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Fig. 2 | BMC Endocrine Disorders

Fig. 2

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. 2

Recombinant CaMKIV incubation reduces ER stress-induced insulin resistance and autophagy dysfunction in mature adipocytes. Adipocytes were pretreated with Tun (2.5 μg/ml) for 4 h, followed by CaMKIV (100 ng/ml) 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 p-mTOR, p-CREB expression and their total protein levels. b ER stress markers including PERK phosphorylation (p-PERK) and cleaved-ATF6 in adipocytes. c Autophagy-related proteins Atg7, p62 and LC3 in adipocytes. d IRS-1 tyrosine phosphorylation (pY), Akt serine 473 phosphorylation (p-Akt), and their total protein levels were examined in mice adipocytes either with IP followed by IB or by direct immunoblotting. 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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