HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 295/5/E1000    most recent 90252.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Laviano, A. Articles by Seelaender, M. Search for Related Content PubMed PubMed Citation Articles by Laviano, A. Articles by Seelaender, M.

REVIEW

Neural control of the anorexia-cachexia syndrome

¹Department of Clinical Medicine, Sapienza University of Rome, Rome, Italy; ²Department of Behavioral Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan; ³Center for the Study of Weight Regulation, Oregon Health and Science University, Portland, Oregon; ⁴Department of Surgery, State University of New York Upstate Medical University, Syracuse, New York; ⁵Clinical Nutrition, Geneva University Hospital, Geneva, Switzerland; and ⁶Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

Submitted 24 February 2008 ; accepted in final form 15 August 2008

ABSTRACT

The anorexia-cachexia syndrome is a debilitating clinical condition characterizing the course of chronic diseases, which heavily impacts on patients' morbidity and quality of life, ultimately accelerating death. The pathogenesis is multifactorial and reflects the complexity and redundancy of the mechanisms controlling energy homeostasis under physiological conditions. Accumulating evidence indicates that, during disease, disturbances of the hypothalamic pathways controlling energy homeostasis occur, leading to profound metabolic changes in peripheral tissues. In particular, the hypothalamic melanocortin system does not respond appropriately to peripheral inputs, and its activity is diverted largely toward the promotion of catabolic stimuli (i.e., reduced energy intake, increased energy expenditure, possibly increased muscle proteolysis, and adipose tissue loss). Hypothalamic proinflammatory cytokines and serotonin, among other factors, are key in triggering hypothalamic resistance. These catabolic effects represent the central response to peripheral challenges (i.e., growing tumor, renal, cardiac failure, disrupted hepatic metabolism) that are likely sensed by the brain through the vagus nerve. Also, disease-induced changes in fatty acid oxidation within hypothalamic neurons may contribute to the dysfunction of the hypothalamic melanocortin system. Ultimately, sympathetic outflow mediates, at least in part, the metabolic changes in peripheral tissues. Other factors are likely involved in the pathogenesis of the anorexia-cachexia syndrome, and their role is currently being elucidated. However, available evidence shows that the constellation of symptoms characterizing this syndrome should be considered, at least in part, as different phenotypes of common neurochemical/metabolic alterations in the presence of a chronic inflammatory state.

melanocortin; cytokines; serotonin; malonyl-coenzyme A; vagus nerve; sympathetic output

This article has been cited by other articles:

				A. Y.-M. Wang, M. M.-M. Sea, N. Tang, C. W.-k. Lam, I. H.-S. Chan, S.-F. Lui, J. E Sanderson, and J. Woo Energy intake and expenditure profile in chronic peritoneal dialysis patients complicated with circulatory congestion Am. J. Clinical Nutrition, November 1, 2009; 90(5): 1179 - 1184. [Abstract] [Full Text] [PDF]