Nonalcoholic fatty liver disease (
NAFLD) is a
chronic disease affecting the health of many people worldwide. Previous studies have shown that
dietary calcium supplementation may alleviate
NAFLD, but the underlying mechanism is not clear. In this study investigating the effect of
calcium on hepatic lipid metabolism, 8-week-old male C57BL/6J mice were divided into four groups (n = 6): (1) mice given a normal chow containing 0.5%
calcium (CN0.5), (2) mice given a normal chow containing 1.2%
calcium (CN1.2), (3) mice given a high-fat diet (HFD) containing 0.5%
calcium (HFD0.5), and (4) mice fed a HFD containing 1.2%
calcium (HFD1.2). To understand the underlying mechanism, cells were treated with
oleic acid and
palmitic acid to mimic the HFD conditions in vitro. The results showed that
calcium alleviated the increase in
triglyceride accumulation induced by
oleic acid and/or
palmitic acid in HepG2, AML12, and primary hepatocyte cells. Our data demonstrated that
calcium supplementation alleviated HFD-induced hepatic steatosis through increased liver
lipase activity, proving
calcium is involved in the regulation of hepatic lipid metabolism. Moreover,
calcium also increased the level of
glycogen in the liver, and at the same time had the effect of reducing glycolysis and promoting
glucose absorption.
Calcium addition increased
calcium levels in the mitochondria and cytoplasm. Taken together, we concluded that
calcium supplementation could relieve HFD-induced hepatic steatosis by changing energy metabolism and
lipase activity.