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Matthew J. Laye

Researcher at Buck Institute for Research on Aging

Publications -  41
Citations -  4582

Matthew J. Laye is an academic researcher from Buck Institute for Research on Aging. The author has contributed to research in topics: Skeletal muscle & Insulin resistance. The author has an hindex of 23, co-authored 39 publications receiving 3871 citations. Previous affiliations of Matthew J. Laye include University of Missouri & University of Copenhagen.

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Lack of exercise is a major cause of chronic diseases

TL;DR: Physical inactivity is a primary cause of most chronic diseases as discussed by the authors, and the body rapidly maladapts to insufficient physical activity, and if continued, results in substantial decreases in both total and quality years of life.
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Mitochondrial dysfunction precedes insulin resistance and hepatic steatosis and contributes to the natural history of non-alcoholic fatty liver disease in an obese rodent model

TL;DR: It is shown that hepatic mitochondrial dysfunction precedes the development of NAFLD and insulin resistance in the OLETF rats, and evidence suggests that progressive mitochondrial dysfunction contributes to the natural history of obesity-associated NA FLD.
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Muscle Specific microRNAs Are Regulated by Endurance Exercise in Human Skeletal Muscle

TL;DR: The data suggest myomiRs respond to physiological stimuli, but their role in regulating human skeletal muscle adaptation remains unknown.
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Daily exercise increases hepatic fatty acid oxidation and prevents steatosis in Otsuka Long-Evans Tokushima Fatty rats.

TL;DR: It is unequivocally demonstrate that daily physical activity attenuates hepatic steatosis and NAFLD in an obese rodent model and suggest that this effect is likely mediated, in part, through enhancement of hepatic fatty acid oxidation and reductions in key protein intermediates of fatty acid synthesis.
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The miRNA plasma signature in response to acute aerobic exercise and endurance training.

TL;DR: In conclusion, acute exercise and chronic endurance training, likely through specific mechanisms unique to each stimulus, robustly modify the miRNA signature of human plasma.