Ankur V. Dnyanmote

TL;DR: Research in type 2 diabetic rats investigated alterations in the renal and hepatic expression of organic anion and cation transporters, multidrug resistance-associated proteins (Mrps), breast cancer resistance protein (Bcrp), P-glycoprotein (Pgp), and hepatatic Na(+)-taurocholate cotransporting polypeptide (Ntcp) in type 1 diabetic rats to investigate changes in chemical disposition and drug pharmacokinetics.

TL;DR: The studies show high sensitivity of type 2 diabetes to model hepatotoxicants and suggest that CCl4 hepatotoxicity is potentiated due to inhibited tissue repair, whereas in the nondiabetic rats robust tissue repair resulted in regression of injury and survival after CCl 4 administration.

TL;DR: It is suggested that advancement of cells in the cell division cycle and higher tissue repair protect DB mice by preventing progression of APAP-initiated liver injury that normally leads to mortality.

TL;DR: It appears that similar to type 1 diabetes, type 2 diabetes also increases sensitivity to dissimilar hepatotoxicants due to inhibited compensatory tissue repair, suggesting that sensitivity to hepatotoxicity in diabetes occurs in the absence as well as presence of insulin.

TL;DR: It is suggested that pre-placement of S-phase cells in the kidney due to diabetes is critical in mitigating the progression of DCVC-initiated renal injury by upregulation of tissue repair, leading to survival of the DB mice by avoiding acute renal failure.