Search

The underlying process leading to insulin-dependent diabetes mellitus (IDDM) is the degeneration of the insulin-secreting pancreatic beta-cells, with subsequent inability to regulate levels of blood sugar. Patients with IDDM frequently also suffer from osteoporosis, a disease in which the bones lose strength and are susceptible to fractures. Previous animal studies investigating the mechanisms behind diabetes-induced changes in bone growth and strength have generally used the drug streptozocin to induce diabetes in the animals, and have not reached a consensus concerning the mechanism. The BB rat, in which diabetes develops spontaneously without any intervention, was used in experiments investigating bone and mineral metabolism in the presence of insulin replacement therapy. Urinary calcium (calcium is an important constituent of bone) was increased in diabetic rats compared with nondiabetic littermates, but blood calcium levels were normal. The levels of several vitamin D-related compounds involved in bone metabolism were decreased in diabetic rats. Absorption of calcium from the duodenum (part of the small intestine) was completely abolished in diabetic rats, and a variety of indices of bone strength and growth were decreased. Blood levels of osteocalcin, a biochemical marker of osteoblast (bone-producing cell) function, were decreased, and the levels were highly correlated with insulin-like growth factor (IGF). IGF stimulates osteoblast replication and bone synthesis, and this correlation suggests that IGF may play a causal role in the development of osteoporosis in diabetic patients. (Consumer Summary produced by Reliance Medical Information, Inc.)