1, rue du Prof. Calmette, F-59019 Lille, France Fax: +33 3 20.44.66.45; e-mail: jorg@xenope.univ-lille2.fr, FR Division of Metabolism, Diabetes and Endocrinology, Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri, USA, US 2 Department of Nutrition, H?tel-Dieu Hospital, 1 place du parvis Notre-Dame, F-75004 Paris, France, FR
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Abstract: | 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 humans, no major obesity gene has been identified to date. In contrast, there are a number of genetically
well defined animal models for obesity. In two of those models (ob/ob and db/db), defects in the same pathway are responsible
for obesity. Recently, some evidence has been found for the OB gene also being involved in human obesity. In this study we
investigated the potential role of the OB receptor (OBR) in the etiology of massive obesity in humans using familial linkage
analyses and case-control association studies. The typing of two microsatellite markers (D1S198 and D1S209), flanking the
OBR gene, in 256 sib pairs showed no evidence for linkage with obesity. 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 (χ2 = 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 glucose load compared to homozygous individuals (P = 0.02). In summary, our results do not support a major role of the human OBR gene in the development of morbid obesity in
our population.
Received: 4 December 1996 / Accepted: 25 June 1997 |
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