Table of Contents
International Journal of Peptides
Volume 2012, Article ID 287457, 13 pages
Review Article

Leptin in Anorexia and Cachexia Syndrome

1Division of Diabetes, Endocrinology and Metabolism, Michael E DeBakey Veterans Affairs Medical Center, Houston, TX 77030, USA
2Baylor College of Medicine, 2002 Holcombe Boulevored, Building 109, Room 210, Houston, TX 77030, USA
3Division of Diabetes, Department of Medicine, Endocrinology and Metabolism, St Luke’s Episcopal Hospital, Houston, TX 77030, USA
4Huffington Center of Aging, Baylor College of Medicine, Houston, TX 77030, USA

Received 22 August 2011; Revised 25 October 2011; Accepted 28 October 2011

Academic Editor: Lloyd D. Fricker

Copyright © 2012 Diana R. Engineer and Jose M. Garcia. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Leptin is a product of the obese (OB) gene secreted by adipocytes in proportion to fat mass. It decreases food intake and increases energy expenditure by affecting the balance between orexigenic and anorexigenic hypothalamic pathways. Low leptin levels are responsible for the compensatory increase in appetite and body weight and decreased energy expenditure (EE) following caloric deprivation. The anorexia-cachexia syndrome is a complication of many chronic conditions including cancer, chronic obstructive pulmonary disease, congestive heart failure, chronic kidney disease, and aging, where the decrease in body weight and food intake is not followed by a compensatory increase in appetite or decreased EE. Crosstalk between leptin and inflammatory signaling known to be activated in these conditions may be responsible for this paradox. This manuscript will review the evidence and potential mechanisms mediating changes in the leptin pathway in the setting of anorexia and cachexia associated with chronic diseases.