While melatonin is usually associated with healthy sleep, there is growing evidence that it also plays an essential role in treating non-alcoholic fatty liver disease (NAFLD).

This condition is estimated to affect about one third of people living in industrialized countries. Extra fat deposits in the liver are serious. They threaten the liver’s ability to filter blood, detoxify harmful substances, metabolize drugs, and properly digest food due to decreased bile production.

Clinical work has found that patients with nonalcoholic steatohepatitis, a form of non-alcoholic fatty liver disease, saw improvements with only 10 mg of melatonin per day for 28 days. The results show how valuable melatonin can be for the overlapping factors of liver disease and metabolic syndrome: insulin resistance was reduced by 60 percent, and plasma levels of adiponectin and leptin rose by 119 percent and 33 percent, respectively.

Adiponectin and leptin are hormones with actions on glucose levels, fat metabolism, appetite and fullness perception, and are considered keys to cardiovascular and liver function and keeping a healthy weight, so melatonin’s effects go far beyond helping you get a good night’s sleep. This one nutrient helps preserve and restore the liver, fights cardiovascular and blood sugar conditions associated with metabolic syndrome, and may even stop weight gain.

Abstract:

Gonciarz M, Bielański W, Partyka R, Brzozowski T, Konturek PC, Eszyk J, Celiński K, Reiter RJ, Konturek SJ. Plasma insulin, leptin, adiponectin, resistin, ghrelin, and melatonin in nonalcoholic steatohepatitis patients treated with melatonin. J Pineal Res. 2013 Mar;54(2):154-61.

Insulin resistance, oxidative stress, and an abnormal production of adipokines and cytokines are implicated in the pathogenesis of nonalcoholic steatohepatitis (NASH). Recently, we reported a significant improvement in plasma liver enzymes among patients with NASH treated with melatonin. In this study, we investigated the effect of melatonin, administered at a dose of 10 mg/day for 28 days to 16 patients with histologically proven NASH on insulin resistance (HOMA-IR), on the plasma levels of adiponectin, leptin, ghrelin, and resistin. Additionally, plasma levels of aminotransferases and gamma glutamyltranspeptidase as well as plasma concentrations of melatonin were evaluated. Median baseline values of HOMA-IR, leptin (ng/mL), and resistin (pg/mL) in patients with NASH were significantly higher in comparison with controls: 4.90 versus 1.60, 10.70 versus 4.30, and 152 versus 91, respectively. Median adiponectin level (μg/mL) was decreased in patients compared to controls: 6.40 versus 16.25; no significant difference in ghrelin levels between patients and controls was found. After melatonin treatment, the median value of HOMA-IR was significantly reduced by 60% as compared to baseline values, whereas adiponectin, leptin, and ghrelin plasma levels rose significantly by 119%, 33%, and 20%, respectively; the difference between pre-/posttreatment in plasma resistin levels was not significant. These findings make melatonin a suitable candidate for testing in patients with NASH in the large controlled clinical trials.