Does glucocorticoid exposure explain the association between metabolic dysfunction and tendinopathy?

Abstract

Background While metabolic health is acknowledged to affect connective tissue structure and function, the mechanisms are unclear. Glucocorticoids are present in almost every cell type throughout the body and control key physiological processes such as energy homeostasis, stress response, inflammatory and immune processes, and cardiovascular function. Glucocorticoid excess manifests as visceral adiposity, dyslipidemia, insulin resistance, and type 2 diabetes. As these metabolic states are also associated with tendinopathy and tendon rupture, it may be that glucocorticoids excess is the link between metabolic health and tendinopathy. Objective To synthesise current knowledge linking glucocorticoid exposure to tendon structure and function. Methods Narrative literature review. Results We provide an overview of endogenous glucocorticoid production, regulation, and signalling. Next we review the impact that oral glucocorticoid has on risk of tendon rupture and the effect that injected glucocorticoid has on resolution of symptoms. Then we highlight the clinical and mechanistic overlap between tendinopathy and glucocorticoid excess in the areas of visceral adiposity, dyslipidemia, insulin resistance and type 2 diabetes. In these areas, we highlight the role of glucocorticoids and how these hormones might underpin the connection between metabolic health and tendon dysfunction. Conclusions There are several plausible pathways through which glucocorticoids might mediate the connection between metabolic health and tendinopathy.

Glucocorticoids Play a Pivotal Role in Analgesic and Blood Glucose Regulatory Effects in C57 Mice Treated by Water Wxtract of Prunella Vulgaris L. Spica

“…For example, as the effector molecules of the stress response, GCs are known to increase the consumption of foods enriched in fat and sugar, but acute stress usually results in decreased eating whereas chronic stress results in increased eating [41]. GCs are known as catabolic molecules, but glucocorticoid excess manifests as visceral adiposity [42]. P. vulgaris treatment in current research showed a decreased appetite but an increased ratio of body weight gain to food intake.…”

Network Pharmacology and ­Experimental Analyses of the Mechanism of Analgesic and Glucose Intolerance Through Glucocorticoid Signaling in C57 Mice Treated with Water Extract of Prunella vulgaris L. Spica

“…48 GCs are known as catabolic molecules, but GC excess manifests as visceral adiposity. 49 Similarly, P. vulgaris treatment shows a decreased appetite, but an increased ratio of body weight gain to food intake. Likewise, an elevated plasma BDNF level and hypothalamic BDNF expression, coupled with a down-regulated hepatic BDNF expression occurred in the current research.…”

Chronic hyperglycemia, hypercholesterolemia, and metabolic syndrome are associated with risk of tendon injury

“…27 BMI was calculated as kg/m 2 , and the subjects were classified as running vs. no running (<0 h/week) smokers vs. non-smokers based on self-reporting. Likewise, regular use of painkillers, the treatment with lipid-lowering statins, 28 and medication as treatment for asthma/bronchitis, 29 which may cause tendon damage, were registered based on self-reporting.…”