Abstract
Diabetic encephalopathy is a complication of diabetes mellitus characterized by impaired cognitive functions. Protein kinase C (PKC) isoforms are rarely reported on diabetic encephalopathy, although they have been believed to play crucial roles in other diabetic complications. In this study, streptozotocin- (STZ-) induced diabetic mice were found to exhibit learning and memory deficits in the Morris water maze test. Meanwhile, the expression of cPKCβII, nPKCε, and cPKCγ did not change in the hippocampus, cortex, and striatum at 2 and 8 weeks after STZ injection. The nPKCε translocation to the membrane, where it is activated, was not altered in the above brain regions at 2 and 8 weeks after STZ injection. Nevertheless, cPKCβII translocation to the membrane was significantly decreased in the cortex and hippocampus at 8 weeks after STZ injection. The translocation of cPKCγ from the cytosol to the membrane was remarkably decreased in the hippocampus at 2 and 8 weeks and in the cortex and striatum at 8 weeks after STZ injection. In addition, deletion of cPKCγ aggravated the impairment of spatial learning and memory. In conclusion, our results suggest that the decrease in the activity of cPKCβII and cPKCγ, especially cPKCγ, may play key roles in the pathogenesis of diabetic encephalopathy.
Highlights
The prevalence rates of diabetes mellitus (DM) have increased rapidly over the past three decades in the world [1]
Several studies in type 2 diabetic patients have demonstrated that activation of nPKCε by hepatic accumulation of the diacylglycerol can result in hepatic insulin resistance and nonalcoholic fatty liver disease [19]. nPKCε deletion enhances the amplifying pathways of glucose-stimulated insulin secretion and lipolysis in diabetic mouse beta-cells [20]
We explored whether cPKCβII, cPKCγ, and nPKCε participated in the pathogenesis of type 1 diabetic encephalopathy induced by streptozocin (STZ) injection in mice
Summary
The prevalence rates of diabetes mellitus (DM) have increased rapidly over the past three decades in the world [1]. It has been demonstrated that the cPKCβII, cPKCγ, and nPKCε, widely expressed in the nervous system, participate in many diabetic complications [10,11,12,13,14]. CPKCβII is the most studied isoform for diabetic complications. Several studies in type 2 diabetic patients have demonstrated that activation of nPKCε by hepatic accumulation of the diacylglycerol can result in hepatic insulin resistance and nonalcoholic fatty liver disease [19]. Few studies investigate the roles of the three specific PKC isoforms in the diabetic encephalopathy. We explored whether cPKCβII, cPKCγ, and nPKCε participated in the pathogenesis of type 1 diabetic encephalopathy induced by streptozocin (STZ) injection in mice
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