Obesity is a chronic disease derived from disequilibrium between energy intake and energy expenditure and evolving as a challenging epidemiological disease in the 21st century. It is urgently necessary to solve this issue by searching for effective strategies and safe drugs. Skeletal muscle could be a potential therapeutic target for the prevention and treatment of obesity and its associated complications due to non-shivering thermogenesis (NST) function. Skeletal muscle NST is based dominantly on futile sarcoplasmic reticulum Ca ATPase (SERCA) pump cycling that leads to a rise in cytosolic Ca, increased adenosine triphosphate (ATP) hydrolysis and heat production. This review will highlight the mechanisms of skeletal muscle NST, including SLN mediated SERCA pump futile cycling, SR-mitochondrial crosstalk and increased mitochondrial biogenesis, and thermogenesis induced by uncoupling proteins 3 (UCP3). We then summarize natural products targeting the pathogenesis of obesity via skeletal muscle NST, offering new insights into pharmacotherapy and potential drug candidates to combat obesity.
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http://dx.doi.org/10.1016/j.lfs.2021.119024 | DOI Listing |
J Cachexia Sarcopenia Muscle
December 2024
Institute for Cancer Outcomes and Survivorship, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Background: Older adults with cancer are at an increased risk of treatment related toxicities and early death. Routinely collected clinico-demographic characteristics inadequately explain this increased risk limiting accurate prognostication. Prior studies have suggested that altered body composition and frailty are independently associated with worse survival among older adults with cancer; however, their combined influence remains unclear.
View Article and Find Full Text PDFCurr Stem Cell Res Ther
December 2024
Center for Rehabilitation Medicine, Rehabilitation & Sports Medicine Research Institute of Zhejiang Province, Department of Rehabilitation Medicine, Zhejiang Provincial People's Hospital(Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, China.
Background: Skeletal muscle atrophy in myotonic dystrophy type 1 (DM1) is caused by abnormal skeletal muscle satellite cell (SSC) proliferation due to increased glycolysis, which impairs muscle regeneration. In DM1, RNA foci sequester muscleblind-like protein 1 (MBNL1) in the nucleus, inhibiting its role in regulating SSC proliferation. Aerobic training reduces glycolysis and increases SSC proliferation and muscle fiber volume.
View Article and Find Full Text PDFExp Brain Res
December 2024
School of Biomedical sciences, University of Leeds, Leeds, UK.
Current clinical assessment tools don't fully capture the genuine neural deficits experienced by chronic stroke survivors and, consequently, they don't fully explain motor function throughout everyday life. Towards addressing this problem, here we aimed to characterise post-stroke alterations in upper-limb control from a novel perspective to the muscle synergy by applying, for the first time, a computational approach that quantifies diverse types of functional muscle interactions (i.e.
View Article and Find Full Text PDFJ Orthop Surg Res
December 2024
Department of Orthopaedic Surgery, Henry Ford Hospital, Henry Ford Health, 2799 W. Grand Blvd CFP-6, Detroit, MI, 48202, USA.
Background: Socioeconomic status has been recognized as a crucial social determinant of health influencing patient outcomes. Area Deprivation Index (ADI) is a validated measure of an area's socioeconomic status. Limited data exists on the impact of ADI and clinical outcomes and complications following rotator cuff repair (RCR).
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!