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)
JournalTrends in Endocrinology and Metabolism
DOIs
StateAccepted/In press - Jan 1 2019

Fingerprint

Energy Intake
Cell Cycle
Obesity
Neurons
Retinoblastoma Genes
Pro-Opiomelanocortin
Retinoblastoma Protein
Cyclin-Dependent Kinases
Nervous System Diseases
Body Weight
Phosphorylation
Diet

Keywords

  • cell cycle
  • diet-induced obesity
  • hypothalamus

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

Neuronal Cell Cycle Events Link Caloric Intake to Obesity. / Iqbal, Niloy; Zhu, LIang I.; Chua, Streamson C.

In: Trends in Endocrinology and Metabolism, 01.01.2019.

Research output: Contribution to journalReview article

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