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We previously demonstrated in streptozotocin-induced diabetic mice that deficiency or inhibition of aldose reductase (AR) caused significant dephosphorylation of hepatic transcriptional factor PPAR  α  , leading to its activation and significant reductions in serum lipid levels. Herein, we report that inhibition of AR by zopolrestat or by a short-hairpin RNA (shRNA) against AR caused a significant reduction in serum and hepatic triglycerides levels in 10-week old diabetic db/db mice. Meanwhile, hyperglycemia-induced phosphorylation of hepatic ERK1/2 and PPAR  α   was significantly attenuated in db/db mice treated with zopolrestat or AR shRNA. Further, in comparison with the untreated db/db mice, the hepatic mRNA expression of  Aco  and  ApoA5 , two target genes for PPAR  α  , was increased by 93% ( P  < 0.05) and 73% ( P  < 0.05) in zopolrestat-treated mice, respectively. Together, these data indicate that inhibition of AR might lead to significant amelioration in hyperglycemia-induced dyslipidemia and nonalcoholic fatty liver disease.

experimental diabetes research

Inhibition of Aldose Reductase Activates Hepatic Peroxisome Proliferator-Activated Receptor-<i>α</i>and Ameliorates Hepatosteatosis in Diabetic db/db Mice

Inhibition of Aldose Reductase Activates Hepatic Peroxisome Proliferator-Activated Receptor-αand Ameliorates Hepatosteatosis in Diabetic db/db Mice