<i>Porphyromonas gingivalis</i> exacerbates the progression of fatty liver disease via CD36-PPARγ pathway

Ahn, Ji-Su; Yang, Ji Won; Oh, Su-Jeong; Shin, Ye Young; Kang, Min‐Jung; Park, Hae Ryoun; Seo, Yoojin; Kim, Hyung–Sik

doi:10.5483/bmbrep.2021.54.6.050

Cited by 14 publications

(8 citation statements)

References 38 publications

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“…Previous animal studies have mainly focused on the effects of a single periodontal pathogen on NAFLD. 8 , 27 , 28 However, the key pathogenic hypothesis may not fully reveal the complexity of the pathogenesis and interactions between periodontitis and NAFLD. Consequently, a mixed bacterial dysbiosis model related to periodontitis may provide better scientific support than a single-species model and can better simulate actual clinical conditions.…”

Section: Discussionmentioning

confidence: 99%

Periodontitis salivary microbiota exacerbates nonalcoholic fatty liver disease in high-fat diet-induced obese mice

Wang¹,

Li²,

Qian³

et al. 2023

iScience

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Section: Discussionmentioning

confidence: 99%

Periodontitis salivary microbiota exacerbates nonalcoholic fatty liver disease in high-fat diet-induced obese mice

Wang¹,

Li²,

Qian³

et al. 2023

iScience

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“…Chronic low-grade inflammation induced by P. gingivalis infection induces insulin resistance, which affects hepatic glucolipid metabolism and consequently leads to lipid accumulation in hepatocytes. In addition to this, a study by Ahn et al., 2021 found that P. gingivalis induced the progression of nonalcoholic fatty liver disease in high-fat-fed mice by upregulating the CD36-PPARγ axis ( Ahn et al., 2021 ). As one of the important metabolic enzymes in fatty acids, fatty acid translocase 36 (CD36) is widely expressed in various cells (myocytes, monocytes, macrophages, hepatocytes) ( Thanakun et al., 2014 ).…”

Section: Association Of P Gingivalis With Systemic...mentioning

confidence: 98%

Host insulin resistance caused by Porphyromonas gingivalis-review of recent progresses

Jia

2023

Front. Cell. Infect. Microbiol.

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Porphyromonas gingivalis (P. gingivalis) is a Gram-negative oral anaerobic bacterium that plays a key role in the pathogenesis of periodontitis. P. gingivalis expresses a variety of virulence factors that disrupt innate and adaptive immunity, allowing P. gingivalis to survive and multiply in the host and destroy periodontal tissue. In addition to periodontal disease, P.gingivalis is also associated with systemic diseases, of which insulin resistance is an important pathological basis. P. gingivalis causes a systemic inflammatory response, disrupts insulin signaling pathways, induces pancreatic β-cell hypofunction and reduced numbers, and causes decreased insulin sensitivity leading to insulin resistance (IR). In this paper, we systematically review the studies on the mechanism of insulin resistance induced by P. gingivalis, discuss the association between P. gingivalis and systemic diseases based on insulin resistance, and finally propose relevant therapeutic approaches. Overall, through a systematic review of the mechanisms related to systemic diseases caused by P. gingivalis through insulin resistance, we hope to provide new insights for future basic research and clinical interventions for related systemic diseases.

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“…[80] Ahn et al showed a streamed result with Pg on fatty liver disease in obese mice through the upregulation CD36-PPARγ pathway. [81] Pg-LPS injected via the oral mucosa in the maxilla has been reported to induce the onset of NASH in the liver of rats fed a high-fat diet. [82] In general prevention and/or elimination of Pg infections with dental treatment may have a beneficial effect on NASH.…”

Section: Periodontal Problems and Non-alcoholic Fatty Liver Diseasementioning

confidence: 99%

Non-Alcoholic Fatty Liver and Periodontal Disease: Is there a Relationship? A Contemporary Review

Hatipoglu

2024

J Inonu Liver Transpl Inst

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T he Non-alcoholic fatty liver disease (NAFLD) it's a term used for several conditions caused by fat accumulation in the liver. One-fourth of the world's population is faced with this clinical situation. It is mostly seen in South America and the Middle East, and least in Africa. [1] Nevertheless, when considering its prevalence within the community, this malady emerges as one of the most frequently encountered liver diseases, demonstrating a notable association with elevated rates of liver-related mortality and morbidity. [2] By definition, NAFLD is a clinical picture in which insulin resistance, histopathological more than 5% steatosis of hepatocytes, or dense fat fractions by radiographic techniques are detected. This clinical situation is examined under two main headings non-alcoholic fatty liver (NAFL) and non-alcoholic steatohepatitis (steatosis coexists with liver-cell injury and inflammation). [3,4] NAFLD has 4 stages for developing; simple fatty liver (steatosis), non-alcoholic steatohepatitis (NASH), fibrosis and cirrhosis, and may liver cancer. [5] In advanced phases, this may result in liver transplantation. The patients with NAFLD show similar histological damage to alcoholic liver disease. [6] Oxidative and inflammatory responses play crucial roles in the shared pathogenesis of both NAFLD and nonalcoholic NASH. [7] Lifestyle is an important point for developing this disease.Periodontal disease is a common inflammatory disease and is known to be related to other systemic diseases. This bidirectional relation between periodontal disease and other disease processes has led to outstanding research recently. In addition, periodontal disease has been advocated to exacerbate metabolic disorders including non-alcoholic fatty liver disease (NAFLD). In this traditional review, general characteristics of periodontal diseases, general characteristics of NAFLD/ Nonalcoholic steatohepatitis (NASH), and their causality were discussed for treatment providers. The collected data significantly corroborate a greater incidence of periodontal disease among individuals with NAFLD in comparison to the general healthy population. Healthcare professionals need to be aware of the association between NAFLD and periodontal disease thus patient management effectiveness can be enhanced.

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Porphyromonas gingivalis exacerbates the progression of fatty liver disease via CD36-PPARγ pathway

Cited by 14 publications

References 38 publications

Periodontitis salivary microbiota exacerbates nonalcoholic fatty liver disease in high-fat diet-induced obese mice

Periodontitis salivary microbiota exacerbates nonalcoholic fatty liver disease in high-fat diet-induced obese mice

Host insulin resistance caused by Porphyromonas gingivalis-review of recent progresses

Non-Alcoholic Fatty Liver and Periodontal Disease: Is there a Relationship? A Contemporary Review

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