|
|
||||||||
I. The OB protein as a satiety factor: Recently, important insights were gained into the control of food intake and energy expenditure by the newly discovered adipocyte-derived hormone OB (the ob gene product, dubbed leptin) as well as into the pathogenetic role of the adipocyte-specific β3-adrenergic receptor, mutations of which predispose to obesity, insulin resistance and early onset of non-insulin dependent diabetes mellitus. The latter studies are the topic of the second part of this month's Highlights section.
The genetically obese mouse strain (ob/ob) suffering from type II diabetes and hypothermia was described over 40 years ago. Early studies elegantly demonstrated the absence of a defect in a circulating factor in these mice, since parabiosis experiments (coupling of the circulatory systems) of an ob/ob mouse with a normal partner induced weight loss and a decrease in food intake in the ob/ob mouse. Similarly, joining two normal mice by parabiosis and
This article has been cited by other articles:
![]() |
M. V. Kumar, G. D. Sunvold, and P. J. Scarpace Dietary vitamin A supplementation in rats: suppression of leptin and induction of UCP1 mRNA J. Lipid Res., May 1, 1999; 40(5): 824 - 829. [Abstract] [Full Text] |
||||
![]() |
H. Li, M. Matheny, N. Tumer, and P. J. Scarpace Aging and fasting regulation of leptin and hypothalamic neuropeptide Y gene expression Am J Physiol Endocrinol Metab, September 1, 1998; 275(3): E405 - E411. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |