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Porphyromonas gingivalis impairs glucose uptake in skeletal muscle associated with altering gut microbiota
The FASEB Journal ( IF 4.4 ) Pub Date : 2020-11-16 , DOI: 10.1096/fj.202001158r
Kazuki Watanabe 1 , Sayaka Katagiri 1 , Hirokazu Takahashi 2, 3 , Naoki Sasaki 1 , Shogo Maekawa 1 , Rina Komazaki 1 , Masahiro Hatasa 1 , Yoichiro Kitajima 2, 4 , Yusuke Maruyama 5 , Takahiko Shiba 1 , Keiji Komatsu 1 , Yujin Ohsugi 1 , Kenichi Tanaka 2 , Ayumi Matsuzawa 6 , Tomomitsu Hirota 7 , Haruka Tohara 8 , Yuichiro Eguchi 3 , Keizo Anzai 2 , Atsuhiko Hattori 5 , Takanori Iwata 1
Affiliation  

Skeletal muscles have a high metabolic capacity, which play key roles in glucose metabolism. Although periodontal disease increases the risk of metabolic syndrome, the relationship between periodontal bacterial infection and skeletal muscle metabolic dysfunction is unclear. We found that anti-Porphyromonas gingivalis (Pg) antibody titers positively correlated with intramuscular adipose tissue content (IMAC), fasting blood glucose, and HOMA-IR in metabolic syndrome patients. In C57BL/6J mice fed a high-fat diet, recipients of oral Pg (HFPg) had impaired glucose tolerance, insulin resistance, and higher IMAC compared to recipients of saline (HFco). The soleus muscle in HFPg mice exhibited fat infiltration and lower glucose uptake with higher Tnfa expression and lower insulin signaling than in HFco mice. Gene set enrichment analysis showed that TNFα signaling via NFκB gene set was enriched in the soleus muscle of HFPg mice. Moreover, TNF-α also decreased glucose uptake in C2C12 myoblast cells in vitro. Based on 16S rRNA sequencing, Pg administration altered the gut microbiome, particularly by decreasing the abundance of genus Turicibacter. Microbial network of the gut microbiome was dramatically changed by Pg administration. Our findings suggest that infection with Pg is a risk factor for metabolic syndrome and skeletal muscle metabolic dysfunction via gut microbiome alteration.

中文翻译:

牙龈卟啉单胞菌损害与改变肠道微生物群相关的骨骼肌中的葡萄糖摄取

骨骼肌具有很高的代谢能力,在葡萄糖代谢中起关键作用。尽管牙周病会增加代谢综合征的风险,但牙周细菌感染与骨骼肌代谢功能障碍之间的关系尚不清楚。我们发现,在代谢综合征患者中,抗牙龈卟啉单胞菌 (Pg) 抗体滴度与肌内脂肪组织含量 (IMAC)、空腹血糖和 HOMA-IR 呈正相关。在喂食高脂肪饮食的 C57BL/6J 小鼠中,与生理盐水 (HFco) 接受者相比,口服 Pg (HFPg) 接受者的葡萄糖耐量受损、胰岛素抵抗和更高的 IMAC。与 HFco 小鼠相比,HFPg 小鼠的比目鱼肌表现出脂肪浸润和较低的葡萄糖摄取,具有更高的 Tnfa 表达和更低的胰岛素信号传导。基因集富集分析表明,通过 NFκB 基因集的 TNFα 信号在 HFPg 小鼠的比目鱼肌中富集。此外,TNF-α 还降低了体外 C2C12 成肌细胞的葡萄糖摄取。基于 16S rRNA 测序,Pg 给药改变了肠道微生物组,特别是通过降低 Turicibacter 属的丰度。Pg 给药显着改变了肠道微生物组的微生物网络。我们的研究结果表明,Pg 感染是通过肠道微生物组改变导致代谢综合征和骨骼肌代谢功能障碍的危险因素。特别是通过减少 Turicibacter 属的丰度。Pg 给药显着改变了肠道微生物组的微生物网络。我们的研究结果表明,Pg 感染是通过肠道微生物组改变导致代谢综合征和骨骼肌代谢功能障碍的危险因素。特别是通过减少 Turicibacter 属的丰度。Pg 给药显着改变了肠道微生物组的微生物网络。我们的研究结果表明,Pg 感染是通过肠道微生物组改变导致代谢综合征和骨骼肌代谢功能障碍的危险因素。
更新日期:2020-11-16
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