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Rethinking Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas.

Isabella D Cooper1, Kenneth H Brookler2, Catherine A P Crofts3

  • 1Translational Physiology Research Group, School of Life Sciences, University of Westminster, 115 New Cavendish Street, London W1W 6UW, UK.

Biomedicines
|September 28, 2021
PubMed
Summary

Patients with type 2 diabetes and cardiovascular disease exhibit "hyperinsulinaemia-osteofragilitas," a bone fragility phenotype with normal to high bone density. This condition increases fracture risk, necessitating investigation for diabetes and hyperinsulinemia in fracture patients with normal bone density.

Keywords:
beta hydroxybutyratebone mineral densitycollagenfragility fractureshydroxyapatitehyperinsulinaemiaosteocalinosteoporosistype 2 diabetesvitamin D

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Area of Science:

  • Endocrinology
  • Bone Biology
  • Metabolic Diseases

Background:

  • Type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD) are linked to hyperinsulinemia, reduced bone remodeling, and increased fragility fractures.
  • Unlike traditional osteoporosis, T2DM-related bone fragility, termed "hyperinsulinaemia-osteofragilitas," presents with normal or increased bone mineral density (BMD).

Purpose of the Study:

  • To elucidate the mechanisms underlying bone fragility in hyperinsulinemic states.
  • To highlight the distinct characteristics of the "hyperinsulinaemia-osteofragilitas" phenotype.
  • To emphasize the role of insulin resistance and hyperinsulinemia in bone health.

Main Methods:

  • Review of existing literature on T2DM, CVD, hyperinsulinemia, and bone fragility.
  • Analysis of the molecular pathways affected by hyperinsulinemia, including oxidative stress, mitochondrial function, and vitamin D metabolism.
  • Examination of the role of osteocytes, osteocalcin, and magnesium in bone integrity.

Main Results:

  • Hyperinsulinemia promotes glucose metabolism, reduces antioxidant activity, increases reactive oxygen species, and impairs osteoblast/osteocyte function.
  • Insulin resistance is associated with increased BMD and fracture risk.
  • Hyperinsulinemia reduces vitamin D availability and magnesium transport, leading to decreased osteocalcin synthesis and increased osteocyte apoptosis.
  • Micropetrosis and magnesium deficiency exacerbate hyperinsulinemia and vitamin D transport issues.

Conclusions:

  • The "hyperinsulinaemia-osteofragilitas" phenotype is characterized by impaired bone remodeling and osteocyte viability despite normal or high BMD.
  • Interventions like carbohydrate restriction, fasting, or ketosis may improve osteocyte viability and bone health by reducing insulin exposure.
  • Patients with fractures and normal BMD should be evaluated for T2DM and hyperinsulinemia.