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Titolo:
INDICATION FOR LINKAGE OF THE HUMAN OB GENE REGION WITH EXTREME OBESITY
Autore:
CLEMENT K; GARNER C; HAGER J; PHILIPPI A; LEDUC C; CAREY A; HARRIS TJR; JURY C; CARDON LR; BASDEVANT A; DEMENAIS F; GUYGRAND B; NORTH M; FROGUEL P;
Indirizzi:
INST PASTEUR,CNRS EP 10,1 RUE CALMETTE,BP 245 F-59019 LILLE FRANCE CHU LILLE F-59019 LILLE FRANCE INSERM U358 PARIS FRANCE HOP HOTEL DIEU,DEPT NUTR PARIS FRANCE SEQUANA THERAPEUT LA JOLLA CA 00000
Titolo Testata:
Diabetes
fascicolo: 5, volume: 45, anno: 1996,
pagine: 687 - 690
SICI:
0012-1797(1996)45:5<687:IFLOTH>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
RADIATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
29
Recensione:
Indirizzi per estratti:
Citazione:
K. Clement et al., "INDICATION FOR LINKAGE OF THE HUMAN OB GENE REGION WITH EXTREME OBESITY", Diabetes, 45(5), 1996, pp. 687-690

Abstract

Obesity is one of the most significant risk factors for hypertension,coronary heart disease, and NIDDM (Frayn RN, Coppack SW: Insulin resistance, adipose tissue and coronary heart disease. Clin Sci 82:1-8, 1992; Kaplan NM: The deadly quartet: upper-body obesity, glucose intolerance, hypertriglyceridemia, and hypertension. Arch Intern Med 149:1514-1520, 1989). While family segregation, adoption, and twin studies have indicated that degree of adiposity has a significant genetic component (Stunkard AJ, Harris JR, Pedersen NL, McClearn GE: The body-mass index of twins who have been reared apart. N Engl J Med 322:1483-1487, 1990; Bouchard C, Despres J-P, Mauriege P: Genetic and nongenetic determinants of regional fat distribution. Endocr Rev 14:72-93, 1993), the genes and predisposing mutations remain poorly understood. This is in contrast to several well-defined genetic models for obesity in rodents, particularly the mouse obese Cab) gene, in which loss-of-function mutations cause severe obesity. Recent studies have demonstrated a substantial reduction in body fat when recombinant ob protein (leptin) is administered to mice. To test the relevance of these observations to human obesity, the location of the human homologue (OB) was established by radiation hybrid mapping and eight microsatellite markers spanning the OB gene region (7q31.3) were genotyped in 101 obese French families. Affected-sib-pair analyses for extreme obesity, defined by BMI >35 kg/m(2), revealed suggestive evidence for linkage to three markers located within 2 cM of the OB gene (D7S514, D7S680, and D7S530). The OB gene is therefore a candidate for genetic predisposition to extreme obesity in a subset of these families.

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Documento generato il 25/09/20 alle ore 07:15:21