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Hanson et al

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However, since lactate is a metabolic byproduct and greater metabolic demand increases lactate production, the remaining muscle cells produce even more lactate than usual due to their increased workload, hastening the accumulation of lactate and exacerbating neuronal destruction and muscular atrophy

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endorsed by international guidelines such as ADA and EASD, to highlight the potential of SGLT2 inhibitors and GLP-1 RAs to improve cardiorenal outcomes for patients with T2D [38, 40]

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