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World J Diabetes. Feb 15, 2014; 5(1): 14-16
Published online Feb 15, 2014. doi: 10.4239/wjd.v5.i1.14
Insulin and bone: Recent developments
Gordon L Klein
Gordon L Klein, Department of Orthopaedic Surgery and Rehabilitation, University of Texas and Shriners Burns Hospital, Galveston, TX 77555, United States
Author contributions: Klein GL contributed to the manuscript.
Correspondence to: Gordon L Klein, MD, MPH, Department of Orthopaedic Surgery and Rehabilitation, University of Texas and Shriners Burns Hospital, 301 University Boulevard, Galveston, TX 77555, United States. gordonklein@ymail.com
Telephone: +1-409-7475750 Fax: +1-409-7706719
Received: November 24, 2013
Revised: December 4, 2013
Accepted: December 17, 2013
Published online: February 15, 2014
Processing time: 87 Days and 13.6 Hours
Abstract

While insulin-like growth factor I is a well-known anabolic agent in bone evidence is beginning to accumulate that its homologue, insulin, also has some anabolic properties for bone. There is specific evidence that insulin may work to stimulate osteoblast differentiation, which in turn would enhance production of osteocalcin, the osteoblast-produced peptide that can stimulate pancreatic β cell proliferation and skeletal muscle insulin sensitivity. It is uncertain whether insulin stimulates bone directly or indirectly by increasing muscle work and therefore skeletal loading. We raise the question of the sequence of events that occurs with insulin resistance, such as type 2 diabetes. Evidence to date suggests that these patients have lower serum concentrations of osteocalcin, perhaps reduced skeletal loading, and reduced bone strength as evidenced by micro-indentation studies.

Keywords: Type 2 diabetes; Insulin; Bone; Osteoblasts; Insulin resistance

Core tip: This is a review of recent publications that suggest an anabolic loop among bone, pancreas, and skeletal muscle.