Hakkak Reza, Korourian Soheila, Foley Steven L, Erickson Bruce D
Department of Dietetics and Nutrition, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America.
Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America.
PLoS One. 2017 Jul 13;12(7):e0181451. doi: 10.1371/journal.pone.0181451. eCollection 2017.
Obesity has been on the rise in the US and worldwide for the last several decades. Obesity has been associated with chronic disease development, such as certain types of cancer, type 2 diabetes, cardiovascular disease, and liver diseases. Previously, we reported that obesity promotes DMBA-induced mammary tumor development using the obese Zucker rat model. The intestinal microbiota is composed of a diverse population of obligate and facultative anaerobic microorganisms, and these organisms carry out a broad range of metabolic activities. Obesity has been linked to changes in the intestinal microbiota, but the composition of the bacterial populations in lean and obese Zucker rats has not been carefully studied. Therefore, the objective of this study was to determine the effects of obesity on the gut microbiota in this model. Lean and obese female Zucker rats (n = 16) were fed an AIN-93G-like diet for 8 weeks. Rats were weighed twice weekly, and fecal samples were collected at the beginning and end of the experiment. 16S rRNA gene sequencing was used to evaluate the composition of the fecal bacterial populations. At the outset of the study, the lean rats exhibited much lower ratios of the Firmicutes to Bacteroidetes phyla than the obese rats, but after 60 days, this ratio in the lean rats exceeded that of the obese. This shift was associated with reductions in the Bacteroidaceae, S24-7 and Paraprevotellaceae families in the lean rats. Obese rats also showed increased levels of the genus Akkermansia at day 60. PCoA plots of beta diversity showed clustering of the different test groups, indicating clear differences in intestinal microbiota populations associated with both the time point of the study and the lean or obese status in the Zucker rat model for obesity.
在过去几十年里，肥胖在美国乃至全球范围内都呈上升趋势。肥胖与慢性疾病的发展相关，比如某些类型的癌症、2型糖尿病、心血管疾病和肝脏疾病。此前，我们利用肥胖的Zucker大鼠模型报道了肥胖会促进二甲基苯并蒽（DMBA）诱导的乳腺肿瘤发展。肠道微生物群由各种各样的专性和兼性厌氧微生物组成，这些微生物进行广泛的代谢活动。肥胖与肠道微生物群的变化有关，但瘦型和肥胖型Zucker大鼠的细菌种群组成尚未得到仔细研究。因此，本研究的目的是确定肥胖对该模型中肠道微生物群的影响。将瘦型和肥胖型雌性Zucker大鼠（n = 16）喂以AIN-93G样饮食8周。每周对大鼠称重两次，并在实验开始和结束时收集粪便样本。采用16S rRNA基因测序来评估粪便细菌种群的组成。在研究开始时，瘦型大鼠中厚壁菌门与拟杆菌门的比例远低于肥胖大鼠，但60天后，瘦型大鼠的这一比例超过了肥胖大鼠。这种转变与瘦型大鼠中拟杆菌科、S24-7和副普雷沃氏菌科的减少有关。肥胖大鼠在第60天时还显示出阿克曼氏菌属水平的增加。β多样性的主坐标分析（PCoA）图显示不同测试组聚类，表明在Zucker大鼠肥胖模型中，与研究时间点以及瘦或胖状态相关的肠道微生物群存在明显差异。
