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非靶向和靶向牙龈代谢组学揭示高脂肪饮食诱导肥胖与牙周炎之间的代谢关联。

Untargeted and targeted gingival metabolome in rodents reveal metabolic links between high-fat diet-induced obesity and periodontitis.

机构信息

Department of Periodontics, Guangzhou Key Laboratory of Basic and Applied Research of Oral Regenerative Medicine, Affiliated Stomatology Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China.

Department of Prosthodontics, Guangdong Provincial Key Laboratory of Stomatology, Guanghua School of Stomatology, Sun Yat-sen University, Guangzhou, China.

出版信息

J Clin Periodontol. 2021 Aug;48(8):1137-1148. doi: 10.1111/jcpe.13486. Epub 2021 May 27.

Abstract

AIM

To characterize gingival metabolome in high-fat diet (HFD)-induced obesity in mice with/without periodontitis.

METHODS

HFD-induced obesity mouse model was established by 16-week feeding, and a lean control group was fed with low-fat diet (n = 21/group). Both models were induced for periodontitis on the left sides by molar ligation for 10 days, whereas the right sides were used as controls. Gingival metabolome and arginine metabolism were analysed by non-targeted/targeted liquid chromatography-mass spectrometry.

RESULTS

Of 2247 reference features, presence of periodontitis altered 165 in lean versus 885 in HFD mice; and HFD altered 525 in absence versus 1435 in presence of periodontitis. Compared with healthy condition, periodontitis and HFD had distinct effects on gingival metabolome. Metabolomic impacts of periodontitis were generally greater in HFD mice versus lean controls. K-medoids clustering showed that HFD amplified the impacts of periodontitis on gingival metabolome in both intensity and extensity. Ten metabolic pathways were enriched, including 2 specific to periodontitis, 5 specific to HFD and 3 shared ones. Targeted validation on arginine metabolism confirmed the additive effects between HFD and periodontitis.

CONCLUSION

The obese population consuming excessive HFD display amplified metabolic response to periodontitis, presenting a metabolic susceptibility to exacerbated periodontal destruction.

摘要

目的

研究高脂饮食(HFD)诱导肥胖伴或不伴牙周炎小鼠的牙龈代谢组学特征。

方法

通过 16 周喂养建立 HFD 诱导肥胖小鼠模型,设立低脂饮食对照组(n=21/组)。两组左侧磨牙结扎诱发牙周炎 10 天,右侧作为对照。采用非靶向/靶向液相色谱-质谱法分析牙龈代谢组学和精氨酸代谢。

结果

在 2247 个参考特征中,与 lean 相比,periodontitis 在 HFD 小鼠中改变了 165 个,而在 absence 中改变了 885 个;与 absence 相比,HFD 在 presence 中改变了 525 个,而改变了 1435 个。与健康状况相比,periodontitis 和 HFD 对牙龈代谢组有明显不同的影响。与 lean 对照组相比,periodontitis 在 HFD 小鼠中的代谢影响更为明显。K-medoids 聚类表明,HFD 放大了 periodontitis 对牙龈代谢组在强度和广度上的影响。富集了 10 条代谢途径,包括 2 条特定于 periodontitis 的途径、5 条特定于 HFD 的途径和 3 条共享途径。对精氨酸代谢的靶向验证证实了 HFD 和 periodontitis 之间的协同作用。

结论

食用过量 HFD 的肥胖人群对牙周炎表现出放大的代谢反应,呈现出对牙周破坏加重的代谢易感性。

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