Neuronal Cell Cycle Events Link Caloric Intake to Obesity

Research output: Contribution to journalReview article

Abstract

Obesity is a neurological disorder that operates by favoring energy storage within adipose depots and increased caloric intake. Most cases of human obesity are acquired without any underlying genetic basis. Here, we suggest that obesity can impair the function of some hypothalamic neurons critical to body weight regulation. Genetic ablation of the retinoblastoma (Rb) gene within pro-opiomelanocortin (POMC) neurons leads to death of the neurons and subsequent obesity. The Rb protein (pRb), a key inhibitor of the cell cycle, can also be inactivated by cyclin dependent kinase (CDK)-mediated phosphorylation. Extensive development led to the production of FDA-approved CDK4/6 inhibitors. Based on our own results, we propose that maintaining or re-instating pRb function using CDK4/6 inhibitors are potentially effective treatments of diet-induced obesity (DIO).

Original languageEnglish (US)
Pages (from-to)46-52
Number of pages7
JournalTrends in Endocrinology and Metabolism
Volume31
Issue number1
DOIs
StatePublished - Jan 2020

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Keywords

  • cell cycle
  • diet-induced obesity
  • hypothalamus

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

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