Circumventing leptin resistance for weight control.

Departments of Neuroscience and Physiology, College of Medicine, University of Florida McKnight Brain Institute, Gainesville, FL 32610-0244, USA.
Proceedings of the National Academy of Sciences (Impact Factor: 9.74). 05/2001; 98(8):4279-81. DOI:10.1073/pnas.091101498
Source: PubMed
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    ABSTRACT: 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.
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S P Kalra