Fatty acid synthase gene regulation in primary hypothalamic neurons.

Kim EK, Kleman AM, Ronnett GV
Neurosci Lett. 2007 423 (3): 200-4

PMID: 17709201 · PMCID: PMC4286184 · DOI:10.1016/j.neulet.2007.06.056

Understanding the mechanisms that regulate feeding is critical to the development of therapeutic interventions for obesity. Many studies indicate that enzymes within fatty acid metabolic pathways may serve as targets for pharmacological tools to treat this epidemic. We, and others have previously demonstrated that C75, a fatty acid synthase (FAS) inhibitor, induced significant anorexia and weight loss by both central and peripheral mechanisms. Because the hypothalamus is important in the regulation of homeostatic processes for feeding control, we have identified pathways that alter the gene expression of FAS in primary hypothalamic neuronal cultures. Insulin, glucose and AICAR (an activator of AMP-activated protein kinase) affected changes in hypothalamic FAS mRNA, which may be regulated via the SREBP1c dependent or independent pathway.

MeSH Terms (18)

Aminoimidazole Carboxamide Animals Cells, Cultured Dose-Response Relationship, Drug Fatty Acid Synthases Fetus Gene Expression Regulation Glucose Hypothalamus Insulin Neurons Protein Isoforms Rats Rats, Sprague-Dawley Ribonucleotides RNA, Messenger Sterol Regulatory Element Binding Protein 1 Time Factors

Connections (1)

This publication is referenced by other Labnodes entities: