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

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 mu m(2), acute group: 8.3 +/- 0.4 cells/100 mu m(2), chronic group: 10.9 +/- 0.9 cells/100 mu m(2), and insulin group: 9.2 +/- 0.8 cells/100 mu m(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 mu m(2), acute group: 0.019 +/- 0.005 cells/100 mu m(2), chronic group: 0.067 +/- 0.015, and insulin group: 0.004 +/- 0.004 cells/100 mu m(2), P < 0.05). Patellar tendon collagen content was similar to 32% greater in the chronic and acute groups compared with the control or insulin groups (control group: 681 +/- 63 mu g collagen/mg dry wt, acute group: 938 +/- 21 mu g collagen/mg dry wt, chronic: 951 +/- 52 mu g collagen/mg dry wt, and insulin group: 596 +/- 84 mu g 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.