| Literature DB >> 25968574 |
Minglong Shao1, Lechu Yu2, Fangfang Zhang1, Xuemian Lu1, Xiaokun Li3, Peng Cheng1, Xiufei Lin1, Luqing He1, Shunzi Jin4, Yi Tan5, Hong Yang2, Chi Zhang6, Lu Cai5.
Abstract
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.Entities:
Keywords: fibroblast growth factor-21; inflammation; insulin resistance; low-dose radiation; oxidative stress
Mesh:
Substances:
Year: 2015 PMID: 25968574 PMCID: PMC4490332 DOI: 10.1152/ajpendo.00026.2015
Source DB: PubMed Journal: Am J Physiol Endocrinol Metab ISSN: 0193-1849 Impact factor: 4.310