Both
lipid accumulation and oxidative stress are major pathologic contributors to the development of hepatic steatosis. Treatment with
molybdate reduces hepatic levels of
lipids in diabetic rats. Potential activities of
molybdate as an
antioxidant have also been demonstrated in various animal models. In the present study, we evaluated the effects of
sodium molybdate dihydrate (SM) on hepatic steatosis and associated disturbances in a widely used mouse model of the
metabolic disease. Male C57Bl/6 mice
at 10 weeks of age were fed a diet deficient in
methionine and
choline (MCD) and
bottled water containing SM for four weeks. The SM treatment markedly attenuated MCD-induced accumulation of
lipids, mainly
triglycerides, in the liver.
Lipid catabolic autophagic pathways were activated by SM in the MCD-fed mouse livers, as evidenced by a decreased level of p62 expression. MCD-induced oxidative damage, such as
lipid and
protein oxidation, was also alleviated by SM in the liver. However, the level of MCD-induced hepatocellular damage was not affected by SM. Taken together, these findings suggest that
molybdate can be used in the treatment and prevention of hepatic steatosis without inducing adverse effects in the liver. To the best of our knowledge, this is the first experimental study to investigate the effects of
molybdate in
non-alcoholic fatty liver disease, and also the first that demonstrates
molybdate-induced autophagy.