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Molecular basis of the obesity associated with Bardet-Biedl syndrome
Journal article   Open access   Peer reviewed

Molecular basis of the obesity associated with Bardet-Biedl syndrome

Deng-Fu Guo and Kamal Rahmouni
Trends in endocrinology and metabolism, Vol.22(7), pp.286-293
07/2011
DOI: 10.1016/j.tem.2011.02.009
PMCID: PMC3130119
PMID: 21514177
url
https://doi.org/10.1016/j.tem.2011.02.009View
Published (Version of record) Open Access

Abstract

Bardet-Biedl Syndrome (BBS) is a rare human hereditary disorder associated with several features including obesity, retinopathy, renal defects, polydactyly, learning disabilities and hypogenitalism. This article discusses the abnormalities accounting for energy imbalance leading to obesity in BBS with emphasis on the recent evidence pointing to aberrations in hypothalamic action of leptin. Indeed, BBS proteins have emerged as important mediators of leptin receptor trafficking, and loss of BBS genes results in leptin resistance that may be due to abnormal leptin receptor handling in a subset of leptin responsive neurons. These recent discoveries hold promise for improved clinical management of BBS patients. The relevance of these findings to non-syndromic common obesity is also discussed.

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