期刊
ALIMENTARY PHARMACOLOGY & THERAPEUTICS
卷 36, 期 4, 页码 345-352出版社
WILEY
DOI: 10.1111/j.1365-2036.2012.05196.x
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Background Low bone mineral density (BMD) has been reported in both paediatric and adult patients with non-alcoholic fatty liver disease (NAFLD). The mechanisms behind the reduced BMD in NAFLD are still not completely understood. Aim To provide a critical overview of the pathophysiological pathways linking NAFLD, reduced BMD and osteoporosis, with a special focus on the alterations of soluble mediators which could link fat accumulation in the liver with bone health. The MEDLINE database was searched by a combination of keywords: non-alcoholic fatty liver disease OR hepatic steatosis OR metabolic syndrome OR insulin resistance AND bone mineral density OR osteoporosis OR bone AND biomarkers OR serum marker. Results Several factors that may influence bone mineralisation and the increased risk of osteoporosis in NAFLD can be discussed. These include the release of cytokines from the inflamed liver which may influence the bone microenvironment, vitamin D deficiency, and limited physical activity. Circulating markers of bone metabolism, including osteopontin, osteoprotegerin, osteocalcin and fetuin-A, have been found to be altered in patients with NAFLD. Conclusion A better understanding of the mechanisms that link bone metabolism and the liver may open a new frontier to fight two highly prevalent conditions like NAFLD and osteoporosis.
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