Probiotics as Renal Guardians: Modulating Gut Microbiota to Combat Diabetes-Induced Kidney Damage.

IF 3.5 3区 生物学 Q1 BIOLOGY Biology-Basel Pub Date : 2025-01-24 DOI:10.3390/biology14020122
Saleh Bakheet Al-Ghamdi
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Abstract

Gut microbiota plays a pivotal role in various health challenges, particularly in mitigating diabetes-induced renal damage. Numerous studies have highlighted that modifying gut microbiota is a promising therapeutic strategy for preserving kidney function and mitigating diabetes-related complications. This study aimed to evaluate the protective effects of Lactobacillus acidophilus ATCC 4356 supplementations on kidney health in a rat model of diabetes-induced renal damage. Four groups were studied: control, probiotic supplementation, diabetic, and diabetic with probiotic supplementation. Diabetes was induced using a single streptozotocin (STZ) injection after a 12 h fast, and probiotic supplementation (1 × 10⁹ CFU/kg daily) was administered two weeks prior to diabetes induction and continued throughout the experimental period. Weekly assessments included fasting blood glucose, insulin, glycation markers, and kidney function tests. Glucose metabolism and insulin sensitivity were analyzed through oral glucose tolerance test (OGTT) and insulin sensitivity test (IST). The microbiome was analyzed using 16S rRNA gene sequencing to evaluate changes in diversity and composition. Probiotic supplementation significantly enhanced microbial diversity and composition. Alpha diversity indices such as Shannon and Chao1 demonstrated higher values in the probiotic-treated diabetic group compared to untreated diabetic rats. The Firmicutes/Bacteroidetes ratio, a key indicator of gut health, was also restored in the probiotic-treated diabetic group. Results: Probiotic supplementation significantly improved glycemic control, reduced fasting blood glucose levels, and enhanced insulin sensitivity in diabetic rats. Antioxidant enzyme levels, depleted in untreated diabetic rats, were restored, reflecting reduced oxidative stress. Histological analysis showed better kidney structure, reduced inflammation, and decreased fibrosis. Furthermore, the Comet assay results confirmed a reduction in DNA damage in probiotic-treated diabetic rats. Conclusion: Lactobacillus acidophilus ATCC 4356 supplementation demonstrated significant protective effects against diabetes-induced renal damage by restoring gut microbiota diversity, improving glycemic control, and reducing oxidative stress. These findings highlight the potential of targeting the gut microbiota and its systemic effects on kidney health as a therapeutic approach for managing diabetes-related complications. Further research is needed to optimize probiotic treatments and assess their long-term benefits in diabetes management and kidney health.

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益生菌作为肾脏守护者:调节肠道微生物群对抗糖尿病引起的肾脏损害。
肠道微生物群在各种健康挑战中起着关键作用,特别是在减轻糖尿病引起的肾损害方面。许多研究强调,改变肠道微生物群是一种很有前途的治疗策略,可以保护肾功能和减轻糖尿病相关并发症。本研究旨在评价补充嗜酸乳杆菌ATCC 4356对糖尿病肾损伤模型大鼠肾脏健康的保护作用。研究分为四组:对照组、补充益生菌组、糖尿病组和补充益生菌的糖尿病组。禁食12 h后,采用单次链脲佐菌素(STZ)诱导糖尿病,并在诱导糖尿病前2周补充益生菌(1 × 10⁹CFU/kg / d),并持续到整个实验期间。每周评估包括空腹血糖、胰岛素、糖化标志物和肾功能检查。通过口服糖耐量试验(OGTT)和胰岛素敏感性试验(IST)分析糖代谢和胰岛素敏感性。利用16S rRNA基因测序分析微生物组的多样性和组成变化。补充益生菌可显著提高微生物的多样性和组成。α多样性指数如Shannon和Chao1在益生菌治疗的糖尿病大鼠中显示高于未治疗的糖尿病大鼠。在益生菌治疗的糖尿病组中,厚壁菌门/拟杆菌门比率(肠道健康的关键指标)也有所恢复。结果:补充益生菌可显著改善糖尿病大鼠的血糖控制,降低空腹血糖水平,增强胰岛素敏感性。抗氧化酶水平,在未治疗的糖尿病大鼠,恢复,反映减少氧化应激。组织学分析显示肾脏结构改善,炎症减轻,纤维化减少。此外,Comet试验结果证实了益生菌治疗的糖尿病大鼠DNA损伤的减少。结论:补充嗜酸乳杆菌ATCC 4356可恢复肠道菌群多样性,改善血糖控制,降低氧化应激,对糖尿病肾损伤具有显著的保护作用。这些发现强调了靶向肠道微生物群及其对肾脏健康的全身性影响作为治疗糖尿病相关并发症的治疗方法的潜力。需要进一步的研究来优化益生菌治疗并评估其在糖尿病管理和肾脏健康方面的长期益处。
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来源期刊
Biology-Basel
Biology-Basel Biological Science-Biological Science
CiteScore
5.70
自引率
4.80%
发文量
1618
审稿时长
11 weeks
期刊介绍: Biology (ISSN 2079-7737) is an international, peer-reviewed, quick-refereeing open access journal of Biological Science published by MDPI online. It publishes reviews, research papers and communications in all areas of biology and at the interface of related disciplines. Our aim is to encourage scientists to publish their experimental and theoretical results in as much detail as possible. There is no restriction on the length of the papers. The full experimental details must be provided so that the results can be reproduced. Electronic files regarding the full details of the experimental procedure, if unable to be published in a normal way, can be deposited as supplementary material.
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