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Bone-Derived Factors: A New Gateway to Regulate Glycemia

Nicolas Bonnet¹

¹Division of Bone Diseases, Department of Internal Medicine Specialties, Geneva University Hospitals and Faculty of Medicine, 64 Av de la Roseraie, 1205, Geneva 14, Switzerland. Nicolas.Bonnet@unige.ch.

Calcified Tissue International

|November 11, 2016

Summary

Type 2 diabetes and osteoporosis share common pathways. Bone-derived factors, like FGF23 and osteocalcin, influence glucose metabolism and may offer new therapeutic targets for diabetes.

Area of Science:

Endocrinology
Metabolic Diseases
Bone Biology

Background:

Type 2 diabetes mellitus (T2DM) and osteoporosis prevalence increase with aging.
Preclinical studies suggest shared pathogenic mechanisms between T2DM and osteoporosis.
Emerging evidence highlights bone as an endocrine organ influencing metabolic health.

Purpose of the Study:

To review emerging perspectives on bone-derived factors regulating glycemia.
To explore the role of bone cells and factors in T2DM pathogenesis.
To re-evaluate the connection between bone and glucose metabolism.

Main Methods:

Review of preclinical investigations and genetic studies (e.g., FGF23, osteocalcin, BMPs deficient mice).
Analysis of the endocrine functions of bone-derived factors.
Exploration of mechanisms linking bone remodeling to glucose homeostasis.

Main Results:

Bone-derived factors (FGF23, osteocalcin) play roles in both bone and glucose homeostasis.
Bone morphogenetic proteins and osteoprotegerin-deficient mice models elucidated their functions.
Bone-derived factors can regulate pancreatic beta cells, liver glucose storage, and adipose tissue.

Conclusions:

Bone-derived factors represent potential regulators of glycemia.
Targeting bone-derived factors may offer novel therapeutic strategies for T2DM.
Further research into inter-organ communication involving bone is crucial for understanding diabetes pathophysiology.

Keywords:

Beta-cell Browning Glucose Insulin Osteokine Steatosis

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