探討Lactobacillus paracasei LM-141對於高脂食物誘導之肥胖鼠代謝功能異常改善之影響

現今全球飲食習慣逐漸改變,尤其高油脂飲食的攝取,許多研究已經指出過多的能量攝取會造成肥胖發展且可能進一步導致代謝性異常,然而益生菌的補充能夠藉由改變腸道菌叢組成達到改善代謝性異常的作用。因此,在本研究中探討新分離的益生菌 Lactobacillusparacasei LM-141 (LPLM-141) 對於高脂飼料餵食誘導的肥胖鼠代謝性異常的影響,以及相關的作用分子機轉。本研究使用動物模式進行實驗,28 隻雄性 Sprague- Dawley (SD) 大鼠分為四組,其中三組餵食高脂飼料且有兩組額外補充低和高劑量的 Lactobacillus paracaseiLM-141。從本次實驗結果當中,觀察到藉由餵食 LPLM-141 可以降低高脂飼料誘導之肥胖鼠體重、脂肪組織重量增加及腹部脂肪堆積。血清中葡萄糖、胰島素、脂聯素(Adiponectin) 及瘦體素(Leptin) 的表現也能夠藉由攝取 LPLM-141 改善高脂飼料所導致的異常狀態。此外,也可以發現到餵食 LPLM-141 具有達到降低肝功能損傷指標(天門冬胺酸轉胺酶及丙胺酸轉胺酶) 和血脂濃度(總膽固醇、三酸甘油脂、低密度脂蛋白/高密度脂蛋白比值)的效果。除此之外,從即時定量聚合酶連鎖反應 (Real time-qPCR) 的結果中可以看出高脂飼料會導致大鼠肝臟內脂肪合成(長鏈脂肪酸合成酶 6、脂肪酸合成酶、固醇調節元素結合蛋白-1c)及脂肪組織內促發炎(腫瘤壞死因子-、介白素-6、介白素-1)相關基因表現量上升,而脂肪組織內抗發炎(過氧化物酶體增殖物活化受體γ)相關基因表現量下降,並且能夠藉由攝取LPLM-141 達到改善的效果。藉由肝臟的 Hematoxylin and Eosin (H&E) 和 Oil red O 染色及脂肪組織 F4/80 染色可以觀察到LPLM-141的補充對於高脂飼料導致的脂肪肝形成及脂肪組織發炎的影響。高脂飼料誘導大鼠體內脂肪肝的形成對於肝臟內胰島素訊息傳遞相關蛋白質表現的影響,包含了胰島素接受器受質(IRS-1)及磷酸化蛋白激酶 B/蛋白激酶 B (p-Akt/Akt) 的表現皆有降低的現象,然而,藉由餵食 LPLM-141 能夠提升且改善 IRS1 及 p-Akt/Akt 的表現量。本篇研究結果顯示出攝取 LPLM-141 乳酸菌可以藉由減緩脂肪組織發炎反應達到改善胰島素抗性及脂肪肝的效果,藉此改善肥胖及減少其所引發之慢性代謝性症候群發生之機率。

關鍵字

益生菌；高脂食物；肥胖；代謝性異常

並列摘要

Due to the changes of eating habits, popularity of fast food culture, and uptake of high-fat diet, several studies have revealed that excess energy intake resulted in the development of obesity, and may further lead to chronic metabolic disorders. However, administration of probiotics could improve the metabolic disorders by modulation of gut microbiota. Therefore, in this study, the effects of the novel probiotics Lactobacillus paracasei LM-141 (LPLM-141) on the metabolic disorders of high-fat diet induced obese rats and relevant mechanism involved were investigated. Twenty-eight male Sprague-Dawley (SD) rats were divided into 4 groups and fed with high-fat diet with or without LPLM-141 probiotics. Our results demonstrated that oral administration of LPLM-141 significantly reduced the increased body and adipose tissue weight, as well as accumulation of abdominal fat in high-fat diet induced obese rats. The increased expressions of serum glucose, insulin, leptin, and decreased serum adiponectin level in high-fat diet induced obese rats were reversed by LPLM-141 administration. In addition, LPLM-141 administration reduced liver function damage index (Aspartate aminotransferase, AST and Alanine aminotransferase, ALT) and serum lipid profile (total cholesterol, triglyceride, and Low-density lipoprotein/High-density lipoprotein ratio (LDL/HDL)) enhanced in high-fat diet induced obese rats. Moreover, administration of LPLM-141 reduced the expression of hepatic lipogenesis-related genes (Elongation of very long chain fatty acids protein (Elovl) 6, Fatty acid synthase (FAS) and Sterol regulatory element-binding protein (Srebp)-1c) increased in high-fat diet induced obese rats. In addition, the upregulation of pro-inflammatory cytokine genes including tumor necrosis factor (TNF)-, interlukin (IL)-6 and interlukin (IL)-1 in adipose tissue of high-fat diet induced obese rats were downregulated by LPLM-141 administration. On the other hand, the decreased Peroxisome proliferator-activated receptor gamma (PPAR)-γ gene in adipose tissue of high-fat diet induced obese rats was increased by administration of LPLM-141. The results from H&E staining, Oil red O staining in liver, and F4/80 staining in adipose tissue showed that the liver steatosis and inflammation in the adipose tissue were alleviated by LPLM-141 treatment. Finally, the reduced insulin receptor substract 1 (IRS-1) and phosphorylated Protein kinase B/ Protein kinase B (p-Akt/Akt) expressions in liver of high-fat diet induced obese rats were enhanced by LPLM-141 administration. Our present results suggested that administration of LPLM-141 improved insulin resistance and hepatic steatosis by reducing the inflammation in the adipose tissue, thereby ameliorating obesity and its related chronic metabolic complications.

並列關鍵字

Lactobacillus ； High-fat diet ； Obesity ； Metabolic syndrome

參考文獻

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探討Lactobacillus paracasei LM-141對於高脂食物誘導之肥胖鼠代謝功能異常改善之影響

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