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Fig. 3 | BMC Endocrine Disorders

Fig. 3

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. 3

CaMKIV rescues autophagy dysfunction induced ER stress and insulin resistance in mature adipocytes. Adipocytes were pretreated with 100 nM Atg7 siRNA (Atg7si) or control siRNA (controlsi) for 24 h, followed by 2 mM CaMKIV for 24 h. For insulin signaling, cells incubated in the absence or presence of 10 nM insulin for 10 min. All indicators were measured at protein level. The relative quantity of protein was analyzed using Quantity One software. a Total protein was isolated from siRNA adipocytes and immunoblotted with antibodies for Atg7. b Effect of CaMKIV on ER stress in Atg7−/− adipocytes. c IRS-1 tyrosine phosphorylation (pY) and Akt serine 473 phosphorylation (p-Akt) in Atg7si transfected adipocytes with or without CaMKIV. Quantitative data are presented as means ± SD from at least 3 independent experiments. IB, immunoblotting; IP, immunoprecipitation. * P < 0.05 or ** P < 0.01

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