Bone as an endocrine organ: Diabetic bone disease as a cause of endocrine disorder via osteocalcin, FGF23 secreted from osteocyte/osteoblast

Abstract

Endocrine effects occur when organs secrete humoral physiologically active substances into the blood or other bodily fluids, and these active substances exert their physiological activities in target tissues. Fibroblast growth factor (FGF) 23, which is secreted by osteocytes, acts on the renal tubule and is involved in phosphorus metabolism. Osteocalcin, which is secreted by osteoblasts, acts on pancreatic β-cells and adipocytes and plays a role in insulin secretion and glycometabolism, in addition to its conventional role as a bone matrix protein. Thus, FGF23 and osteocalcin secreted from bone tissues function as endocrine hormones. Osteocyte and osteoblast functions are decreased in diabetes. Consequently, the secretion of FGF23 and osteocalcin is hindered. The decreased function of FGF23 causes hyperphosphatemia and leads to the progression of arteriosclerosis. The decreased function of osteocalcin results in decreased insulin secretion and increased insulin resistance. In this article, we describe the role of bone as an endocrine organ and its association with diabetes.