Diabetes mellitus adversely affects the bone. Basically, it is related to weakening of the anabolic effect of insulin and other pancreatic hormones. Mechanisms underlying the decrease in bone density are not fully understood. However, many of the systemic changes related to metabolic abnormalities in diabetes have a damaging effect on the bone tissue. Inadequate compensation of glycemic profile in this disease, both directly (non-enzymatic glycosylation of proteins, activation of polyol pathway of glucose metabolism, oxidative stress) and indirectly (violation of gene expression), damages the bone structure. Another anabolic hormone produced by β-cells of the pancreas is amylin. It is a potent hypoglycemic and antiresorptive hormone affecting calcium homeostasis and influencing the preservation of bone density. The studies have shown that amylin, on the one hand, stimulates osteoblast proliferation, and on the other hand, inhibits osteoclast motility, thus acting similar to calcitonin. Inefficient redistribution of bone mass occurs. This may explain the increased incidence of fractures in patients with type 2 diabetes on the background of high bone density according to densitometry. In this regard, further studies are required to clarify the effect of amylin deficiency on the development of osteoporosis.
Overlapping Phenotypes in Osteopetrosis and Pycnodysostosis in Asian-Indians