[Is ucOC a novel bone-derived anti-diabetogenic hormone in humans?]

Clin Calcium. 2009 Sep;19(9):1304-10.
[Article in Japanese]

Abstract

Recent studies have indicated that osteocalcin, a peptide secreted by osteoblasts, functions as an anti-diabetogenic hormone in mice. Osteocalcin knock out mice exhibit obesity, hyperglycemia, and decreased insulin secretion relative to wild-type mice. Treatment with non-carboxylated osteocalcin upregulates energy expenditure, and ameliorates obesity and diabetes in mouse models of obesity-related diabetes. Of interest, the beneficial effects of osteocalcin were shown to be specific to non-carboxylated osteocalcin. This appears, however, inconsistent with recent clinical studies showing insulin-sensitizing effects of vitamin K, which promotes gamma-carboxylation of osteocalcin. These findings shed new light on the crosstalk between bone and energy expenditure, and lead to new questions. These questions include: (1) Does non-carboxylated osteocalcin exert the beneficial effects in humans?; (2) Does warfarin, a vitamin K antagonist, improve insulin, sensitivity and lower blood glucose levels?; (3) and Do estrogen and bisphosphonate, which reduce circulating osteocalcin, contribute to insulin resistance and obesity? These issues await further investigations.

Publication types

  • Review

MeSH terms

  • Animals
  • Bone Density Conservation Agents
  • Diabetes Mellitus / drug therapy
  • Diphosphonates
  • Estrogens
  • Humans
  • Hyperglycemia / etiology
  • Hypoglycemic Agents*
  • Insulin Resistance
  • Mice
  • Obesity / drug therapy
  • Obesity / etiology
  • Osteoblasts / metabolism*
  • Osteocalcin / metabolism
  • Osteocalcin / physiology*
  • Osteocalcin / therapeutic use
  • Vitamin K / physiology
  • Warfarin

Substances

  • Bone Density Conservation Agents
  • Diphosphonates
  • Estrogens
  • Hypoglycemic Agents
  • Osteocalcin
  • Vitamin K
  • Warfarin