Journal article
The concept of selective leptin resistance: evidence from agouti yellow obese mice
Diabetes (New York, N.Y.), Vol.51(2), pp.439-442
02/2002
DOI: 10.2337/diabetes.51.2.439
PMID: 11812752
Abstract
Leptin, a hormone secreted by adipose tissue, acts to inhibit appetite and promote metabolism, thereby reducing body weight. Leptin also increases sympathetic activity and arterial pressure. Several murine models of obesity, including agouti obese mice, exhibit resistance to the anorexic and weight-reducing effects of leptin. Hypertension in agouti mice has been attributed to hyperleptinemia. These observations pose a seeming paradox. If these mice are leptin-resistant, then how can leptin contribute to hypertension? We tested the novel hypothesis that these mice have selective leptin resistance, with preservation of the sympathoexcitatory action despite resistance to the weight-reducing actions. Leptin-induced decreases in food intake and body weight were less in agouti obese mice than in lean littermates. In contrast, leptin-induced increases in sympathetic nerve activity did not differ in obese and lean mice. These findings support the concept of selective leptin resistance, with resistance to the metabolic actions of leptin but preservation of the sympathoexcitatory actions. This finding may have potential implications for human obesity, which is associated with elevated plasma leptin and is thought to be a leptin-resistant state. If leptin resistance is selective in obese humans, then leptin could contribute to sympathetic overactivity and its adverse consequences in human obesity.
Details
- Title: Subtitle
- The concept of selective leptin resistance: evidence from agouti yellow obese mice
- Creators
- Marcelo L G Correia - Hypertension Genetics Specialized Center of Research and Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, Iowa 52242-1101, USAWilliam G HaynesKamal RahmouniDonald A MorganWilliam I SivitzAllyn L Mark
- Resource Type
- Journal article
- Publication Details
- Diabetes (New York, N.Y.), Vol.51(2), pp.439-442
- Publisher
- United States
- DOI
- 10.2337/diabetes.51.2.439
- PMID
- 11812752
- ISSN
- 0012-1797
- eISSN
- 1939-327X
- Grant note
- HL44546 / NHLBI NIH HHS HL14388 / NHLBI NIH HHS
- Language
- English
- Date published
- 02/2002
- Academic Unit
- Iowa Neuroscience Institute; Neuroscience and Pharmacology; Endocrinology and Metabolism; Internal Medicine
- Record Identifier
- 9984040243602771
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