Monogenic models of obesity

被引：15

作者：

Chua Jr. S.C. ^{[1
]}

机构：

[1] Rockefeller University, New York, NY 10021

来源：

Behavior Genetics | 1997年 / 27卷 / 4期

基金：

美国国家卫生研究院;

关键词：

Monogenic models; Obesity;

D O I：

10.1023/A:1025679728948

中图分类号：

学科分类号：

摘要：

The study of rodent monogenic models of obesity has yielded significant insights into the pathogenesis of obesity. Multiple independent mutations in several genes can produce obesity. As these genes act in different regulatory pathways, it is clear that multiple mechanisms can produce obesity. Furthermore, a single gene defect can produce regulatory deficits in multiple modes of energy expenditure. The most severe forms of genetic obesity involve multiple pathogenic processes. It is significant that regulatory defects in any single component of caloric intake or energy expenditure appear to be sufficient to produce obesity. Finally, the systems regulating energy balance are loosely coupled; positive and negative influences are not completely balanced, both in strength as well as temporally.

引用

页码：277 / 284

页数：7

共 55 条

[1] Assimacopoulous-Jeannet F., Moinat M., Muzzin P., Colomb C., Jeanrenaud B., Girardier L., Giacobino J.P., Seydoux J., Effects of a peroxisome proliferator on beta-oxidation and overall energy balance in obese (fa/fa) rats, Am. J. Physiol., 260, 2 PT 2, (1991)
[2] Batt R.A., Hambi M., Development of the hypothermia in obese mice (genotype ob/ob), Int. J. Obesity, 6, 4, pp. 391-397, (1982)
[3] Bell G.E., Stern J.S., Evaluation of body composition of young obese and lean Zucker rats, Growth, 41, pp. 63-80, (1977)
[4] Boulange A., Planche E., Degasquet P., Onset of genetic obesity in the absence of hyperphagia during the first week of life in the Zucker rat (fa/fa), J. Lipid Res., 20, pp. 857-864, (1979)
[5] Bultman S.J., Michaud E.J., Woychik R.P., Molecular characterization of the mouse agouti locus, Cell, 71, 7, pp. 1195-1204, (1992)
[6] Campfield L.A., Smith F.J., Guisez Y., Devos R., Burn P., Recombinant mouse OB protein: Evidence for a peripheral signal linking adiposity and central neural networks, Science, 269, pp. 546-549, (1995)
[7] Chanussot F., Ulmer M., Ratanasavanh R., Max J.P., Debry G., Influence of diet composition on obesity, hyperlipemia and liver steatosis in Zucker fa/fa rats pair-fed with Zucker Fa/-rats, Int. J. Obesity, 8, 3, pp. 259-270, (1984)
[8] Chen H., Charlat O., Tartaglia L.A., Woolf E.A., Weng X., Ellis S.J., Lakey N.D., Culpepper J., Moore K.J., Breitbart R.E., Duyk G.M., Tepper R.I., Morgenstern J.P., Evidence that the diabetes gene encodes the leptin receptor identification of a mutation in the leptin receptor gene in db/db mice, Cell, 84, 3, pp. 491-495, (1996)
[9] Chua S.C., Chung W.K., Wu-Peng X.S., Zhang Y., Liu S.-M., Tartaglia L., Leibel R.L., Phenotypes of mouse diabetes and rat fatty due to mutations in the OB (leptin) receptor, Science, 27, 5251, pp. 994-996, (1996)
[10] Chua S.C., White D.W., Wu-Peng X.S., Liu S.-M., Okada N., Kershaw E.E., Chung W.K., Power-Kehoe L., Chua M., Tartaglia L.A., Leibel R.L., Phenotype of fatty due to Gln269Pro mutation in the leptin receptor (Lepr), Diabetes, 45, 8, pp. 1141-1143, (1996)

← 1 2 3 4 5 6 →