Arellano-García Laura Isabel, Milton-Laskibar Iñaki, Martínez J Alfredo, Arán-González Miguel, Portillo María P
Nutrition and Obesity Group, Department of Pharmacy and Food Sciences, Faculty of Pharmacy and Lucio Lascaray Research Centre, University of the Basque Country (UPV/EHU), Vitoria-Gasteiz, Spain.
CIBERobn Physiopathology of Obesity and Nutrition, Institute of Health Carlos III, Madrid, Spain.
Biofactors. 2025 Jan-Feb;51(1):e2116. doi: 10.1002/biof.2116. Epub 2024 Aug 12.
Nonalcoholic fatty liver disease (NAFLD) is one of the most prevalent chronic liver alterations worldwide, being gut microbiota dysbiosis one of the contributing factors to its development. The aim of this research is to compare the potential effects of a viable probiotic (Lactobacillus rhamnosus GG) with those exerted by its heat-inactivated paraprobiotic counterpart in a dietary rodent model of NAFLD. The probiotic administration effectively prevented the hepatic lipid accumulation induced by a high-fat high-fructose diet feeding, as demonstrated by chemical (lower TG content) and histological (lower steatosis grade and lobular inflammation) analyses. This effect was mainly mediated by the downregulation of lipid uptake (FATP2 protein expression) and upregulating liver TG release to bloodstream (MTTP activity) in rats receiving the probiotic. By contrast, the effect of the paraprobiotic preventing diet-induced liver lipid accumulation was milder, and mainly derived from the downregulation of hepatic de novo lipogenesis (SREBP-1c protein expression and FAS activity) and TG assembly (DGAT2 and AQP9 protein expression). The obtained results demonstrate that under these experimental conditions, the effects induced by the administration of viable L. rhamnosus GG preventing liver lipid accumulation in rats fed a diet rich in saturated fat and fructose differ from those induced by its heat-inactivated paraprobiotic counterpart.
非酒精性脂肪性肝病（NAFLD）是全球最普遍的慢性肝脏病变之一，肠道微生物群失调是其发病的促成因素之一。本研究的目的是在非酒精性脂肪性肝病的饮食啮齿动物模型中，比较一种活益生菌（鼠李糖乳杆菌GG）与其热灭活的副益生菌对应物所产生的潜在影响。化学分析（较低的甘油三酯含量）和组织学分析（较低的脂肪变性分级和小叶炎症）表明，给予益生菌可有效预防高脂高果糖饮食诱导的肝脏脂质积累。在接受益生菌的大鼠中，这种作用主要是通过下调脂质摄取（FATP2蛋白表达）和上调肝脏甘油三酯向血液中的释放（MTTP活性）来介导的。相比之下，副益生菌预防饮食诱导的肝脏脂质积累的作用较轻微，主要源于肝脏从头脂肪生成（SREBP-1c蛋白表达和FAS活性）和甘油三酯组装（DGAT2和AQP9蛋白表达）的下调。所得结果表明，在这些实验条件下，给予活的鼠李糖乳杆菌GG预防喂食富含饱和脂肪和果糖饮食的大鼠肝脏脂质积累所产生的作用，与其热灭活的副益生菌对应物所产生的作用不同。
