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This potential action may be possible by enhancing skeletal muscle response to the activation of AMPK activation, which appears to sequentially increase the expression of glucose transporters

Considering the consistent reports of suppressed AGXT in MASH 12,15,16,17 , recent evidence linking AGXT dysfunction and primary hyperoxaluria with liver disease 12,15,20,21 , the known deleterious effects of oxalate in renal and cardiovascular diseases 22,23,24,25,26 , together with the rising prevalence of MASH and limited therapy available 1,6,7 , there is a strong rationale to better understand impaired oxalate metabolism in MASH and to evaluate the therapeutic potential of targeting this dysregulated metabolic pathway

doi:10.1093/humupd/dmx001

7: e016434