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Fig. 1 | BMC Endocrine Disorders

Fig. 1

From: In vitro treatment of 3 T3-L1 adipocytes with recombinant Calcium/calmodulin-dependent Protein Kinase IV (CaMKIV) limits ER stress and improves insulin sensitivity through inhibition of autophagy via the mTOR/CREB signaling pathway

Fig. 1

Induction of autophagic dysfunction due to ER stress induced by tunicamycin in adipocytes treated with 0, 1, 2.5 or 5 μg/ml Tun for 4 h. All indicators were measured at protein level. The relative quantity of protein was analyzed using Quantity One software. a ER stress markers including PERK phosphorylation (p-PERK) and cleaved-ATF6 in adipocytes. b Autophagy-related proteins Atg7, p62 and LC3 in adipocytes treated with 2.5 μg/ml Tun for 4 h. c Representation electron micrographs of adipocytes treated with 2.5 μg/ml Tun for 4 h. Quantification of autophagolysosome-like vacuoles per field in the EM images, Scale bars, 0.5 μm. Quantitative data are presented as means ± SD from at least 3 independent experiments. * P < 0.05 or ** P < 0.01

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