Original Article


, Volume 44, Issue 1, pp 87-98

First online:

Rosiglitazone protects against palmitate-induced pancreatic beta-cell death by activation of autophagy via 5′-AMP-activated protein kinase modulation

  • Jie WuAffiliated withDepartment of Endocrinology, Chang Hai Hospital, The Second Military Medical UniversityDepartment of Endocrinology, Tong Ji Hospital, Tong Ji University
  • , Jun-jie WuAffiliated withNational Ministry of Education Key Laboratory of Contemporary Anthropology, School of Life Sciences, Fudan University
  • , Lin-jun YangAffiliated withDepartment of Oncology, Chang Hai Hospital, The Second Military Medical University
  • , Li-xin WeiAffiliated withDepartment of Tumor Immunology and Gene Therapy Center, Eastern Hepatobiliary Surgery Hospital, The Second Military Medical University
  • , Da-jin ZouAffiliated withDepartment of Endocrinology, Chang Hai Hospital, The Second Military Medical University Email author 

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Promoting beta-cell survival is crucial for the prevention of beta-cell failure in diabetes. Thiazolidinediones, a widely used drug to improve insulin sensitivity in clinical practice, is found to have a protective effect on islet beta-cell. To date, the mechanism underlying the protective role of thiazolidinedione on beta-cell survival remain largely unknown. Activation of autophagy was detected by transmission electron microscopy, western blot, and GFP-LC3 transfection. Cell viability was examined by WST-8. Cell apoptosis was demonstrated by DAPI and Annexin V/PI staining. Colony formation assay was used to detect long-term cell viability. We demonstrated that rosiglitazone-treated beta-cells were more resistant to palmitate-induced apoptosis. The conversion of LC3-I to LC3-II and accumulated autophagosomes were found to be upregulated in rosiglitazone-treated cells. Inhibition of autophagy augmented palmitate-induced apoptosis with rosiglitazone treatment, suggesting that autophagy plays an important role in the survival function of rosiglitazone on beta-cells. Furthermore, we showed that rosiglitazone could induce AMP-activated protein kinase (AMPK) phosphorylation and reduce p70S6 kinase phosphorylation. Inhibition of AMPK impaired autophagy activation and enhanced palmitate-induced apoptosis during rosiglitazone treatment. These findings reveal that rosiglitazone-induced autophagy contributes to its protective function on beta-cells during palmitate treatment.


Rosiglitazone Autophagy Palmitate AMPK