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장내세균, 구강세균과 간 건강

작성일 2020-09-09 첨부파일 링크

 

 

 

 

 

 

 

 

 

 

간은 다 아다시피…장을 통해 들어온 외부물질을 검색하고, 해독하고, 우리 몸에 필요한 물질로 바꾸어 혈액으로 내보내고, 쓰고 남는 영양소를 보관하는 내 몸의 포털싸이트이고 화학공장입니다.

간 기능이 손상되면, 간세포에 있던 ALT ASL 라는 효소가 혈류로 흘러나오게 되어 증가하게 됩니다. 하지만, 이런 효소의 수치가 정상범위를 벗어났다 하더라도, 바로 간이 안 좋다 결론내릴 수 없고, 그 진행정도도 알기 어렵습니다. 추가적으로 초음파나 CT, MRI, 심지어 조직검사 같은 것도 봐야 겠죠.

그 전에 장내세균이나 구강세균을 검사해 보면 어떨까요.

장에서 흡수된 영양소는 바로 간으로 향하고, 간은 장에 소화효소를 만들어 분비함으로 장과 간은 늘 순환하고 소통합니다. 이를 장-간 축(Gut Liver Axis) 이라 합니다. 이 장간축이 잘 돌아가려면 장내세균의 역할이 중요한 건 물론이고요.

장내세균중 Collinsella 이나 대장균(E. coli) 가 정상상태의 간에서 지방간(NAFLD, NASH) 을 걸쳐 간경화로 갈수록 증가하는 경향이 있습니다.(Astbury, Atallah et al. 2020) 반대로 패칼리박테리움의 수가 적다면, 장내환경이 악화되어 염증성장염들을 가져올 수 있고, 간에도 비알콜성간질환(NAFLD) 등을 만들 수 있습니다.(Iino, Endo et al. 2019) 패칼리박테리움은 대장까지 들어온 식이섬유를 분해하여 단쇄지방산을 만들어 장내환경을 개선하고, 몸 전체로는 염증을 낮추고 면역을 높이는 기능을 합니다. 한국인의 경우, 장내세균중 패칼리박테리움은 평균 8% 정도입니다. 또 장내세균중 항염 세균으로 알려진 아카멘시아 라는 세균들역시 장내에 많이 서식하면 장 점막의 방어기능을 더 좋게해서 간으로 가는 여러 독소들을 미리 차단하는 효과가 기대됩니다. (Adolph, Grander et al. 2018)

장내에서 패칼리박테리움을 증가시키려면, 채식위주의 식사로 대장으로 가는 식이섬유의 양을 증가시키는 것이 좋습니다. 대표적으로 우리음식 김치는 장내에서 패칼리박테리움을 증가시킵니다.(Kim and Park 2018)

구강세균중 진지발리스는 간질환의 시작과 진행에 영향을 미칩니다. 진지발리스는 탄수화물과 지방의 대사과정을 방해하고, 면역에 영향을 주어 간세포의 손상을 초래합니다. (Sasaki, Katagiri et al. 2018) 비알콜성 지방간이 있는 사람과 없는 사람의 구강에서 Pg 가 발견되는 비율은 확연히 구분되고, 비알콜성 지방간이 있는 사람의 잇몸관리를 통해 구강세균을 낮추어 주면 AST ALT 같은 간효소 수치가 좋아집니다.

간 건강을 위해서도 구강위생관리가 중요하다는 거지요.

 

 

 

Adolph, T. E., et al. (2018). "Liver–Microbiome Axis in Health and Disease." Trends in immunology 39(9): 712-723.

The intestinal and hepatobiliary tract exhibits host-specific commensal colonization. The resident microbiota has emerged as a key player in intestinal and hepatic diseases. Alcoholic and nonalcoholic fatty liver diseases (ALD/NAFLD), primary sclerosing cholangitis (PSC), liver cirrhosis, and some of their clinical complications, such as hepatic encephalopathy (HE), have been linked to a microbial signature, as also observed for severe liver inflammation in alcoholic hepatitis. In turn, the liver impacts, and communicates with, the microbiota through hepatic mediators, such as bile acids or inflammatory signals. Therefore, a liver–microbiome bidirectional crosstalk appears to be critical in health and various liver diseases and could be therapeutically targeted, such as by fecal microbiota transplantation.

Astbury, S., et al. (2020). "Lower gut microbiome diversity and higher abundance of proinflammatory genus Collinsella are associated with biopsy-proven nonalcoholic steatohepatitis." Gut Microbes 11(3): 569-580.

Iino, C., et al. (2019). "Significant decrease in Faecalibacterium among gut microbiota in nonalcoholic fatty liver disease: a large BMI- and sex-matched population study." Hepatology International 13(6): 748-756.

Compositional changes of the gut microbiota are known to occur in patients with nonalcoholic fatty liver disease (NAFLD); however, the changes did not corroborate between the studies. We evaluated the gut microbiota between NAFLD and non-NAFLD participants, excluding the influence of obesity and sex in this study involving a large number of participants.

Kim, H.-Y. and K.-Y. Park (2018). "Clinical trials of kimchi intakes on the regulation of metabolic parameters and colon health in healthy Korean young adults." Journal of Functional Foods 47: 325-333.

Kimchi intakes significantly increased dietary fiber levels in volunteers. Intakes of standardized kimchi (SK) and functional kimchi (FK) tended to reduce body fat mass and percentage. Both kimchi groups showed reduced levels of LDL-C (p < 0.05), and increased levels of HDL-C (p < 0.01). However, FK intake was associated with reduction of TC, TG, and IL-6 levels, as well as an increase in adiponectin level (p < 0.05). In the fecal analysis, the SK and FK groups showed decreased pH, β-glucosidase, and β-glucuronidase levels (p < 0.01). Further, intakes of kimchi, especially FK, reduced the abundance of Firmicutes, but increased levels of Bacteroidetes. In addition, intakes of both types of kimchi increased the abundance of short chain fatty acid production related genera (Faecalibacterium, Roseburia, and Phascolactobacterium) and reduced Clostridium sp. and Escherichia coli group counts. Thus, kimchi intakes regulated metabolic parameters and colon health, and FK clearly increased health function in humans.

Sasaki, N., et al. (2018). "Endotoxemia by Porphyromonas gingivalis Injection Aggravates Non-alcoholic Fatty Liver Disease, Disrupts Glucose/Lipid Metabolism, and Alters Gut Microbiota in Mice." 9(2470).

Many risk factors related to the development of non-alcoholic fatty liver disease (NAFLD) have been proposed, including the most well-known of diabetes and obesity as well as periodontitis. As periodontal pathogenic bacteria produce endotoxins, periodontal treatment can result in endotoxemia. The aim of this study was to investigate the effects of intravenous, sonicated Porphyromonas gingivalis (Pg) injection on glucose/lipid metabolism, liver steatosis, and gut microbiota in mice. Endotoxemia was induced in C57BL/6J mice (8 weeks old) by intravenous injection of sonicated Pg; Pg was deactivated but its endotoxin remained. The mice were fed a high-fat diet and administered sonicated Pg (HFPg) or saline (HFco) injections for 12 weeks. Liver steatosis, glucose metabolism, and gene expression in the liver were evaluated. 16S rRNA gene sequencing with metagenome prediction was performed on the gut microbiota. Compared to HFco mice, HFPg mice exhibited impaired glucose tolerance and insulin resistance along with increased liver steatosis. Liver microarray analysis demonstrated that 1278 genes were differentially expressed between HFco and HFPg mice. Gene set enrichment analysis showed that fatty acid metabolism, hypoxia, and TNFα signaling via NFκB gene sets were enriched in HFPg mice. Although sonicated Pg did not directly reach the gut, it changed the gut microbiota and decreased bacterial diversity in HFPg mice. Metagenome prediction in the gut microbiota showed enriched citrate cycle and carbon fixation pathways in prokaryotes. Overall, intravenous injection of sonicated Pg caused impaired glucose tolerance, insulin resistance, and liver steatosis in mice fed high-fat diets. Thus, blood infusion of Pg contributes to NAFLD and alters the gut microbiota.

 

 

 

 

 

 


 

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