Medium-chain triglycerides reduce glomerulosclerosis and induce expression of redox genes in NSY mice with diabetic nephropathy

IF 2.4 Q3 NUTRITION & DIETETICS PharmaNutrition Pub Date : 2023-03-01 DOI:10.1016/j.phanu.2022.100325
Mai Hagiwara , Shiori Ishiyama , Kazuki Mochizuki
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引用次数: 1

Abstract

Background

Nephropathy is a type of complication of type 2 diabetes, and medium chain triglycerides (MCTs) potentially improve metabolic abnormalities. This study examined whether MCT intake inhibits nephropathy development in a type 2 diabetic mouse model.

Methods

Six-week-old control non-diabetic ICR mice and type 2 diabetic Nagoya Shibata Yasuda (NSY) mice were fed a diet enriched with long-chain saturated/mono-unsaturated triglycerides, including palmitic-, stearic-, and oleic acids (C16/C18-rich group). NSY mice were fed a diet containing medium-chain triglycerides with either caprylic acid (C8-rich group) or capric acid (C10-rich group). Feeding was performed for 20 weeks. Plasma biomarker levels were measured using ELISA or enzymatic methods. Kidney pathology was evaluated using periodic acid–Schiff staining, and the expression of redox genes and proteins were determined using qRT-PCR and western blotting.

Results

The C16/C18-rich group of NSY mice exhibited expansion of the mesangial region in the kidney. Plasma cystatin C and creatinine concentrations were not different between ICR mice and C16/C18-rich group of NSY mice and between C16/C18-rich and C8- or C10-rich groups of NSY mice. The C8- and C10-rich groups had suppressed mesangial region than the C16/C18-rich groups. The mRNA expression of Sod1, Prdx1, and Gpx2, and SOD1 protein levels were higher in the C8- and/or C10-rich groups than in the C16/C18-rich group of NSY mice.

Conclusions

MCT intake in NSY mice at the stage without increased markers indicating glomerular filtration decrease, reduces glomerulosclerosis, with induction of redox gene expression, in the kidney.

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中链甘油三酯减少糖尿病肾病NSY小鼠肾小球硬化并诱导氧化还原基因表达
背景肾病是2型糖尿病的一种并发症,中链甘油三酯(MCTs)可能会改善代谢异常。本研究在2型糖尿病小鼠模型中检测MCT摄入是否抑制肾病的发展。方法6周龄对照非糖尿病ICR小鼠和2型糖尿病名古屋-柴田-安田(NSY)小鼠喂食富含长链饱和/单不饱和甘油三酯的饮食,包括棕榈酸、硬脂酸和油酸(富含C16/C18的组)。NSY小鼠喂食含有中链甘油三酯和辛酸(富含C8组)或癸酸(富含C10组)的饮食。喂食20周。使用ELISA或酶法测量血浆生物标志物水平。使用碘酸-希夫染色评估肾脏病理学,并使用qRT-PCR和蛋白质印迹测定氧化还原基因和蛋白质的表达。结果富含C16/C18的NSY小鼠肾系膜区扩张。ICR小鼠和富含C16/C18的NSY小鼠组之间以及富含C16/C8和富含C8或C10的NSY小鼠组之间的血浆胱抑素C和肌酸酐浓度没有差异。富含C8和C10的组比富含C16/C18的组具有抑制系膜区的作用。富含C8和/或C10的NSY小鼠组的Sod1、Prdx1、Gpx2和Sod1蛋白水平的mRNA表达高于富含C16/C18的NSY小鼠组。结论在NSY小鼠未增加肾小球滤过标志物的阶段摄入sMCT,可减少肾小球硬化,并诱导肾脏氧化还原基因表达。
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来源期刊
PharmaNutrition
PharmaNutrition Agricultural and Biological Sciences-Food Science
CiteScore
5.70
自引率
3.10%
发文量
33
审稿时长
12 days
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