Helicobacter pylori infection might have a potential role in hepatocyte ballooning in nonalcoholic fatty liver disease

Sumida, Yoshio; Kanemasa, Kazuyuki; Imai, Shoichi; Mori, Kumiko; Tanaka, Saiyu; Shimokobe, Hideto; Kitamura, Yoko; Fukumoto, Kohei; Kakutani, Akira; Ohno, Tomoyuki; Taketani, Hiroyoshi; Seko, Yuya; Ishiba, Hiroshi; Hara, Tasuku; Okajima, Akira; Yamaguchi, Kanji; Moriguchi, Michihisa; Mitsuyoshi, Hironori; Yasui, Kohichiroh; Minami, Masahito; Itoh, Yoshito

doi:10.1007/s00535-015-1039-2

Cited by 72 publications

(91 citation statements)

References 52 publications

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“…This study also found that H. pylori infection could independently predict NASH in logistic regression analysis ( p = 0.003). And it further confirmed that H. pylori infection may represent a contributing factor to NAFLD (Sumida et al, 2015). Similarly, another two studies from Turkey and Japan, respectively, also suggested H. pylori infection as one of the independent risk factors for the development of NAFLD (Takuma, 2011; Sumida et al, 2015).…”

Section: Epidemiology and Clinical Experimentsmentioning

confidence: 57%

“…We know that H. pylori infection has been implicated in the pathogenesis of insulin resistance (IR) (Polyzos et al, 2011), which contributes to the development of NAFLD. Recently, many studies have reported that H. pylori infection is closely related to the development of NAFLD (Polyzos et al, 2013a; Sumida et al, 2015). However, the mechanisms underlying NAFLD remains unclear, and therapeutic options to this disorder are fairly limited nowadays.…”

Section: Introductionmentioning

confidence: 99%

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The Possible Role of Helicobacter pylori Infection in Non-alcoholic Fatty Liver Disease

Cheng

et al. 2017

Front. Microbiol.

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Helicobacter pylori (H. pylori) which colonizes the stomach can cause a wide array of gastric disorders, including chronic gastritis, peptic ulcer, and gastric cancer. Recently, accumulating evidence has implicated H. pylori infection in extragastrointestinal diseases such as cardiovascular diseases, neurological disorders, and metabolic diseases. At the same time, many scholars have noted the relationship between H. pylori infection and non-alcoholic fatty liver disease (NAFLD). Despite the positive association between H. pylori and NAFLD reported in some researches, there are opposite perspectives denying their relationship. Due to high prevalence, unclear etiology and difficult treatment of NAFLD, confirming the pathogenicity of H. pylori infection in NAFLD will undoubtedly provide insights for novel treatment strategies for NAFLD. This paper will review the relationship between H. pylori infection and NAFLD and the possible pathogenic mechanisms.

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Section: Epidemiology and Clinical Experimentsmentioning

confidence: 57%

Section: Introductionmentioning

confidence: 99%

The Possible Role of Helicobacter pylori Infection in Non-alcoholic Fatty Liver Disease

Cheng

et al. 2017

Front. Microbiol.

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“…The contributing effect of HP infection to the development of NAFLD has also been suggested, as well as for the progression from hepatic steatosis to NASH [13, 36–38]. In addition to insulin resistance, invasion of HP in the small bowel mucosa might increase intestinal permeability and facilitate the passage of bacterial endotoxins via the portal vein to the liver [13].…”

Section: Discussionmentioning

confidence: 99%

“…In this way, the severity of steatosis in humans has been correlated with the disruption of intercellular tight junctions in the gut, increasing intestinal permeability, and the intestinal bacterial overgrowth in the small bowel microbiota [39]. In a recent work, the prevalence of NASH, the total NAFLD activity score, and the grade of hepatocyte ballooning were significantly higher in patients positive for anti-HP immunoglobulin G than in those negative [36]. Similarly, higher rates of anti-HP IgG were detected in patients with biopsy-proven NAFLD compared to control group [38].…”

Section: Discussionmentioning

confidence: 99%

The Role of Morbid Obesity in the Promotion of Metabolic Disruptions and Non-Alcoholic Steatohepatitis by Helicobacter Pylori

et al. 2016

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BackgroundHelicobacter pylory (HP) infection has been associated to an increased rate of type 2 diabetes (T2D) and liver disease through its effect on insulin resistance and systemic inflammation. However, results are inconstant and no studies exist in morbidly obese patients, in which both insulin resistance and inflammation coexist.Material and MethodsCross-sectional study to evaluate the relationship between HP infection and alterations in carbohydrate metabolism, lipid profile, inflammation markers, and liver disease in patients awaiting for bariatric surgery. HP infection was histologically assessed in gastric antrum biopsy from 416 subjects. Liver biopsy was also available in 93 subjects.ResultsBoth impaired fasting glucose and T2D were similar when comparing subjects with and without HP infection (24.2% vs. 22%, p = 0.290 and 29.4% vs. 29.1%, p = 0.916, respectively), with no differences between groups in the HOMA-IR, lipid profile neither inflammatory parameters. However, HP infection was higher among subjects with a BMI ≥ 40.0 kg/m2 in comparison with lower degrees of obesity (71.7% vs. 60.0%, p = 0.041). In addition, subjects without HP infection showed higher degrees of steatosis (44.1±26.4% vs. 32.0±20.7%, p = 0.038), as well as a lower prevalence of non-alcoholic steatohepatitis (9.3% vs. 30.7%, p = 0.023).ConclusionsIn patients with morbid obesity, HP infection does not seem to be associated with abnormal carbohydrate metabolism. In addition, less advanced degrees of non-alcoholic fatty disease were observed. We suggest that low-grade inflammation that accompanies obesity mitigates the diabetogenic effect of HP, so the presence of obesity should be considered in studies that evaluate the HP metabolic effects.

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“…Moreover, we describe for the first time the association between high fat dietinduced NAFLD and enhanced Helicobacter genus detection. Even though is a controversial issue [45,46], it has been suggested the role of Helicobacter pilory as a contributing factor in the progression of NAFLD [47][48][49], considering its eradication as effective preventive or treatment measures [50,51]. Interestingly, Helicobacter genus was dramatically reduced by quercetin treatment in our model of NAFLD, corroborating its anti-Helicobacter activity observed in in vitro and in vivo models of infection [52,53], and supporting therapeutic potential of quercetin for prevention of the spectrum of non-alcoholic fatty liver diseases.…”

Section: Thus Quercetin Reduced the Increased Firmicutes/bacteroidetesmentioning

confidence: 99%

Protective effect of quercetin on high-fat diet-induced non-alcoholic fatty liver disease in mice is mediated by modulating intestinal microbiota imbalance and related gut-liver axis activation

Porras

Nistal

Martínez‐Flórez

et al. 2017

Free Radical Biology and Medicine

412

259

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Abbreviations: ALT, alanine aminotransferase; C/EBPα, CCAAT/enhancer binding protein alpha; CHOP, CCAAT-enhancer-binding protein homologous protein; CYP2E1, cytochrome P450 2E1; DAMPs, danger-associated molecular patterns; FABP1, fatty acid binding protein 1; FAS, fatty acid synthase; FAT/CD36, fatty acid translocase CD36; FFA, free fatty acid; FOXA1, forkhead box protein A1; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; GRP78, 78 kDa glucose-regulated protein; HFD, high fat diet; HOMA-IR, homeostasis model assessment of insulin resistance; IAP, intestinal phosphatase alkaline; IL-6, interleukin 6; LPO, lipid peroxidation; LPS, lipopolysaccharide; LXRα, liver X receptor alpha; NAFLD, non-alcoholic fatty liver disease; NAS, NAFLD activity score; NASH, non-alcoholic steatohepatitis; NF-B , nuclear factor kappa B; NLRP3, NOD-like receptor family pyrin domain containing 3;PAMPs, pathogen-associated molecular patterns; PRRs, pattern recognition receptors; SCFAs, short-chain fatty acids; SREBP-1c, sterol regulatory element binding protein 1c; TG, triglycerides; TLR, Toll-like receptor; TNF-αtumor necrosis factor; UPR, unfolded protein response. AbstractGut microbiota is involved in obesity, metabolic syndrome and the progression of nonalcoholic fatty liver disease (NAFLD). It has been recently suggested that the flavonoid quercetin may have the ability to modulate the intestinal microbiota composition, suggesting a prebiotic capacity which highlights a great therapeutic potential in NAFLD. The present study aims to investigate benefits of experimental treatment with quercetin on gut microbial balance and related gut-liver axis activation in a nutritional animal model of NAFLD associated to obesity. C57BL/6J mice were challenged with high fat diet (HFD) supplemented or not with quercetin for 16 weeks.

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Helicobacter pylori infection might have a potential role in hepatocyte ballooning in nonalcoholic fatty liver disease

Abstract: The association of H. pylori seropositivity with hepatocyte ballooning suggests that H. pylori infection may represent another contributing factor in the progression from NAFL to NASH. Eradicating H. pylori infection may have therapeutic prospects in NASH treatment.

Cited by 72 publications

References 52 publications

The Possible Role of Helicobacter pylori Infection in Non-alcoholic Fatty Liver Disease

The Possible Role of Helicobacter pylori Infection in Non-alcoholic Fatty Liver Disease

The Role of Morbid Obesity in the Promotion of Metabolic Disruptions and Non-Alcoholic Steatohepatitis by Helicobacter Pylori

Protective effect of quercetin on high-fat diet-induced non-alcoholic fatty liver disease in mice is mediated by modulating intestinal microbiota imbalance and related gut-liver axis activation

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