Evidence map›Paper›PMID 26860515›Full record

ArticleEndocrine2016

Blood glucose fluctuation accelerates renal injury involved to inhibit the AKT signaling pathway in diabetic rats.

Changjiang Ying, Xiaoyan Zhou, Zhenzhen Chang, Hongwei Ling, Xingbo Cheng, Wei Li

Abstract read
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In one paragraph

Article in Endocrine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.2field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 45 citations in OpenAlex.

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  17. Angiopoietin-1: an early biomarker of diabetic nephropathy?Journal of translational medicine · 2021
    Article
  18. Glucose Variability: How Does It Work?International journal of molecular sciences · 2021
    Review
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  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Changjiang YingDepartment of Endocrinology, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, Jiangsu, People's Republic of China.
Xiaoyan ZhouLaboratory of Morphology, Xuzhou Medical College, Xuzhou, 221004, Jiangsu, People's Republic of China.
Zhenzhen ChangDepartment of Endocrinology, Affiliated Hospital of Xuzhou Medical College, Xuzhou, 221002, Jiangsu, People's Republic of China.
Hongwei LingDepartment of Endocrinology, Affiliated Hospital of Xuzhou Medical College, Xuzhou, 221002, Jiangsu, People's Republic of China.
Xingbo ChengDepartment of Endocrinology, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, Jiangsu, People's Republic of China. chengxingbo1107@163.com.
Wei LiDepartment of Endocrinology, Affiliated Hospital of Xuzhou Medical College, Xuzhou, 221002, Jiangsu, People's Republic of China. liwei0190@163.com.
Xuzhou Medical College · CNFirst Affiliated Hospital of Soochow University · CNAffiliated Hospital of Xuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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, high-fat diet, and a single dose of STZ (35 mg/kg)-injected 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. T-SOD 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 (p-AKT) (phosphor-Ser473), phosphorylated glycogen synthase kinase-3 beta (p-GSK-3β) (phosphor-Ser9), Bcl-2-associated X protein (BAX), B cell lymphoma/leukemia 2 (BCL-2), and cleaved-cysteinyl aspartate-specific proteinase-3 (caspase-3) 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 p-AKT level and BCL-2, and increased p-GSK-3β, BAX, cleaved-caspase-3 levels, and ratio of BAX/BCL-2 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 rats.

Indexed as

AnimalsBlood GlucoseDiabetes Mellitus, ExperimentalDiabetic NephropathiesDiet, High-FatKidneyKidney Function TestsMalePhosphorylationProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleySignal TransductionBlood GlucoseProto-Oncogene Proteins c-aktBlood glucose fluctuationCleaved-caspase-3Diabetic nephropathyp-AKT

Identifiers

PMID26860515
OpenAlexW2272834153

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.