Abstract
Non-alcoholic fatty liver disease (NAFLD) is a common disease, which is characterized by the accumulation of triglycerides in the hepatocytes without excess alcohol intake. Circadian rhythms can participate in lipid, glucose, and cholesterol metabolism and are closely related to metabolism seen in this disease. Circadian clock genes can modulate liver lipid metabolism. Desynchrony of circadian rhythms and the influences imparted by external environmental stimuli can increase morbidity. By contrast, synchronizing circadian rhythms can help to alleviate the metabolic disturbance seen in NAFLD. In this review, we have discussed the current research connections that exist between the circadian clock and the metabolism of NAFLD, and we have specifically focused on the key circadian clock genes, Bmal1, Clock, Rev-Erbs, Rors, Pers, Crys, Nocturnin, and DECs.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is a form of triglyceride (TG) accumulation at or exceeding 5% of the liver weight without excess alcohol intake (Andronescu et al, 2018)
The histological classification distinguishes a range of conditions within NAFLD that vary from hepatic steatosis to non-alcoholic steatohepatitis (NASH), which might evolve to many subsequent conditions that include fibrosis, cirrhosis, liver failure, and hepatocellular carcinoma (Ipsen et al, 2018)
We have revealed that the prevalence of NAFLD in employees of the city of Shanghai, China was 38.17%; a rate that was much higher than we had previously appreciated (Hu et al, 2012; Sherif et al, 2016)
Summary
Non-alcoholic fatty liver disease (NAFLD) is a form of triglyceride (TG) accumulation at or exceeding 5% of the liver weight without excess alcohol intake (Andronescu et al, 2018). The global prevalence of NAFLD has dramatically increased during the past three decades, as a result of a global epidemic in the incidence of metabolic disorders. Circadian Clock Genes in the Metabolism of NAFLD the decomposition of fat cells is weakened where IR is seen, resulting in lipolysis from the adipose tissue, and increased uptake of free fatty acids into the liver. Mitochondrial dysfunction could impair fatty acid beta-oxidation and cause lipid accumulation, which usually precedes NAFLD. With impaired fatty acid beta-oxidation or TG transport, the capacity of the liver to clear lipids efficiently is reduced, which might lead to the development of NAFLD (Figure 1). The circadian rhythm system plays a key role in human physiology and disease systems. We will discuss current research connections between the circadian clock and the metabolism seen in NAFLD, with a particular focus on key circadian clock genes
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