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This review aims to evaluate KD as a therapeutic intervention for neurodegenerative diseases by examining its effects on pathological mechanisms, such as mitochondrial dysfunction, neuroinflammation, and alterations in energy metabolism, to assess its feasibility and potential in managing neurological disorders

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The proteins examined are: HSL, ATGL, adiponutrin, triacylglycerol hydrolase, / hydrolase containing mRNA 5 (also known as CGI-58) and 11 (also known as Beuren-Williams Syndrome Critical Region 21), acylpeptide hydrolase, esterase 1, esterase D, carboxylesterase ML1, and membrane-associated calcium-independent phospholipase A 2

After 4 weeks, L-glutamine decreased HbA1c and fructosamine irrespective of sitagliptin in patients with T2DM, and postprandial glucose decreased with significant time-treatment interactions, while HbA1c and fructosamine decreased without significant time-treatment interactions [38]

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