Diabetes is characterized by a hyperglycemic environment, which promotes accumulation of advanced glycation end products (AGEs). In tendon tissue, AGEs build-up results in alterations in collagen structure and binding along with changes in the noncollagenous components of tendon tissue. These changes are believed to result in stiffening of the tendon tissue; however, experimental data suggest that the impact of AGEs to tendon mechanics may be more nuanced. For example, alterations in tendon biochemistry and sliding mechanics may lead to impaired homeostasis and consequent degenerative changes that could lead to decreased stiffness. Additional investigation translating the effect of AGEs in tendon tissue to specific tendon-related clinical syndromes would be beneficial to identify specific treatment targets and better tailor medical and rehabilitative intervention for individuals with diabetes.