Vanessa D Sherk1, Irene Schauer2,3, Viral N Shah4. 1. Department of Orthopedics, School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, 80045, USA. vanessa.sherk@cuanschutz.edu. 2. Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Colorado Anschutz Medical Campus, Aurora, CO, 80045, USA. 3. Rocky Mountain Regional VA Medical Center, Aurora, CO, USA. 4. Barbara Davis Center for Diabetes, University of Colorado Anschutz Medical Campus, Aurora, CO, 80045, USA.
Abstract
PURPOSE OF REVIEW: To provide an update on the acute effects of glucose, insulin, and incretins on markers of bone turnover in those with and without diabetes. RECENT FINDINGS: Bone resorption is suppressed acutely in response to glucose and insulin challenges in both healthy subjects and patients with diabetes. The suppression is stronger with oral glucose compared with intravenous delivery. Stronger responses with oral glucose may be related to incretin effects on insulin secretion or from a direct effect on bone turnover. Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-2 (GLP-2) infusion acutely suppresses bone resorption without much effect on bone formation. The bone turnover response to a metabolic challenge may be attenuated in type 2 diabetes, but this is an understudied area. A knowledge gap exists regarding bone turnover responses to a metabolic challenge in type 1 diabetes. The gut-pancreas-bone link is potentially an endocrine axis. This linkage is disrupted in diabetes, but the mechanism and progression of this disruption are not understood.
PURPOSE OF REVIEW: To provide an update on the acute effects of glucose, insulin, and incretins on markers of bone turnover in those with and without diabetes. RECENT FINDINGS: Bone resorption is suppressed acutely in response to glucose and insulin challenges in both healthy subjects and patients with diabetes. The suppression is stronger with oral glucose compared with intravenous delivery. Stronger responses with oral glucose may be related to incretin effects on insulin secretion or from a direct effect on bone turnover. Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-2 (GLP-2) infusion acutely suppresses bone resorption without much effect on bone formation. The bone turnover response to a metabolic challenge may be attenuated in type 2 diabetes, but this is an understudied area. A knowledge gap exists regarding bone turnover responses to a metabolic challenge in type 1 diabetes. The gut-pancreas-bone link is potentially an endocrine axis. This linkage is disrupted in diabetes, but the mechanism and progression of this disruption are not understood.
Entities:
Keywords:
Bone turnover; Glycemic control; Incretin; Insulin; Type 1 diabetes; Type 2 diabetes
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