Non-alcoholic fatty liver, adipose tissue, and the bone: a new triumvirate on the block

Excerpt

In the latest years, a growing body of evidence has connected metabolic syndrome and obesity to bone loss and osteoporosis [1], thereby challenging the conventional view that excessive body weight protects against osteoporosis through increased mechanical load to the skeleton and enhanced cortical bone deposition [2]. In a parallel way, available data suggest that excess body weight may be detrimental to the skeleton, and that excessive adipose tissue plays a key role in this relationship [3]. Within this frame of research, recent studies focused on the relationship between bone health and non-alcoholic fatty liver (NAFLD), the hepatic manifestation of the metabolic syndrome, which recognizes in altered adipose tissue adipokine secretion a key pathogenic factor [4]. The two published studies on endocrine add importantly to the existing literature on the association between NAFLD and osteoporosis. First, ultrasonographic NAFLD was linked to low bone mass in a large cohort of Korean postmenopausal women, independently of age, BMI, smoking status, alcohol intake, and metabolic syndrome [5]. Second, the effect of a multidisciplinary weight-losing regimen on NAFLD, bone mineral density (BMD), and adipokine profile was assessed in post-puberal obese adolescents: weight loss improved NAFLD, BMD, insulin resistance, and plasma lipids. Importantly, bone mineral content changes were related to a reduction in insulin resistance and plasma leptin levels [6]. Consistent with these data, a recent cross-sectional study, connected the histological severity of NAFLD to the degree of BMD changes in obese children [7]. …