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肠道甲烷短杆菌史密斯氏菌而非总细菌与大鼠饮食诱导的体重增加有关。

Intestinal Methanobrevibacter smithii but not total bacteria is related to diet-induced weight gain in rats.

机构信息

Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.

出版信息

Obesity (Silver Spring). 2013 Apr;21(4):748-54. doi: 10.1002/oby.20277.

Abstract

UNLABELLED

It is increasingly understood that gastrointestinal (GI) methanogens, including Methanobrevibacter smithii, influence host metabolism.

OBJECTIVE

Therefore, we compared M. smithii colonization and weight gain in a rat model under different dietary conditions.

DESIGN AND METHODS

Sprague-Dawley rats were inoculated with M. smithii or vehicle (N = 10/group), fed normal chow until day 112 postinoculation, high-fat chow until day 182, then normal chow until day 253. Thereafter, five rats from each group were fed high-fat and normal chow until euthanasia.

RESULTS

Both groups exhibited M. smithii colonization, which increased following inoculation only for the first 9 days. Change to high-fat chow correlated with significant increases in weight (P < 0.00001) and stool M. smithii (P < 0.01) in all rats, with stool M. smithi decreasing on return to normal chow. Rats switched back to high-fat on day 253 further increased weight (P < 0.001) and stool M. smithii (P = 0.039). Euthanasia revealed all animals had higher M. smithii, but not total bacteria, in the small intestine than in the colon. Rats switched back to high-fat chow had higher M. smithii levels in the duodenum, ileum, and cecum than those fed normal chow; total bacteria did not differ in any bowel segment. Rats which gained more weight had more bowel segments colonized, and the lowest weight recorded was in a rat on high-fat chow which had minimal M. smithii colonization.

CONCLUSIONS

We conclude that M. smithii colonization occurs in the small bowel as well as in the colon, and that the level and extent of M. smithii colonization is predictive of degree of weight gain in this animal model.

摘要

未加标签

越来越多的人认为胃肠道(GI)产甲烷菌,包括史密斯甲烷杆菌,会影响宿主的新陈代谢。

目的

因此,我们比较了不同饮食条件下大鼠模型中史密斯甲烷杆菌的定植和体重增加情况。

设计和方法

将 Sprague-Dawley 大鼠接种史密斯甲烷杆菌或载体(每组 10 只),接种后至第 112 天给予普通饲料,至第 182 天给予高脂肪饲料,然后至第 253 天给予普通饲料。此后,每组 5 只大鼠分别给予高脂肪和普通饲料,直至处死。

结果

两组大鼠均出现史密斯甲烷杆菌定植,定植仅在接种后前 9 天增加。改为高脂肪饮食与所有大鼠体重显著增加(P < 0.00001)和粪便史密斯甲烷杆菌(P < 0.01)显著增加相关,所有大鼠返回普通饲料后粪便史密斯甲烷杆菌减少。第 253 天改为高脂肪饮食的大鼠体重进一步增加(P < 0.001),粪便史密斯甲烷杆菌(P = 0.039)增加。安乐死时发现所有动物小肠中的史密斯甲烷杆菌比结肠中的更多,但总细菌则不然。改为高脂肪饮食的大鼠空肠、回肠和盲肠中的史密斯甲烷杆菌水平高于正常饮食的大鼠;各肠段的总细菌无差异。体重增加较多的大鼠有更多的肠段定植,记录到的最低体重是在一只高脂肪饮食的大鼠身上,其史密斯甲烷杆菌定植最少。

结论

我们的结论是,史密斯甲烷杆菌定植于小肠和结肠,并且该细菌的定植水平和范围可预测该动物模型中体重增加的程度。

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