Diet-induced obese mice retain endogenous leptin action.

Published

Journal Article

Obesity is characterized by hyperleptinemia and decreased response to exogenous leptin. This has been widely attributed to the development of leptin resistance, a state of impaired leptin signaling proposed to contribute to the development and persistence of obesity. To directly determine endogenous leptin activity in obesity, we treated lean and obese mice with a leptin receptor antagonist. The antagonist increased feeding and body weight (BW) in lean mice, but not in obese models of leptin, leptin receptor, or melanocortin-4 receptor deficiency. In contrast, the antagonist increased feeding and BW comparably in lean and diet-induced obese (DIO) mice, an increase associated with decreased hypothalamic expression of Socs3, a primary target of leptin. These findings demonstrate that hyperleptinemic DIO mice retain leptin suppression of feeding comparable to lean mice and counter the view that resistance to endogenous leptin contributes to the persistence of DIO in mice.

Full Text

Duke Authors

Cited Authors

  • Ottaway, N; Mahbod, P; Rivero, B; Norman, LA; Gertler, A; D'Alessio, DA; Perez-Tilve, D

Published Date

  • June 2, 2015

Published In

Volume / Issue

  • 21 / 6

Start / End Page

  • 877 - 882

PubMed ID

  • 25980347

Pubmed Central ID

  • 25980347

Electronic International Standard Serial Number (EISSN)

  • 1932-7420

Digital Object Identifier (DOI)

  • 10.1016/j.cmet.2015.04.015

Language

  • eng

Conference Location

  • United States