title: Influence of acute and chronic streptozotocin-induced diabetes on the rat tendon extracellular matrix and mechanical properties.
abstract: Diabetes is a major risk factor for tendinopathy, and tendon abnormalities are common in diabetic patients. The purpose of the present study was to evaluate the effect of streptozotocin (60 mg/kg)-induced diabetes and insulin therapy on tendon mechanical and cellular properties. Sprague-Dawley rats (n = 40) were divided into the following four groups: nondiabetic (control), 1 wk of diabetes (acute), 10 wk of diabetes (chronic), and 10 wk of diabetes with insulin treatment (insulin). After 10 wk, Achilles tendon and tail fascicle mechanical properties were similar between groups (P > 0.05). Cell density in the Achilles tendon was greater in the chronic group compared with the control and acute groups (control group: 7.8 ± 0.5 cells/100 μm(2), acute group: 8.3 ± 0.4 cells/100 μm(2), chronic group: 10.9 ± 0.9 cells/100 μm(2), and insulin group: 9.2 ± 0.8 cells/100 μm(2), P < 0.05). The density of proliferating cells in the Achilles tendon was greater in the chronic group compared with all other groups (control group: 0.025 ± 0.009 cells/100 μm(2), acute group: 0.019 ± 0.005 cells/100 μm(2), chronic group: 0.067 ± 0.015, and insulin group: 0.004 ± 0.004 cells/100 μm(2), P < 0.05). Patellar tendon collagen content was ∼32% greater in the chronic and acute groups compared with the control or insulin groups (control group: 681 ± 63 μg collagen/mg dry wt, acute group: 938 ± 21 μg collagen/mg dry wt, chronic: 951 ± 52 μg collagen/mg dry wt, and insulin group: 596 ± 84 μg collagen/mg dry wt, P < 0.05). In contrast, patellar tendon hydroxylysyl pyridinoline cross linking and collagen fibril organization were unchanged by diabetes or insulin (P > 0.05). Our findings suggest that 10 wk of streptozotocin-induced diabetes does not alter rat tendon mechanical properties even with an increase in collagen content. Future studies could attempt to further address the mechanisms contributing to the increase in tendon problems noted in diabetic patients, especially since our data suggest that hyperglycemia per se does not alter tendon mechanical properties.
authors: Department of Physiology, Arizona College of Osteopathic Medicine, Midwestern University, Glendale, Arizona; Department of Basic Medical Sciences, University of Arizona College of Medicine, Phoenix, Arizona.
authors: Brent D
authors: BD
authors: Volper
authors: Department of Physiology, Arizona College of Osteopathic Medicine, Midwestern University, Glendale, Arizona; Department of Basic Medical Sciences, University of Arizona College of Medicine, Phoenix, Arizona.
authors: Richard T
authors: RT
authors: Huynh
authors: Department of Physiology, Arizona College of Osteopathic Medicine, Midwestern University, Glendale, Arizona;
authors: Kathryn A
authors: KA
authors: Arthur
authors: Laboratory of Systems Physiology, Department of Kinesiology, University of North Carolina at Charlotte, Charlotte, North Carolina;
authors: Joshua
authors: J
authors: Noone
authors: Laboratory of Systems Physiology, Department of Kinesiology, University of North Carolina at Charlotte, Charlotte, North Carolina;
authors: Benjamin D
authors: BD
authors: Gordon
authors: Laboratory of Systems Physiology, Department of Kinesiology, University of North Carolina at Charlotte, Charlotte, North Carolina;
authors: Emily W
authors: EW
authors: Zacherle
authors: Laboratory of Systems Physiology, Department of Kinesiology, University of North Carolina at Charlotte, Charlotte, North Carolina;
authors: Eduardo
authors: E
authors: Munoz
authors: Musculoskeletal Rehabilitation Research Unit and Institute of Sports Medicine, Copenhagen Bispebjerg Hospital Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark; and.
authors: Mikkel A
authors: MA
authors: Sørensen
authors: Musculoskeletal Rehabilitation Research Unit and Institute of Sports Medicine, Copenhagen Bispebjerg Hospital Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark; and.
authors: René B
authors: RB
authors: Svensson
authors: Department of Physiology, Arizona College of Osteopathic Medicine, Midwestern University, Glendale, Arizona;
authors: Tom L
authors: TL
authors: Broderick
authors: Musculoskeletal Rehabilitation Research Unit and Institute of Sports Medicine, Copenhagen Bispebjerg Hospital Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark; and.
authors: S Peter
authors: SP
authors: Magnusson
authors: Laboratory of Systems Physiology, Department of Kinesiology, University of North Carolina at Charlotte, Charlotte, North Carolina;
authors: Reuben
authors: R
authors: Howden
authors: Department of Basic Medical Sciences, University of Arizona College of Medicine, Phoenix, Arizona.
authors: Taben M
authors: TM
authors: Hale
authors: Department of Physiology, Arizona College of Osteopathic Medicine, Midwestern University, Glendale, Arizona; ccarro@midwestern.edu.
authors: Chad C
authors: CC
authors: Carroll
mesh_terms: D000208:Acute Disease; D000818:Animals; D002908:Chronic Disease; D003094:Collagen / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000473:pathology* / Q000503:physiopathology*; D055119:Elastic Modulus; D005109:Extracellular Matrix / Q000378:metabolism* / Q000473:pathology; D016326:Extracellular Matrix Proteins / Q000378:metabolism*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D013311:Streptozocin; D013314:Stress, Mechanical; D013710:Tendons / Q000473:pathology* / Q000503:physiopathology*; D013718:Tensile Strength
chemical_list: D016326:Extracellular Matrix Proteins; D013311:Streptozocin; D003094:Collagen
keywords: collagen; cross linking; diabetes; mechanical strength; tendinopathy; tendon; tenocytes