Influence of acute and chronic streptozotocin-induced diabetes on the rat tendon extracellular matrix and mechanical properties
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Influence of acute and chronic streptozotocin-induced diabetes on the rat tendon extracellular matrix and mechanical properties. / Volper, Brent D; Huynh, Richard T; Arthur, Kathryn A; Noone, Joshua; Gordon, Benjamin D; Zacherle, Emily W; Munoz, Eduardo; Sørensen, Mikkel; Svensson, René B; Broderick, Tom L; Magnusson, S Peter; Howden, Reuben; Hale, Taben M; Carroll, Chad C.
I: American Journal of Physiology: Regulatory, Integrative and Comparative Physiology, Bind 309, Nr. 9, 01.11.2015, s. R1135-43.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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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 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.
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 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.
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
VL - 309
SP - R1135-43
JO - American Journal of Physiology
JF - American Journal of Physiology
SN - 0363-6119
IS - 9
ER -
ID: 161697788