Protective effects of asiatic acid in a spontaneous type 2 diabetic mouse model.

Asiatic acid (AA) has been demonstrated to exhibit anti-diabetic activity. However, the mechanisms and underlying signaling pathways remain to be elucidated. The present study was performed to confirm the protective effect of AA and demonstrate its ability to regulate the phosphatidylinositol 3‑kinase (PI3K)/protein kinase B (AKT)/glycogen synthase kinase‑3β (GSK‑3β) signaling pathway in db/db mice. Db/db mice fed on a high‑fat diet were used to model diabetes mellitus. Modeled mice were divided randomly into the model control, pioglitazone hydrochloride tablet (PH) and AA groups. Age‑matched C57 BL/6J mice served as normal controls. Lipid and glucose levels, and glycogen synthesis rates were assessed following treatment. Pathological changes were detected using hematoxylin and eosin staining. Expression of the PI3K/AKT/GSK‑3β signaling pathway at the mRNA level was measured using quantitative polymerase chain reaction analysis. The model control group revealed typical characteristics of obesity and diabetes, including high glucose and lipid levels, and decreased glycogen synthesis. Four weeks of treatment with AA or PH ameliorated these abnormalities. AA and PH treatments mitigated the upregulation of PI3K, AKT, insulin receptor, and insulin receptor substrate‑1 mRNA expression in modeled mice. Furthermore, AA and PH treatments decreased GSK‑3β and glucose‑6‑phosphatase mRNA expression compared with the normal control group. The results of the present study confirmed that AA possesses anti‑diabetic activity in db/db mice. The PI3K/AKT/GSK‑3β signaling pathway may mediate this protective effect.