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Propofol is the most common intravenous anesthetic agent used in clinical practice. Propofol can induce insulin resistance in mouse primary hepatocytes, however the molecular mechanism through which propofol acts remains largely unknown. Based on previous studies, it was hypothesized that phosphatase and tensin homolog (PTEN) is involved in propofol-mediated insulin resistance. The aim of the present study was to investigate the biological function of PTEN and its molecular mechanism in propofol-induced insulin resistance in mouse primary hepatocytes. Mouse primary hepatocytes were treated with propofol and transfected with small interfering RNA (siRNA)-996 to silence the endogenous expression of PTEN. The current study assessed the effects of propofol and PTEN knockdown on the expression of PTEN and several key enzymes of the phosphoinositide 3-kinase/protein kinase B/glycogen synthase kinase-3β signaling pathway, as well as the glycogen content in mouse primary hepatocytes. Treatment with propofol significantly increased protein and mRNA PTEN expression in mouse primary hepatocytes. In addition, knockdown of PTEN reversed propofol-induced insulin resistance in mouse primary hepatocytes. The present study indicated that PTEN serves a role in the physiological process of propofol-induced insulin resistance in mouse primary hepatocytes, and PTEN inhibition may be a potential target for therapeutic intervention against propofol-induced adverse effects.

PTEN in propofol‑induced insulin resistance in mouse primary hepatocytes