Research

Tendon degeneration and poor healing are significant clinical challenges for persons with diabetes. However, treatment strategies are lacking due to a poor understanding of the mechanisms contributing to the high rate of tendon pathology in persons with diabetes. Dr. Carroll and his team is determining the role of AGEs in the development of tendon pathology and delayed healing in individuals with diabetes. AGEs are elevated in the serum of persons with diabetes. Circulating AGEs activate receptors for AGEs (RAGE), initiating a cascade of events leading to impaired cell proliferation, oxidative stress, inflammation, and cell death. We have hypothesized that AGEs drive tendinopathy and poor healing in persons with diabetes via activation of RAGE. Our team is utilizing cell culture, mouse, and human subjects to determine the relationship of AGEs to tendinopathy.  

Loss of estrogen is a risk factor for tendon pain and degeneration, a significant clinical problem impacting the ~25 million women in the US who reach menopause each year. This line of work builds on our previous work utilizing the OVX rat model, in which he demonstrated that loss of estrogen leads to significant declines in tendon collagen and fascicle function. Further, consumption of the phytoestrogen genistein prevents the declines in tendon collagen and function.  

In collaboration with Wayne Campbell, Ph.D. from Nutrition Sciences, we have evaluated if a high protein diet combined with resistance exercise training can enhance tendon functional properties in elderly adults. Lower protein intake in older adults contributes to the loss of muscle mass with aging. Further, while exercise improves tendon function in young adults, such changes appear blunted in older adults. Emerging studies suggest that protein nutrition may be an option for improving tendon exercise adaptations in older adults. Drs. Carroll and Campbell have recently completed work related to our extramural support from the National Cattlemen’s Beef Association (NCBA).