1 Division of Gastroenterology, University of California, San Diego, La Jolla, CA.
2 Division of Gastroenterology, University of California, San Diego, La Jolla, CA; VA Health Sciences San Diego, La Jolla, CA; Institute of Diabetes and Metabolic Health, University of California, San Diego, La Jolla, CA; Center for Microbiome Innovation, University of California, San Diego, La Jolla, CA. Electronic address: firstname.lastname@example.org.
Circadian clock proteins are endogenous timing mechanisms that control the transcription of hundreds of genes. Their integral role in coordinating metabolism has led to their scrutiny in a number of diseases, including NAFLD. Discoordination between central and peripheral circadian rhythms is a core feature of nearly every genetic, dietary, or environmental model of metabolic syndrome and NAFLD. Restricting feeding to a defined daily interval (time-restricted feeding) can synchronize the central and peripheral circadian rhythms, which in turn can prevent or even treat the metabolic syndrome and hepatic steatosis. Importantly, a number of proteins currently under study as drug targets in NAFLD (SREBP, ACC, PPARs, and incretins) are modulated by circadian proteins. Thus, the clock can be used to maximize the benefits and minimize the side effects of pharmaceutical agents for NAFLD. The circadian clock itself has the potential for use as a target for the treatment of NAFLD.