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Lactobacillus casei Zhang stimulates lipid metabolism in hypercholesterolemic rats by affecting gene expression in the liver

干酪乳杆菌 脂质代谢 分解代谢 生物化学 益生菌 新陈代谢 脂肪酸 乳酸菌 脂肪酸代谢 发酵乳杆菌 生物 化学 乳酸 细菌 植物乳杆菌 遗传学 发酵
作者
Zhi Zhong,Wenyi Zhang,Ruiting Du,He Meng,Heping Zhang
出处
期刊:European Journal of Lipid Science and Technology [Wiley]
卷期号:114 (3): 244-252 被引量:39
标识
DOI:10.1002/ejlt.201100118
摘要

Abstract In this study, we show that administration of Lactobacillus casei Zhang evokes a significant reduction in the levels of cholesterol, triglycerides (TGs), and low‐density lipoprotein cholesterol (LDL‐C) from the serum and liver of hypercholesterolemic rats. After administration of L. casei Zhang, there was 31.5 and 30.8% reduction in the levels of serum TG and LDL‐C. DNA microarray results revealed that 755 genes, mainly involved in biological regulation, and cellular and metabolic processes, were differentially expressed in the liver from rats treated with probiotic bacteria, wherein, 324 genes were up‐regulated and 431 were down‐regulated, respectively. In the up‐regulated group, we characterized genes including Acsl1, Hadh, Acaa2, Acads, and gcdH, which are involved in β‐oxidation of fatty acids and encodes enzymes catalyzing critical steps for CoA synthesis and dehydrogenation. It is possible that Lactobacillus could accelerate the fatty acid catabolism by enhancing β‐oxidation step, thus reducing the level of free fatty acid and TG in the serum and liver. Subsequently, it may trigger lipid homeostasis that converts TGs, which are the main storage form of fatty acids, into free fatty acids, and lower TG concentrations both in the serum and liver. Practical applications: Lactobacillus casei Zhang has the ability to reduce cholesterol level in the blood by stimulating gene expression related to lipid metabolism, particularly through β‐oxidation of fatty acids in liver, thereby, making it an effective candidate probiotic to treat hypercholesterolemia. The findings of this study should provide very useful information in understanding the molecular mechanism of the hypocholesterolemic effect of the strain in an animal model.
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