Sharma Tanvi, Ranawat Pavitra, Garg Ayushi, Rastogi Pulkit, Kaushal Naveen
Department of Biophysics, Panjab University, Chandigarh, 160014, India.
Department of Hematology, Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh, 160012, India.
Mol Cell Biochem. 2025 May;480(5):3169-3184. doi: 10.1007/s11010-024-05185-9. Epub 2024 Dec 21.
Metabolic syndrome (MetS) is driven by a complex interplay of genetic, lifestyle, and dietary factors, leading to weight gain, insulin resistance, dyslipidemia, and chronic inflammation. Gut microbiota dysbiosis has been recently recognized as a key contributor to MetS, leading to advancements in gut microbiome-based interventions to improve health outcomes. Considering the unique challenges associated with the use of pre/probiotics, short-chain fatty acids (SCFA), also known as postbiotics, have emerged as promising therapeutic agents due to their role in modulating host metabolism and physiology. Considering this, the aim of the current study was to explore the therapeutic potential of SCFA (butyrate, propionate, and acetate) supplementation against a high-fat diet (HFD)-induced experimental model of MetS in male Wistar rats. Alterations in body weight, lipid profile, histopathology, and adipose tissue accumulation were assessed to establish SCFA-mediated amelioration of experimental MetS. Further, the enzymatic (GPx, Catalase, GR, and GST) and non-enzymatic (LPO, total ROS, and Redox ratio were evaluated. The results indicated that SCFA supplementation could effectively mitigate key features of MetS. A significant reduction in body weight gain and fasting blood glucose levels, along with markedly lowered triglycerides, total cholesterol, and LDL levels, with partial restoration of HDL levels was observed following SCFA supplementation. SCFA administration also attenuated MetS-associated hepatic damage as studied by histopathological investigation and analysis of liver function marker enzyme activities. Such ameliorative effects of SCFA against HFD-induced MetS were owed to potential redox modulation studied using enzymatic and non-enzymatic oxidative stress markers. In conclusion, the study's outcomes show that SCFA supplementation could potentially be used against managing MetS. It underscores the therapeutic potential of SCFA by placing them as a novel gut microbiome-based dietary approach to improve metabolic health and reduce the risk of MetS-associated complications. However, more detailed mechanistic explorations are warranted in the future, leading to their beneficial role in MetS contributing to holistic health outcomes.
代谢综合征（MetS）是由遗传、生活方式和饮食因素的复杂相互作用驱动的，会导致体重增加、胰岛素抵抗、血脂异常和慢性炎症。肠道微生物群失调最近被认为是代谢综合征的一个关键因素，这促使基于肠道微生物群的干预措施取得进展，以改善健康状况。考虑到使用益生元/益生菌存在的独特挑战，短链脂肪酸（SCFA），也被称为后生元，因其在调节宿主代谢和生理方面的作用，已成为有前景的治疗剂。考虑到这一点，本研究的目的是探讨补充SCFA（丁酸、丙酸和乙酸）对雄性Wistar大鼠高脂饮食（HFD）诱导的代谢综合征实验模型的治疗潜力。评估体重、血脂谱、组织病理学和脂肪组织积累的变化，以确定SCFA介导的实验性代谢综合征的改善情况。此外，还评估了酶促指标（谷胱甘肽过氧化物酶、过氧化氢酶、谷胱甘肽还原酶和谷胱甘肽S-转移酶）和非酶促指标（脂质过氧化、总活性氧和氧化还原比）。结果表明，补充SCFA可以有效减轻代谢综合征的关键特征。补充SCFA后，体重增加和空腹血糖水平显著降低，甘油三酯、总胆固醇和低密度脂蛋白水平明显降低，高密度脂蛋白水平部分恢复。通过组织病理学研究和肝功能标记酶活性分析发现，SCFA给药还减轻了与代谢综合征相关的肝损伤。SCFA对HFD诱导的代谢综合征的这种改善作用归因于使用酶促和非酶促氧化应激标记物研究的潜在氧化还原调节。总之，该研究结果表明，补充SCFA可能有助于管理代谢综合征。它强调了SCFA的治疗潜力，将其作为一种基于肠道微生物群的新型饮食方法，以改善代谢健康并降低代谢综合征相关并发症的风险。然而，未来需要进行更详细的机制探索，以明确它们在代谢综合征中对整体健康结果的有益作用。
