科研成果详情

题名Additive protection by LDR and FGF21 treatment against diabetic nephropathy in type 2 diabetes model
作者
发表日期2015-07-01
发表期刊AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM   影响因子和分区
语种英语
原始文献类型Article
关键词low-dose radiation fibroblast growth factor-21 insulin resistance inflammation oxidative stress
其他关键词LOW-DOSE-RADIATION ; ATOMIC-BOMB SURVIVORS ; GROWTH-FACTOR 21 ; MALE GERM-CELLS ; GAMMA-IRRADIATION ; INSULIN-RESISTANCE ; ADAPTIVE RESPONSE ; RENAL INJURY ; MICE ; HORMESIS
摘要The onset of diabetic nephropathy (DN) is associated with both systemic and renal changes. Fibroblast growth factor (FGF)-21 prevents diabetic complications mainly by improving systemic metabolism. In addition, low-dose radiation (LDR) protects mice from DN directly by preventing renal oxidative stress and inflammation. In the present study, we tried to define whether the combination of FGF21 and LDR could further prevent DN by blocking its systemic and renal pathogeneses. To this end, type 2 diabetes was induced by feeding a high-fat diet for 12 wk followed by a single dose injection of streptozotocin. Diabetic mice were exposed to 50 mGy LDR every other day for 4 wk with and without 1.5 mg/kg FGF21 daily for 8 wk. The changes in systemic parameters, including blood glucose levels, lipid profiles, and insulin resistance, as well as renal pathology, were examined. Diabetic mice exhibited renal dysfunction and pathological abnormalities, all of which were prevented significantly by LDR and/or FGF21; the best effects were observed in the group that received the combination treatment. Our studies revealed that the additive renal protection conferred by the combined treatment against diabetes-induced renal fibrosis, inflammation, and oxidative damage was associated with the systemic improvement of hyperglycemia, hyperlipidemia, and insulin resistance. These results suggest that the combination treatment with LDR and FGF21 prevented DN more efficiently than did either treatment alone. The mechanism behind these protective effects could be attributed to the suppression of both systemic and renal pathways.
资助项目National Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [81000294, 81370917, 81471045]; Research Development Fund of Wenzhou Medical University [QTJ13005]; National Institutes of HealthUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USA [1R01 DK091338-01A1]; Natural Science Foundation of Zhejiang ProvinceNatural Science Foundation of Zhejiang Province [Y14H070033]; NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASESUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK) [R01DK091338] Funding Source: NIH RePORTER
出版者AMER PHYSIOLOGICAL SOC
出版地BETHESDA
ISSN0193-1849
EISSN1522-1555
卷号309期号:1页码:E45-E54
DOI10.1152/ajpendo.00026.2015
页数10
WOS类目Endocrinology & Metabolism ; Physiology
WOS研究方向Endocrinology & Metabolism ; Physiology
WOS记录号WOS:000357514300005
收录类别SCIE ; PUBMED ; SCOPUS
URL查看原文
PubMed ID25968574
PMC记录号PMC4490332
SCOPUSEID2-s2.0-84935507294
通讯作者地址[Zhang, Chi]Chinese-American Research Institute for Diabetic Complications,Wenzhou Medical University,Chashan Univ. Town,Wenzhou,325035,China
Scopus学科分类Medicine (all)
引用统计
被引频次:19[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符https://kms.wmu.edu.cn/handle/3ETUA0LF/6609
专题温州医科大学
通讯作者Zhang, Chi
作者单位
1.Chinese-American Research Institute for Diabetic Complications,Wenzhou Medical University,Wenzhou,China;
2.Ruian Center of Chinese-American Research Institute for Diabetic Complications,Wenzhou Medical University,Wenzhou,China;
3.Key Laboratory of Radiobiology (Ministry of Health),School of Public Health of Jilin University,Changchun,China;
4.Kosair Children’s Hospital Research Institute,Department of Pediatrics,University of Louisville School of Medicine,Louisville,United States
第一作者单位温州医科大学;  
通讯作者单位温州医科大学
第一作者的第一单位温州医科大学
推荐引用方式
GB/T 7714
Shao, Minglong,Yu, Lechu,Zhang, Fangfang,et al. Additive protection by LDR and FGF21 treatment against diabetic nephropathy in type 2 diabetes model[J]. AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM,2015,309(1):E45-E54.
APA Shao, Minglong., Yu, Lechu., Zhang, Fangfang., Lu, Xuemian., Li, Xiaokun., ... & Cai, Lu. (2015). Additive protection by LDR and FGF21 treatment against diabetic nephropathy in type 2 diabetes model. AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 309(1), E45-E54.
MLA Shao, Minglong,et al."Additive protection by LDR and FGF21 treatment against diabetic nephropathy in type 2 diabetes model".AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM 309.1(2015):E45-E54.

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