The hyperleptinemia of obesity-regulator of caloric surpluses

Cell. 2004 Apr 16;117(2):145-6. doi: 10.1016/s0092-8674(04)00339-3.

Abstract

New evidence suggests that leptin and other anorexigenic agents reduce appetite by inactivating hypothalamic AMP-activated protein kinase (AMPK), thereby increasing malonyl CoA levels. This preview examines AMP biology and its role in malonyl-CoA generation and attempts to integrate its central actions with its peripheral antilipotoxic actions within the context of leptin physiology in obesity.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • AMP-Activated Protein Kinases
  • Animals
  • Eating / physiology
  • Energy Intake / physiology*
  • Energy Metabolism / physiology
  • Humans
  • Hypothalamus / metabolism
  • Leptin / blood
  • Leptin / metabolism*
  • Malonyl Coenzyme A / metabolism*
  • Multienzyme Complexes / metabolism*
  • Obesity / metabolism*
  • Obesity / physiopathology
  • Protein-Serine-Threonine Kinases / metabolism*

Substances

  • Leptin
  • Multienzyme Complexes
  • Malonyl Coenzyme A
  • Protein-Serine-Threonine Kinases
  • AMP-Activated Protein Kinases