Novel insights into the relationship between nonalcoholic fatty liver disease and osteoporosis

• Published in: Clinical interventions in aging Vol. 13; pp. 1879 - 1891
• Main Authors: Filip, Rafał, Radzki, Radosław P, Bieńko, Marek
• Format: Journal Article
• Language: English
• Published: New Zealand Dove Medical Press Limited 01.01.2018; Taylor & Francis Ltd; Dove Medical Press
• Subjects: Adipose tissue; Adipose Tissue - metabolism; Aging; Alcohol; Analysis; Bone and Bones - metabolism; Bone and Bones - physiopathology; Bone density; bone metabolism; Care and treatment; Celiac disease; Etiology (Medicine); Fatty liver; Fibroblasts; Fractures; Gastroenterology; Homeostasis; Hormones; Humans; Inflammation; Inflammation - metabolism; Insulin; Insulin resistance; Lead; Liver - metabolism; Liver - physiopathology; Liver diseases; Metabolic syndrome; Middle age; Non-alcoholic Fatty Liver Disease - metabolism; Non-alcoholic Fatty Liver Disease - physiopathology; nonalcoholic fatty liver disease; nonalcoholic steatohepatitis; Novels; Obesity; Osteoporosis; Osteoporosis - metabolism; Osteoporosis - physiopathology; Permeability; Population; Practice guidelines (Medicine); Review; Risk factors; Somatotropin; Transcription factors; Type 2 diabetes; Womens health; Poland; nonalcoholic steatohepatitis; nonalcoholic fatty liver disease; bone metabolism; osteoporosis; inflammation
• ISSN: 1178-1998; 1176-9092; 1178-1998
• DOI: 10.2147/CIA.S170533

Excess fat deposition and insulin resistance are considered the main risk factors for nonalcoholic fatty liver disease (NAFLD), and therefore, not surprisingly, the global prevalence of NAFLD increases in parallel with both obesity and type 2 diabetes. Although deterioration of bone homeostasis in patients with NAFLD is commonly observed, its etiology has not been fully elucidated yet. It was shown in several studies that bone tissue seems to be independently associated with NAFLD. A mechanistic perspective puts the liver at the center of mutual interdependencies obviously involving adipose tissue and muscles and also the bone matrix and bone cells, which are relatively novel. In this review, various pathophysiological mechanisms and possible mediating molecules that may interplay between NAFLD and bone tissue are described. Chronic inflammation, vitamin D3, growth hormone, insulin-like growth factor 1, osteopontin, fetuin-A, irisin, osteocalcin, and osteoprotegerin from osteoblasts have been proposed as mediators of mutual interactions among the skeleton, fatty tissue, and liver. Although to date there are still many issues that have not been elucidated, growing evidence suggests that screening and surveillance of bone mineral density in patients with NAFLD should be considered in future strategies and guidelines for NAFLD management.