3-Deoxyglucosone induces insulin resistance by impairing insulin signaling in HepG2 cells.

摘要: 3-Deoxyglucosone (3DG), a highly reactive dicarbonyl intermediate generated during glycation, has been confirmed to be markedly elevated in the plasma of patients with diabetes. Our previous study found that there is an association between increasing accumulation 3DG and impaired glucose regulation non-diabetic seniors (females, >50 years old; males, >55 old). It was also led homeostasis healthy mice, however, mechanisms underlying deleterious effect diabetes remain fully elucidated. The present aimed investigate ability cause hepatic insulin resistance cell model by assessing uptake glycogen content. In addition, molecular signaling events, including phosphoinositide 3‑kinase (PI3K)/AKT/glucose transporter 2 (GLUT2) PI3K/AKT/glycogen synthase kinase‑3 (GSK‑3) pathways, which affect resistance, were further investigated using Western blot analysis. results showed (10‑300 ng/ml) had no significant on HepG2 viability, viability cells decreased exposure concentrations 500 1,000 ng/ml. Treatment non‑cytotoxic resulted content stimulation, but not under basal conditions. insulin‑induced expression GLUT2 p‑GSK‑3 eliminated (80 300 ng/ml), addition inhibiting phosphorylation downstream effectors pathway, receptor substrate 1, PI3K AKT. conclusion, findings indicated exogenous directly contributed induction impairing cells, suggested may involved worsening diabetic condition.