Endogenous synthesis of n-3 polyunsaturated fatty acids in fat-1 transgenic mice ameliorates streptozocin-induced diabetic nephropathy. (June 2018)

• Record Type: Journal Article
• Authors: Zhang, Yuan-Ming; Zhang, Xiao-Hong; Zhu, Pan; Tan, Rong-Hui; Zhao, Jin-Shun; Wang, Feng; Zhang, Jin-Jie; Yan, Wang; Xi, Yang; Wan, Jian-Bo; Kang, Jing-Xuan; Zou, Zu-Quan; Bu, Shi-Zhong
• Is Part Of: Journal of functional foods. Volume 45(2018)
• Page Start: 427
• Page End: 434
• Publication Date: 2018-06
• Subjects: Fat-1 -- n-3 PUFAs -- NLRP3 inflammasome -- Lipid mediators -- E-cadherin -- Diabetic nephropathy; Functional foods -- Analysis -- Periodicals; Food -- Biotechnology -- Periodicals; Nutrition -- Periodicals; 613.2
• DOI: 10.1016/j.jff.2018.04.010
• Languages: English
• ISSNs: 1756-4646

Abstract

Graphical abstract: Highlights: Streptozocin-induced hyperglycemia led to renal dysfunctions and renal injury, which were attenuated by endogenous n-3 PUFAs in fat-1 transgenic mice. The renoprotective effects of endogenous n-3 PUFAs against DN were linked with the production of n-3 lipid mediators, increased expression of E-cadherin and NLRP3 inflammasome inhibition in renal tissues. Abstract: Although n-3 polyunsaturated fatty acids (PUFAs) exhibit biological activity in many inflammatory diseases, their renoprotective effects against diabetic nephropathy (DN) have been controversial. Here, fat-1 transgenic mice were used to investigate the effects of n-3 PUFAs on streptozocin (STZ)-induced DN. Fat-1 mice exhibited increased renal n-3 PUFAs and n-3 PUFA-derived lipid mediators, compared to wild type (WT) mice. Endogenous n-3 PUFAs protected STZ-treated fat-1 mice against hyperglycemia-induced renal dysfunction, as reflected by significant decreases in kidney/body weight ratio, urinary protein, blood urea nitrogen levels and creatinine clearance. In addition, endogenous n-3 PUFAs significantly ameliorated hyperglycemia-induced renal damage by modulating E-cadhein expression. It was also found that DN-induced NLRP3 inflammasome activation was attenuated by endogenous n-3 PUFAs in STZ-treated fat-1 mice. Our findings suggest that endogenous n-3 PUFAs ameliorate DN potentially through the: (i) formation of n-3 lipid mediators, (ii) induction of E-cadherin expression and (iii) inhibition of NLRP3 inflammasome.