Institut National de la Santé et de la Recherche Médicale (INSERM), Toulouse, France.
Université Paul Sabatier (UPS), Unité Mixte de Recherche (UMR) 1297, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), F-31432, Toulouse Cedex 4, France.
Int J Obes (Lond). 2023 Oct;47(10):1008-1022. doi: 10.1038/s41366-023-01341-1. Epub 2023 Jul 24.
Metabolic inflammation mediated obesity requires bacterial molecules to trigger immune and adipose cells leading to inflammation and adipose depot development. In addition to the well-established gut microbiota dysbiosis, a leaky gut has been identified in patients with obesity and animal models, characterized by the presence of a tissue microbiota in the adipose fat pads.
To determine its potential role, we sequenced the bacterial 16 S rRNA genes in the visceral adipose depot of patients with obesity. Taking great care (surgical, biochemical, and bioinformatic) to avoid environmental contaminants. We performed statistical discriminant analyses to identify specific signatures and constructed network of interactions between variables.
The data showed that a specific 16SrRNA gene signature was composed of numerous bacterial families discriminating between lean versus patients with obesity and people with severe obesity. The main discriminant families were Burkholderiaceae, Yearsiniaceae, and Xanthomonadaceae, all of which were gram-negative. Interestingly, the Morganellaceae were totally absent from people without obesity while preponderant in all in patients with obesity. To generate hypotheses regarding their potential role, we inferred metabolic pathways from the 16SrRNA gene signatures. We identified several pathways associated with adenosyl-cobalamine previously described to be linked with adipose tissue development. We further identified chorismate biosynthesis, which is involved in aromatic amino-acid metabolism and could play a role in fat pad development. This innovative approach generates novel hypotheses regarding the gut to adipose tissue axis.
This innovative approach generates novel hypotheses regarding the gut to adipose tissue axis in obesity and notably the potential role of tissue microbiota.
代谢性炎症介导的肥胖需要细菌分子来触发免疫和脂肪细胞,导致炎症和脂肪储存的发展。除了已经确立的肠道微生物失调外,肥胖患者和动物模型中还存在肠道通透性增加,其特征是脂肪垫组织中存在微生物群。
为了确定其潜在作用,我们对肥胖患者内脏脂肪组织中的细菌 16S rRNA 基因进行了测序。我们非常小心地(通过手术、生化和生物信息学)避免环境污染物的干扰。我们进行了统计判别分析,以确定特定的特征,并构建了变量之间的相互作用网络。
数据显示,一个特定的 16SrRNA 基因特征由许多区分瘦人与肥胖患者和严重肥胖患者的细菌家族组成。主要的判别家族是伯克霍尔德氏菌科、年尼亚菌科和黄单胞菌科,都是革兰氏阴性菌。有趣的是,没有肥胖的人摩根氏菌科完全不存在,而肥胖患者中则占优势。为了生成关于它们潜在作用的假设,我们从 16SrRNA 基因特征推断出代谢途径。我们确定了几个与先前描述的与脂肪组织发育相关的腺苷钴胺素途径有关的途径。我们进一步确定了色氨酸生物合成途径,它涉及芳香族氨基酸代谢,可能在脂肪垫发育中发挥作用。这种创新的方法为肥胖症中肠道到脂肪组织轴的假说提供了新的依据。
这种创新的方法为肥胖症中肠道到脂肪组织轴的假说提供了新的依据,特别是组织微生物群的潜在作用。