50 research outputs found

    Arctigenin Efficiently Enhanced Sedentary Mice Treadmill Endurance

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    Physical inactivity is considered as one of the potential risk factors for the development of type 2 diabetes and other metabolic diseases, while endurance exercise training could enhance fat oxidation that is associated with insulin sensitivity improvement in obesity. AMP-activated protein kinase (AMPK) as an energy sensor plays pivotal roles in the regulation of energy homeostasis, and its activation could improve glucose uptake, promote mitochondrial biogenesis and increase glycolysis. Recent research has even suggested that AMPK activation contributed to endurance enhancement without exercise. Here we report that the natural product arctigenin from the traditional herb Arctium lappa L. (Compositae) strongly increased AMPK phosphorylation and subsequently up-regulated its downstream pathway in both H9C2 and C2C12 cells. It was discovered that arctigenin phosphorylated AMPK via calmodulin-dependent protein kinase kinase (CaMKK) and serine/threonine kinase 11(LKB1)-dependent pathways. Mice treadmill based in vivo assay further indicated that administration of arctigenin improved efficiently mice endurance as reflected by the increased fatigue time and distance, and potently enhanced mitochondrial biogenesis and fatty acid oxidation (FAO) related genes expression in muscle tissues. Our results thus suggested that arctigenin might be used as a potential lead compound for the discovery of the agents with mimic exercise training effects to treat metabolic diseases

    Role of biomechanics in the understanding of normal, injured, and healing ligaments and tendons

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    Ligaments and tendons are soft connective tissues which serve essential roles for biomechanical function of the musculoskeletal system by stabilizing and guiding the motion of diarthrodial joints. Nevertheless, these tissues are frequently injured due to repetition and overuse as well as quick cutting motions that involve acceleration and deceleration. These injuries often upset this balance between mobility and stability of the joint which causes damage to other soft tissues manifested as pain and other morbidity, such as osteoarthritis

    Mechanisms and time course of impaired skeletal muscle glucose transport activity in streptozocin (STZ) diabetic rats.

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    Skeletal muscle glucose transport activity after an oral glucose load in rats.

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    Chronic growth hormone treatment in normal rats reduces post-prandial skeletal muscle plasma membrane GLUT-1 content, but not glucose transport or GLUT-4 expression and localization

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    Glucose ingestion causes GLUT-4 translocation in human skeletal muscle

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    Epinephrine and insulin stimulate different mitogen-activated protein kinase pathways in rat skeletal muscle

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