4.5 Article

Cilia and Obesity

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COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/cshperspect.a028217

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资金

  1. NIAMS NIH HHS [R01 AR054396] Funding Source: Medline
  2. NIDDK NIH HHS [R01 DK106404, R01 DK060540, P30 DK098722, P30 DK097512] Funding Source: Medline
  3. NIGMS NIH HHS [R01 GM095941] Funding Source: Medline

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The ciliopathies Bardet-Biedl syndrome and Alstrom syndrome cause obesity. How ciliary dysfunction leads to obesity has remained mysterious, partly because of a lack of understanding of the physiological roles of primary cilia in the organs and pathways involved in the regulation of metabolism and energy homeostasis. Historically, the study of rare monogenetic disorders that present with obesity has informed our molecular understanding of the mechanisms involved in nonsyndromic forms of obesity. Here, we present a framework, based on genetic studies in mice and humans, of the molecular and cellular pathways underlying long-term regulation of energy homeostasis. We focus on recent progress linking these pathways to the function of the primary cilia with a particular emphasis on the roles of neuronal primary cilia in the regulation of satiety.

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