Anabolic effects of insulin on bone suggest a role for chromium picolinate in preservation of bone density

Med Hypotheses. 1995 Sep;45(3):241-6. doi: 10.1016/0306-9877(95)90112-4.


Activation of osteoclasts by parathyroid hormone (PTH) is mediated by PTH stimulation of osteoblasts, and is dependent on a PTH-induced rise in protein kinase C activity. Physiological levels of insulin reduce the ability of PTH to activate protein kinase C in osteoblasts, suggesting that insulin may be a physiological antagonist of bone resorption. In addition, insulin is known to promote collagen production by osteoblasts. These findings imply that efficient insulin activity may exert an anabolic effect on bone, and rationalize the many clinical studies demonstrating reduced bone density in Type I diabetes. Recently, the insulin-sensitizing nutrient chromium picolinate has been found to reduce urinary excretion of hydroxyproline and calcium in postmenopausal women, presumably indicative of a reduced rate of bone resorption. This nutrient also raised serum levels of dehydroepiandrosterone-sulfate, which may play a physiological role in the preservation of postmenopausal bone density. The impact of chromium picolinate (alone or in conjunction with calcium and other micronutrients) on bone metabolism and bone density, merits further evaluation in controlled studies.

MeSH terms

  • Animals
  • Bone Density / drug effects*
  • Bone Resorption / physiopathology
  • Bone Resorption / prevention & control*
  • Calcium / metabolism
  • Collagen / biosynthesis
  • Dehydroepiandrosterone / analogs & derivatives
  • Dehydroepiandrosterone / physiology
  • Dehydroepiandrosterone Sulfate
  • Enzyme Activation / drug effects
  • Female
  • Humans
  • Insulin / pharmacology*
  • Insulin Resistance
  • Mice
  • Models, Biological
  • Osteoblasts / drug effects*
  • Osteoblasts / metabolism
  • Osteoclasts / drug effects*
  • Osteoclasts / enzymology
  • Osteoclasts / physiology
  • Osteoporosis, Postmenopausal / physiopathology
  • Osteoporosis, Postmenopausal / prevention & control*
  • Parathyroid Hormone / physiology
  • Picolinic Acids / pharmacology
  • Picolinic Acids / therapeutic use*
  • Protein Kinase C / antagonists & inhibitors


  • Insulin
  • Parathyroid Hormone
  • Picolinic Acids
  • Dehydroepiandrosterone
  • Dehydroepiandrosterone Sulfate
  • Collagen
  • Protein Kinase C
  • picolinic acid
  • Calcium