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新型益生菌菌株在高脂肪饮食诱导肥胖的小鼠模型中的抗肥胖作用。

Antiobesity Effect of Novel Probiotic Strains in a Mouse Model of High-Fat Diet-Induced Obesity.

机构信息

College of Life Sciences and Biotechnology, Korea University, Seoul, 02841, Republic of Korea.

Institute of Life Science and Natural Resources, Korea University, Seoul, 02841, Republic of Korea.

出版信息

Probiotics Antimicrob Proteins. 2021 Aug;13(4):1054-1067. doi: 10.1007/s12602-021-09752-0. Epub 2021 Feb 10.

DOI:10.1007/s12602-021-09752-0
PMID:33569747
Abstract

Obesity is one of the major causes of the development of metabolic diseases, particularly cardiovascular diseases and type-2 diabetes mellitus. Increased lipid accumulation and abnormal adipocyte growth, which is an increase in cell numbers and differentiation, have been documented as major pathological characteristics of obesity. Thus, the inhibition of adipogenic differentiation prevents and suppresses obesity. Recently, specific probiotic strains have been known to regulate lipid metabolism in vitro and/or in vivo. Previously, we demonstrated that Lactobacillus johnsonni 3121 and Lactobacillus rhamnosus 86 could act as novel probiotic strains and reduce cholesterol levels. Moreover, both strains significantly reduced lipid accumulation and inhibited adipocyte differentiation by downregulating the adipogenic transcription factor in 3T3-L1 adipocytes. Therefore, L. johnsonni 3121 and L. rhamnosus 86 were selected for in vivo evaluation of their anti-obesity effects using a high-fat diet-induced obese mouse model. Daily oral administration of L. johnsonni 3121 and L. rhamnosus 86 for 12 weeks significantly improved serum lipid profile and downregulated the expression of genes related to adipogenesis and lipogenesis in epididymal white adipose tissue of high-fat diet fed obese mice (p < 0.05). Fecal analysis also suggested that the two probiotic strains could normalize the altered obesity-related gut microbiota in high-fat diet-fed obese mice. These results collectively demonstrate that oral administration of L. johnsonni 3121 and L. rhamnosus 86 could prevent obesity, thereby improving metabolic health.

摘要

肥胖是代谢性疾病发展的主要原因之一,尤其是心血管疾病和 2 型糖尿病。脂质积累增加和异常脂肪细胞生长(即细胞数量和分化增加)已被证明是肥胖的主要病理特征。因此,抑制脂肪生成分化可预防和抑制肥胖。最近,特定的益生菌菌株已被证明可在体外和/或体内调节脂质代谢。此前,我们证明了 Johnson 氏乳杆菌 3121 和鼠李糖乳杆菌 86 可以作为新型益生菌菌株,降低胆固醇水平。此外,这两种菌株通过下调 3T3-L1 脂肪细胞中的脂肪生成转录因子,显著减少脂肪积累并抑制脂肪细胞分化。因此,选择 Johnson 氏乳杆菌 3121 和鼠李糖乳杆菌 86 用于高脂肪饮食诱导肥胖小鼠模型的体内抗肥胖效果评估。每天口服 Johnson 氏乳杆菌 3121 和鼠李糖乳杆菌 86 12 周,可显著改善血清脂质谱,并下调高脂肪饮食喂养肥胖小鼠附睾白色脂肪组织中与脂肪生成和脂肪生成相关的基因表达(p < 0.05)。粪便分析还表明,这两种益生菌菌株可使高脂肪饮食喂养肥胖小鼠中改变的肥胖相关肠道微生物群正常化。这些结果共同表明,口服 Johnson 氏乳杆菌 3121 和鼠李糖乳杆菌 86 可预防肥胖,从而改善代谢健康。

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