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高糖饮食诱导的小鼠脂质代谢异常与肠道菌群失调有关。

High sucrose diet-induced abnormal lipid metabolism in mice is related to the dysbiosis of gut microbiota.

机构信息

Laboratory of Nutritional Biochemistry, Nagoya University, Nagoya 464-8601, Japan.

Academic Institute, College of Agriculture, Shizuoka University, Shizuoka 422-8529, Japan.

出版信息

Clin Nutr ESPEN. 2024 Oct;63:491-500. doi: 10.1016/j.clnesp.2024.06.042. Epub 2024 Jun 29.

DOI:10.1016/j.clnesp.2024.06.042
PMID:39018242
Abstract

BACKGROUND & AIMS: Excess sucrose intake induces metabolic syndrome. In human, abnormal lipids metabolism like obesity, hyperlipidemia and fatty liver are induced. However, excess sucrose causes different phenotypes in different species. Based on our previous study, excess sucrose induced fatty liver and hyperlipidemia in rats. The phenotypes and mechanism of abnormal lipid metabolism in mice is unclear. We investigated the different phenotypes in 5 strains of mice and the relationship between gut microbiome and abnormal lipid metabolism in C57BL/6N mice.

METHODS

We examined the effect of a high sucrose diet in 5 different strains of mice. Besides, to find out the relationship between gut microbiome and metabolic disorder induced by excess sucrose, C57BL/6N mice were fed with a high sucrose diet with or without antibiotics cocktail.

RESULTS

A high sucrose diet induced obesity and fatty liver in inbred mice, whereas did not induce hyperlipidemia in all strains of mice. Moreover, a high sucrose diet changed the composition of gut microbiota in C57BL/6N mice. Antibiotics treatment alleviated the abnormal lipid metabolism induced by high sucrose diet by changing the composition of gut short chain fatty acids.

CONCLUSIONS

These results indicates that the phenotypes of metabolic syndrome are influenced by genetic factors. Furthermore, the dysbiosis of gut microbiome caused by excess sucrose may contribute to the development of abnormal lipid metabolism via its metabolites.

摘要

背景与目的

过量蔗糖摄入会导致代谢综合征。在人体中,会引起肥胖、高血脂和脂肪肝等异常脂质代谢。然而,过量蔗糖会在不同物种中引起不同的表型。基于我们之前的研究,过量蔗糖会在大鼠中引起脂肪肝和高血脂。在小鼠中,异常脂质代谢的表型和机制尚不清楚。我们研究了 5 种不同品系小鼠的不同表型,以及 C57BL/6N 小鼠肠道微生物组与异常脂质代谢之间的关系。

方法

我们检测了高蔗糖饮食对 5 种不同品系小鼠的影响。此外,为了探究肠道微生物组与过量蔗糖诱导的代谢紊乱之间的关系,我们用高蔗糖饮食喂养 C57BL/6N 小鼠,同时给予或不给予抗生素鸡尾酒。

结果

高蔗糖饮食会导致近交系小鼠肥胖和脂肪肝,但不会引起所有品系小鼠的高血脂。此外,高蔗糖饮食改变了 C57BL/6N 小鼠的肠道微生物群组成。抗生素处理通过改变肠道短链脂肪酸的组成,缓解了高蔗糖饮食引起的异常脂质代谢。

结论

这些结果表明,代谢综合征的表型受遗传因素的影响。此外,过量蔗糖引起的肠道微生物组失调可能通过其代谢产物导致异常脂质代谢的发生。

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