Journalartikel

Obese people and mice


AutorenlisteDaniel, H; Herget, M

Jahr der Veröffentlichung1996

Seiten4-&

ZeitschriftErnährungs-Umschau : Forschung & Praxis

Bandnummer43

Heftnummer1

ISSN0340-2371

VerlagUmschau Verlag Breidenstein GMBH


Abstract
The new age of obesity research started only a year ago with the cloning of the ob (obesity)-gene. Meanwhile a large number of studies have been published that investigated the tissue specific expression of the ob-gene and the action of its gene product leptin. Injections of recombinant human and murine leptin into obese (ob/ob) mice or lean mice caused a significant reduction of food intake and body weight while energy expenditure increased. Whereas mutations in the ob-gene appear to cause a lack of leptin production in the ob/ob mice that is associated with morbid obesity, similar mutations in the human ob-gene have not been found as yet. A striking finding is that in humans leptin plasma levels increase parallel to the BMI. The current hypothesis to explain the increased plasma leptin levels in obese humans is based on a reduced sensitivity of the hypothalamic leptin receptor that could cause increased energy intake, reduced energy expenditure and a progressively increasing body fat mass with increased ob-gene expression. New insights into the control of leptin secretion and action is provided by studies that show that insulin affects ob-gene expression in adipocytes and that leptin may alter neuropeptide Y expression and secretion in the brain. It becomes obvious now that leptin is only one player in the control of body fat stores and energy balance.



Zitierstile

Harvard-ZitierstilDaniel, H. and Herget, M. (1996) Obese people and mice, Ernährungs-Umschau : Forschung & Praxis, 43(1), pp. 4-&

APA-ZitierstilDaniel, H., & Herget, M. (1996). Obese people and mice. Ernährungs-Umschau : Forschung & Praxis. 43(1), 4-&.



Schlagwörter


ob-gene

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