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Leptin antagonist prevents the homeostatic downregulation following high‐fat enhanced caloric intake
Author(s) -
Zhang Jiejin,
Matheny Michael K.,
Scarpace Philip J.
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a832-a
Subject(s) - leptin , endocrinology , medicine , downregulation and upregulation , energy homeostasis , caloric theory , antagonist , homeostasis , hypothalamus , chemistry , obesity , receptor , biochemistry , gene
High‐fat feeding induces a transient increase in caloric intake and enhances energy expenditure. We hypothesized that leptin is necessary for the homeostatic downregulation of the high‐fat enhanced caloric intake and may mediate the increase in energy expenditure. Our previous study indicated that acute central leptin antagonist administration blocks leptin‐induced hypothalamic STAT3 phosphorylation. Young (5m) F344XBN male rats were provided with a high‐fat (HF) diet (60% kcal as fat) or chow and simultaneously infused with antagonist (Ant) (25ug/d, lateral ventricle) or vehicle (Con) by mini pump for 7d. Daily caloric intake of both HF groups peaked on day 2. In Con/HF, caloric intake nearly attenuated by day 6, whereas Ant/HF remained elevated. On day 6, oxygen consumption was parallel to caloric intake with Ant/HF>Con/HF>Con/Chow. Visceral adiposity was significantly elevated in Con/HF with even a greater increase in Ant/HF. These results demonstrate that leptin is essential for the homeostatic downregulation of caloric intake following high‐fat feeding, however the high‐fat feeding induced increase in energy expenditure appears to be independent of leptin. Supported by NIH AG20985