Conclusions
Our study suggested that the liver-lipid-bone interactions may play a key role in the abnormal bone metabolism in NAFLD, and circulating sclerostin may be a surrogate marker to reflect bone metabolism status in NAFLD subjects.
Methods
A cross-sectional study was designed and 168 NAFLD subjects and 85 control subjects were included in this study. Serum sclerostin and metabolic parameters were measured. Mouse models of NAFLD were also induced by high-fat diet. Bone structural parameters were determined using microCT and mRNA expression levels of sclerostin in bone and liver tissues were measured.
Results
Our study suggested that circulating sclerostin levels were significantly lower in NAFLD subjects compared with normal controls. In NAFLD subjects, sclerostin was negatively correlated with multiple metabolic parameters, including waist circumference, urea, hepatic enzyme, gamma-glutamyl transpeptidase, and triglyceride, while such correlation was not significant in control subjects. Circulating sclerostin was also negatively correlated with fatty liver index in NAFLD subjects but not in control subjects. Mice fed on a high-fat diet had reduced bone mass and lower sclerostin expression levels in both the bone and liver tissues. Conclusions: Our study suggested that the liver-lipid-bone interactions may play a key role in the abnormal bone metabolism in NAFLD, and circulating sclerostin may be a surrogate marker to reflect bone metabolism status in NAFLD subjects.