DOI: 10.1101/143149May 27, 2017Paper

Obesity/Type II Diabetes Promotes Function-Limiting Changes In Flexor Tendon Extracellular Matrix Organization That Are Not Reversed By Restoring Normal Metabolic Function

BioRxiv : the Preprint Server for Biology
Valentina Studentsova, Keshia M Mora

Abstract

Type II Diabetes (T2DM) negatively alters baseline functions of flexor tendon range of motion and mechanical properties leading to impaired hand movement. As of yet, the biological mechanism(s) leading to diabetic flexor tendinopathy have not been characterized. Here, we use a murine model of diet-induced obesity (DIO) and T2DM to characterize progressive changes in tendon function and organization and to determine if these changes can be reversed through restoration of normal metabolic function. We show that induction of T2DM/obesity is sufficient to initiate an irreversible cascade of pathological events leading to impaired gliding function and mechanical properties specifically in the flexor tendon. Furthermore, we demonstrate that collagen extracellular matrix (ECM) organization is irreversibly compromised during T2DM/obesity and that restoration of normal metabolism is not sufficient to halt these changes. Finally, western blot analysis demonstrate changes in insulin receptor (IR) signaling in obese/diabetic tendons. Collectively, these results establish and characterize a murine model of diabetic flexor tendinopathy, which will aid in identification of novel targets to treat diabetic flexor tendinopathy.

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