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Obesity/ Type II Diabetes Promotes Function-limiting Changes in Flexor Tendon Extracellular Matrix that are not Reversed by Restoring Normal Metabolic Function

Valentina Studentsova, Keshia M. Mora, Melissa F. Glasner, Mark R. Buckley, Alayna E. Loiselle
doi: https://doi.org/10.1101/143149
Valentina Studentsova
1Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY
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Keshia M. Mora
1Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY
2Department of Biomedical Engineering, University of Rochester, Rochester, NY
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Melissa F. Glasner
3Cell Biology of Disease Graduate Program, University of Rochester Medical Center, Rochester, NY
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Mark R. Buckley
1Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY
2Department of Biomedical Engineering, University of Rochester, Rochester, NY
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Alayna E. Loiselle
1Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY
4Department of Orthopaedics & Rehabilitation, University of Rochester Medical Center, Rochester, NY
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  • For correspondence: Alayna_Loiselle@urmc.rochester.edu
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Abstract

Type II Diabetes (T2DM) negatively alters baseline tendon function, including decreased range of motion and mechanical properties; however, the biological mechanisms that promote diabetic tendinopathy are unknown. To facilitate identification of therapeutic targets we developed a novel murine model of diabetic tendinopathy. Mice fed a High Fat Diet (HFD) developed diet induced obesity and T2DM. Obesity/ T2DM resulted in progressive impairments in tendon gliding function and mechanical properties, relative to mice fed a Low Fat Diet (LFD), as well as a decrease in collagen fibril diameter by transmission electron microscopy. We then determined if restoration of normal metabolic function, by switching mice from HFD to LFD, is sufficient to halt the pathological changes in tendon due to obesity/T2DM. However, switching from a HFD to LFD resulted in greater impairments in tendon gliding function than mice maintained on a HFD. Mechanistically, IRβ signaling is decreased in obese/T2DM murine tendons, suggesting altered IRβ signaling as a driver of diabetic tendinopathy. However, knock-down of IRβ expression in S100a4-lineage cells (IRcKOS100a4) was not sufficient to induce diabetic tendinopathy as no impairments in tendon gliding function or mechanical properties were observed in IRcKOS100a4 relative to WT. Collectively, these data define a murine model of diabetic tendinopathy, and demonstrate that tendon-specific, rather than systemic treatment approaches are needed.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted December 12, 2017.
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Obesity/ Type II Diabetes Promotes Function-limiting Changes in Flexor Tendon Extracellular Matrix that are not Reversed by Restoring Normal Metabolic Function
Valentina Studentsova, Keshia M. Mora, Melissa F. Glasner, Mark R. Buckley, Alayna E. Loiselle
bioRxiv 143149; doi: https://doi.org/10.1101/143149
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Obesity/ Type II Diabetes Promotes Function-limiting Changes in Flexor Tendon Extracellular Matrix that are not Reversed by Restoring Normal Metabolic Function
Valentina Studentsova, Keshia M. Mora, Melissa F. Glasner, Mark R. Buckley, Alayna E. Loiselle
bioRxiv 143149; doi: https://doi.org/10.1101/143149

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