| [ Summary ] |
Patients with metabolic syndrome present abnormal lipid profiles, impaired glucose tolerance and hypertension, all of which are caused by excess visceral fat deposition and insulin resistance. Either hyperinsulinemia or leptin resistance has anabolic effects on bone, while increasing TNF-α actions decrease bone mineral density in patients with visceral adiposity. Hyperglycemia is involved in increases in fracture risk. In contrast, either increased serum levels of triglycerides or low HDL-cholesterol levels reduce fracture risk. Several epidemiological studies have demonstrated that subjects with metabolic syndrome are likely to acquire higher bone mineral density and less fracture risk than control subjects. However, if these data are corrected by body mass indexes, obesity alone may be involved in favorable effects on bone. Taken together, excess visceral fat may be involved in impairment of bone metabolism resulting in higher levels of fracture risk. However, obesity itself may have anabolic effects on bone that may overcome metabolic derangement which acts against bone. In conclusion, since it is difficult at this time to determine the effects of various components of metabolic syndrome on fractures, we need to establish new strategies to investigate bone metabolism in patients with metabolic syndrome. |