Effects of high salt intake on glucose metabolism, liver function, and the microbiome in rats: influence of ACE inhibitors and angiotensin II receptor blockers.

IF 5 2区 生物学 Q2 CELL BIOLOGY
Xiaoli Zhang, Mohamed M S Gaballa, Ahmed A Hasan, Yvonne Liu, Johann-Georg Hocher, Xin Chen, Liping Liu, Jian Li, Dominik Wigger, Christoph Reichetzeder, Saban Elitok, Burkhard Kleuser, Bernhard K Krämer, Berthold Hocher
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Abstract

High-salt diets (HSDs) are known to impact blood pressure and cardiovascular health, but their effects on glucose metabolism, liver function, and gut microbiota remain poorly understood. This study investigates how long-term HSD affects these physiological processes and evaluates the potential therapeutic effects of ACE inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs). Male Sprague-Dawley rats were fed a normal salt diet (0.3% NaCl), a moderate salt diet (2% NaCl), or a high-salt diet (8% NaCl) for 12 wk. Two subgroups in the HSD condition received telmisartan or enalapril. We assessed blood pressure, glucose homeostasis, liver inflammation, pancreatic function, and gut microbiota composition. HSD rats exhibited significantly higher blood pressure [130 ± 2 mmHg in normal diet (ND) vs. 144 ± 4 mmHg in HSD; P < 0.01], reduced fasting insulin (1.33 ± 0.14 ng/mL in ND vs. 0.60 ± 0.05 ng/mL in HSD; P < 0.01), and gut microbiota dysbiosis, with a 71% reduction in Ruminococcus species (P = 0.018). Liver inflammation, indicated by an increase in CD68+ macrophages, was also observed in the HSD group. Telmisartan treatment significantly reduced liver inflammation but did not fully restore metabolic homeostasis. HSD disrupts multiple physiological systems, including glucose metabolism and liver function, partly through gut microbiota alterations. ACEIs and ARBs provided partial protection, highlighting the need for multitargeted interventions to mitigate high-salt diet effects.NEW & NOTEWORTHY High-salt diet induces multisystem disruptions, including liver inflammation, reduced insulin levels, and gut microbiota imbalance. ACEIs and ARBs showed limited efficacy, highlighting the need for comprehensive therapeutic approaches.

高盐摄入对大鼠葡萄糖代谢、肝功能和微生物组的影响:ACE抑制剂和血管紧张素II受体阻断剂的影响
背景:高盐饮食(HSD)已知会影响血压和心血管健康,但其对葡萄糖代谢、肝功能和肠道微生物群的影响尚不清楚。本研究探讨了长期HSD如何影响这些生理过程,并评估了ACE抑制剂(ACEIs)和血管紧张素II受体阻滞剂(ARBs)的潜在治疗效果。方法:雄性Sprague-Dawley大鼠分别饲喂正常盐(0.3% NaCl)、中盐(2% NaCl)和高盐(8% NaCl) 3组,为期12周。两个HSD亚组接受替米沙坦或依那普利治疗。我们评估了血压、葡萄糖稳态、肝脏炎症、胰腺功能和肠道微生物群组成。结果:HSD大鼠血压明显升高(ND组130±2 mmHg, HSD组144±4 mmHg);p < 0.01),空腹胰岛素降低(ND组为1.33±0.14 ng/mL, HSD组为0.60±0.05 ng/mL;p < 0.01),肠道菌群失调,瘤胃球菌减少71% (p = 0.018)。HSD组还观察到肝脏炎症,表现为CD68+巨噬细胞增加。替米沙坦治疗可显著减轻肝脏炎症,但不能完全恢复代谢稳态。结论:HSD破坏多种生理系统,包括葡萄糖代谢和肝功能,部分通过肠道微生物群的改变。acei和arb提供了部分保护,强调需要多目标干预来减轻高盐饮食的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
9.10
自引率
1.80%
发文量
252
审稿时长
1 months
期刊介绍: The American Journal of Physiology-Cell Physiology is dedicated to innovative approaches to the study of cell and molecular physiology. Contributions that use cellular and molecular approaches to shed light on mechanisms of physiological control at higher levels of organization also appear regularly. Manuscripts dealing with the structure and function of cell membranes, contractile systems, cellular organelles, and membrane channels, transporters, and pumps are encouraged. Studies dealing with integrated regulation of cellular function, including mechanisms of signal transduction, development, gene expression, cell-to-cell interactions, and the cell physiology of pathophysiological states, are also eagerly sought. Interdisciplinary studies that apply the approaches of biochemistry, biophysics, molecular biology, morphology, and immunology to the determination of new principles in cell physiology are especially welcome.
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