Influence of acute and chronic streptozotocin-induced diabetes on the rat tendon extracellular matrix and mechanical properties

TY - JOUR

T1 - Influence of acute and chronic streptozotocin-induced diabetes on the rat tendon extracellular matrix and mechanical properties

AU - Volper, Brent D

AU - Huynh, Richard T

AU - Arthur, Kathryn A

AU - Noone, Joshua

AU - Gordon, Benjamin D

AU - Zacherle, Emily W

AU - Munoz, Eduardo

AU - Sørensen, Mikkel

AU - Svensson, René B

AU - Broderick, Tom L

AU - Magnusson, S Peter

AU - Howden, Reuben

AU - Hale, Taben M

AU - Carroll, Chad C

N1 - Copyright © 2015 the American Physiological Society.

PY - 2015/11/1

Y1 - 2015/11/1

N2 - 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 μm2, acute group: 8.3 ± 0.4 cells/100 μm2, chronic group: 10.9 ± 0.9 cells/100 μm2, and insulin group: 9.2 ± 0.8 cells/100 μm2, 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 μm2, acute group: 0.019 ± 0.005 cells/100 μm2, chronic group: 0.067 ± 0.015, and insulin group: 0.004 ± 0.004 cells/100 μm2, 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.

AB - 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 μm2, acute group: 8.3 ± 0.4 cells/100 μm2, chronic group: 10.9 ± 0.9 cells/100 μm2, and insulin group: 9.2 ± 0.8 cells/100 μm2, 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 μm2, acute group: 0.019 ± 0.005 cells/100 μm2, chronic group: 0.067 ± 0.015, and insulin group: 0.004 ± 0.004 cells/100 μm2, 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.

KW - Acute Disease

KW - Animals

KW - Chronic Disease

KW - Collagen

KW - Diabetes Mellitus, Experimental

KW - Elastic Modulus

KW - Extracellular Matrix

KW - Extracellular Matrix Proteins

KW - Male

KW - Rats

KW - Rats, Sprague-Dawley

KW - Streptozocin

KW - Stress, Mechanical

KW - Tendons

KW - Tensile Strength

U2 - 10.1152/ajpregu.00189.2015

DO - 10.1152/ajpregu.00189.2015

M3 - Journal article

C2 - 26310937

SN - 0363-6119

VL - 309

SP - R1135-43

JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology

JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology

IS - 9

ER -