Calcium supplementation relieves high-fat diet-induced liver steatosis by reducing energy metabolism and promoting lipolysis

• Published in: The Journal of nutritional biochemistry 2021-08, Vol.94, p.108645, Article 108645
• Main Authors: Zhang, Zhiwang, Liu, Siqi, Qi, Yilin, Aluo, Zhier, Zhang, Lifang, Yu, Lin, Li, Qiang, Luo, Zupeng, Sun, Zheng, Zhou, Lei, Li, Yixing
• Format: Article
• Language: English
• Subjects: Animals; Calcium; Calcium - administration & dosage; Calcium - metabolism; Calcium distribution; Cell Line; Cell Survival - drug effects; Diet, High-Fat - adverse effects; Dietary Supplements; Energy metabolism; Energy Metabolism - drug effects; Fatty Liver - chemically induced; Fatty Liver - drug therapy; Humans; Lipolysis; Liver; Male; Mice; Mice, Inbred C57BL; Mitochondria - drug effects; Mitochondria - metabolism; Mitoxantrone - pharmacology; NAFLD; Ruthenium Compounds - pharmacology
• ISSN: 0955-2863; 1873-4847
• DOI: 10.1016/j.jnutbio.2021.108645

•Calcium supplementation relieves liver steatosis induced by high-fat diet.•Calcium increases the glucose uptake and reduces glycolysis.•Calcium addition reduces cell energy metabolism under high-fat conditions.•Calcium supplementation promotes lipase activity. 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.