The hyperleptinemia of obesity-regulator of caloric surpluses.
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.
Unger
Roger H
RH
Touchstone Center for Diabetes Research, Department of Internal Medicine, UT Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Y8.212, Dallas, TX 75390, USA.
D055372:AMP-Activated Protein Kinases; D000818:Animals; D004435:Eating / Q000502:physiology; D002149:Energy Intake / Q000502:physiology*; D004734:Energy Metabolism / Q000502:physiology; D006801:Humans; D007031:Hypothalamus / Q000378:metabolism; D020738:Leptin / Q000097:blood / Q000378:metabolism*; D008316:Malonyl Coenzyme A / Q000378:metabolism*; D009097:Multienzyme Complexes / Q000378:metabolism*; D009765:Obesity / Q000378:metabolism* / Q000503:physiopathology; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism*
D020738:Leptin; D009097:Multienzyme Complexes; D008316:Malonyl Coenzyme A; D017346:Protein Serine-Threonine Kinases; D055372:AMP-Activated Protein Kinases