Review ARTICLE

Front. Endocrinol., 03 November 2011 | http://dx.doi.org/10.3389/fendo.2011.00060

Hypothalamic obesity after craniopharyngioma: mechanisms, diagnosis, and treatment

  • Department of Pediatrics, University of California San Francisco, San Francisco, CA, USA

Obesity is a common complication after craniopharyngioma therapy, occurring in up to 75% of survivors. Its weight gain is unlike that of normal obesity, in that it occurs even with caloric restriction, and attempts at lifestyle modification are useless to prevent or treat the obesity. The pathogenesis of this condition involves the inability to transduce afferent hormonal signals of adiposity, in effect mimicking a state of CNS starvation. Efferent sympathetic activity drops, resulting in malaise and reduced energy expenditure, and vagal activity increases, resulting in increased insulin secretion and adipogenesis. Lifestyle intervention is essentially useless in this syndrome, termed “hypothalamic obesity.” Pharmacologic treatment is also difficult, consisting of adrenergics to mimic sympathetic activity, or suppression of insulin secretion with octreotide, or both. Recently, bariatric surgery (Roux-en-Y gastric bypass, laparoscopic gastric banding, truncal vagotomy) have also been attempted with variable results. Early and intensive management is required to mitigate the obesity and its negative consequences.

Keywords: craniopharyngioma, hypothalamic obesity, leptin resistance, insulin, octreotide, vagus nerve, symapthetic nervous system, ghrelin

Citation: Lustig RH (2011) Hypothalamic obesity after craniopharyngioma: mechanisms, diagnosis, and treatment. Front. Endocrin. 2:60. doi: 10.3389/fendo.2011.00060

Received: 29 July 2011; Paper pending published: 29 August 2011;
Accepted: 06 October 2011; Published online: 03 November 2011.

Edited by:

Hermann Lothar Mueller, Klinikum Oldenburg gGmbH, Germany

Reviewed by:

Fahrettin Kelestimur, Erciyes University, Turkey
Vera Popovic-Brkic, University Belgrade, Serbia

Copyright: © 2011 Lustig. This is an open-access article subject to a non-exclusive license between the authors and Frontiers Media SA, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and other Frontiers conditions are complied with.

*Correspondence: Robert H. Lustig, Division of Pediatric Endocrinology, University of California San Francisco, Box 0434, 500 Parnassus Avenue, San Francisco, CA 94143-0434, USA. e-mail: rlustig@peds.ucsf.edu