Alemasi Akehu, Gu Lijiang, Zhou Yilun
Department of Nephrology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
Department of Urology, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Ren Fail. 2024 Dec;46(1):2328320. doi: 10.1080/0886022X.2024.2328320. Epub 2024 Mar 12.
Obesity can induce dysbiosis in the gut microbiota and is considered a separate risk factor for kidney function decline. Nonetheless, the precise function of intestinal microorganisms in facilitating the connection between obesity and kidney function decline remains uncertain. Hence, the objective of this study was to investigate the alterations in the gut microbiota composition that take place during obesity and their correlations with renal function utilizing a rat model.
For 20 weeks, 25 Sprague-Dawley rats were fed either a high-fat diet (HFD) or a normal-fat normal diet (ND). Physiological indices, peripheral plasma, kidney tissue, and colon contents were collected for comparison between groups. Metagenomic analysis of intestinal flora was performed.
The HFD group demonstrated significantly increased levels of creatinine and urea nitrogen in the peripheral blood. Additionally, the HFD rats exhibited a significantly larger glomerular diameter compared to the ND group, accompanied by the presence of glomerulosclerosis, tubular vacuolar transformation, and other pathological changes in certain glomeruli. Metagenomics analysis revealed a notable rise in the prevalence of the Firmicutes phylum within the HFD group, primarily comprising the genus. Functional analysis indicated that the gut microbiota in the HFD group primarily correlated with infectious diseases, signal transduction, and signaling molecules and interactions.
This study provides evidence that the consumption of a HFD induces modifications in the composition and functionality of the gut microbiome in rats, which may serve as a potential mechanism underlying the relationship between obesity and the progression of kidney function decline.
肥胖可导致肠道微生物群失调,被认为是肾功能下降的一个独立危险因素。然而,肠道微生物在促进肥胖与肾功能下降之间联系的确切作用仍不确定。因此,本研究的目的是利用大鼠模型研究肥胖过程中肠道微生物群组成的变化及其与肾功能的相关性。
25只Sprague-Dawley大鼠分别喂食高脂饮食(HFD)或正常脂肪正常饮食(ND)20周。收集生理指标、外周血浆、肾组织和结肠内容物进行组间比较。对肠道菌群进行宏基因组分析。
HFD组外周血肌酐和尿素氮水平显著升高。此外,与ND组相比,HFD大鼠的肾小球直径显著增大,部分肾小球出现肾小球硬化、肾小管空泡变性等病理变化。宏基因组分析显示,HFD组厚壁菌门的患病率显著上升,主要包括属。功能分析表明,HFD组的肠道微生物群主要与传染病、信号转导以及信号分子和相互作用相关。
本研究提供了证据,表明食用高脂饮食会导致大鼠肠道微生物群的组成和功能发生改变,这可能是肥胖与肾功能下降进展之间关系的潜在机制。