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Title of Journal: Endocrine

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Abbravation: Endocrine

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Springer US

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10.1002/cmdc.201500383

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1559-0100

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Blood glucose fluctuation accelerates renal injury

Authors: Changjiang Ying Xiaoyan Zhou Zhenzhen Chang Hongwei Ling Xingbo Cheng Wei Li
Publish Date: 2016/02/09
Volume: 53, Issue: 1, Pages: 81-96
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Abstract

Blood glucose fluctuation is associated with diabetic nephropathy However the mechanism by which blood glucose fluctuation accelerates renal injury is not fully understood The aim of the present study was to assess the effects of blood glucose fluctuation on diabetic nephropathy in rats and investigate its underlying mechanism Diabetes in the rats was induced by a high sugar highfat diet and a single dose of STZ 35 mg/kginjected intraperitoneally Unstable blood sugar models were induced by subcutaneous insulin injection and intravenous glucose injection alternately Body weight glycosylated hemoglobin A1c HbAlc blood urea nitrogen BUN serum creatinine Scr and Creatinine clearance Ccr were assessed TSOD activity and MDA level were measured by assay kit Change in renal tissue ultrastructure was observed by light microscopy and electron microscopy Phosphorylated ser/thr protein kinase pAKT phosphorSer473 phosphorylated glycogen synthase kinase3 beta pGSK3β phosphorSer9 Bcl2associated X protein BAX B cell lymphoma/leukemia 2 BCL2 and cleavedcysteinyl aspartatespecific proteinase3 caspase3 levels were detected by immunohistochemistry and Western blot We observed that BUN and Scr were increased in diabetic rats and Ccr was decreased Furthermore blood glucose fluctuations could exacerbate the Ccr changes Renal tissue ultrastructure was also seriously injured by glucose variability in diabetic rats In addition glucose fluctuation increased the oxidative stress of renal tissue Moreover fluctuating blood glucose decreased pAKT level and BCL2 and increased pGSK3β BAX cleavedcaspase3 levels and ratio of BAX/BCL2 in the kidneys of diabetic rats In conclusion these results suggest that blood glucose fluctuation accelerated renal injury is due at least in part to its oxidative stress promoting and inhibiting the AKT signaling pathway in diabetic ratsWe thank Xiaoyan Zhou and Linlin Li Department of Pathology Affiliated Hospital of Xuzhou Medical College for technical support and valuable assistance with histology This work was supported by a grant from the Department of Science Technology Xuzhou Jiangsu China No KC14SH094

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