Increased Orocecal Transit Time in Patients with Nonalcoholic Fatty Liver Disease

Soza, Alejandro; Riquelme, Arnoldo; Gonzalez, Robinson G.; Álvarez, Manuel; Pérez-Ayuso, Rosa María; Glasinovic, J C; Arrese, Marco

doi:10.1007/s10620-005-2720-8

Cited by 49 publications

(46 citation statements)

References 20 publications

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“…Other authors have shown that Anti-LPS EndoCAb levels in peripheral blood may not correlate with L/M ratio in patients with abnormal sugar absorption tests or with increased orocecal transit time. 14,44 An altered intestinal barrier function could cause an increase in plasma levels of proinflammatory cytokines, released after exposure of Kupffer and other reticuloendo-thelial cells to endotoxin delivered by the portal vein. However, among four cytokines measured in peripheral blood, only a mild (not significant) increase in IL-6 was observed in ICP patients and also in normal pregnant women.…”

Section: Discussionmentioning

confidence: 99%

Is a leaky gut involved in the pathogenesis of intrahepatic cholestasis of pregnancy?

et al. 2006

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I ntrahepatic cholestasis of pregnancy (ICP) is a rare disorder of unknown cause that may develop during the third or second trimester of pregnancy and resolves rapidly after delivery. The chief complaint is pruritus, and serum liver tests reveal a mild cholestasis with increased levels of bile salts and aminotransferases. ICP may cause fetal distress, with stillbirths or premature deliveries leading to increased perinatal morbidity and mortality. 1,2 The pathogenesis of ICP appears to be multifactorial. Potential contributors include a genetic predisposition interacting with the effects of estrogen and progesterone metabolites on bile secretory mechanisms. 3 The influence of environmental factors has been suggested by the observation of a seasonal variability in the incidence of ICP, with highest rates reported during winter, a recurrence rate of only 45% to 70% in subsequent pregnancies of multiparous women, and the decrease in the prevalence of ICP detected in Sweden and Chile during recent decades. 4 Therefore, identifying factors that may explain these epidemiological changes appear to be important.The gastrointestinal mucosal epithelium is an essential barrier that normally restricts the passage of harmful molecules into the mucosa and systemic circulation. An increased intestinal permeability has been observed in patients with enteric damage, such as in inflammatory From the

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Section: Discussionmentioning

confidence: 99%

Is a leaky gut involved in the pathogenesis of intrahepatic cholestasis of pregnancy?

et al. 2006

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“…Small intestinal bacterial overgrowth has been reported to place a role in the pathogenesis of NASH, endotoxin and TNF-α being the possible mediator [19][20][21] . But contrary to this hypothesis, in another study, antibiotic treatment did not normalize aminotransferase levels in NASH patients [22] . Therefore more study is needed on the influence of SIBO on the pathogenesis of NASH and the curative effect of antibiotic on NASH.…”

Section: Introductionmentioning

confidence: 78%

“…Therefore more study is needed on the influence of SIBO on the pathogenesis of NASH and the curative effect of antibiotic on NASH. Alejandro S [22] found that prolonged Orocecal Transit Time (OCTT) in NAFLD patients coexist with SIBO. It is generally thought that prolonged OCTT is the cause of SIBO.…”

Section: Introductionmentioning

confidence: 99%

Small intestinal bacteria overgrowth decreases small intestinal motility in the NASH rats

Zhao²,

Li³

2008

WJG

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AIM: To explore the relationship between small intestinal motility and small intestinal bacteria overgrowth (SIBO) in Nonalcoholic steatohepatitis (NASH), and to investigate the effect of SIBO on the pathogenesis of NASH in rats. The effect of cidomycin in alleviating severity of NASH is also studied. METHODS:Forty eight rats were randomly divided into NASH group (n = 16), cidomycin group (n = 16) and control group (n = 16). Then each group were subdivided into small intestinal motility group (n = 8), bacteria group (n = 8) respectively. A semi-solid colored marker was used for monitoring small intestinal transit. The proximal small intestine was harvested under sterile condition and processed for quantitation for aerobes (E. coli ) and anaerobes (Lactobacilli). Liver pathologic score was calculated to qualify the severity of hepatitis. Serum ALT, AST levels were detected to evaluate the severity of hepatitis. RESULTS:Small intestinal transit was inhibited in NASH group (P < 0.01). Rats treated with cidomycin had higher small intestine transit rate than rats in NASH group (P < 0.01). High fat diet resulted in quantitative alterations in the aerobes (E. coli ) but not in the anoerobics (Lactobacill). There was an increase in the number of E. coli in the proximal small intestinal flora in NASH group than in control group (1.70 ± 0.12 log10 (CFU/g) vs 1.28 ± 0.07 log10 (CFU/g), P < 0.01). TNF-α concentration was significantly higher in NASH group than in control group (1.13 ± 0.15 mmol/L vs 0.57 ± 0.09 mmol/L, P < 0.01). TNF-α concentration was lower in cidomycin group than in NASH group (0.63 ± 0.09 mmol/L vs 1.13 ± 0.15 mmol/L, P < 0.01). Treatment with cidomycin showed its effect by significantly lowering serum ALT, AST and TNF-α levels of NASH rats.CONCLUSION: SIBO may decrease small intestinal movement in NASH rats. SIBO may be an important pathogenesis of Nash. And treatment with cidomycin by mouth can alleviate the severity of NASH.

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“…Elevated levels of TNF-α induce liver fibrosis and insulin resistance [25,26]. Some studies in humans and in animals however have failed to document differences between NASH and controls in respect to serum LPS levels [27,28]. In addition, SIBO may contribute to hepatic steatosis by increased levels of trimethylamine-N-oxide (TMAO).…”

Section: Discussionmentioning

confidence: 99%

Small Intestinal Bacterial Overgrowth Is Associated with Non- Alcoholic Fatty Liver Disease

Fialho

André

Thota

et al. 2016

JGLD

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Background: Changes in gut bacteria play a role in type 2 diabetes mellitus (DM) and hepatic steatosis. There is a lack of studies evaluating the frequency and risk factors for non-alcoholic fatty liver disease (NAFLD) in patients tested for small intestinal bacterial overgrowth (SIBO). Aim: To evaluate the frequency of NAFLD and associated risk factors in patients tested for SIBO. Methods: In this case-control study, 372 eligible patients submitted to glucose hydrogen/methane breath test for SIBO who also had an abdominal imaging study were included. Patients were divided into SIBO-positive and SIBO-negative groups. Clinical, demographic and laboratory variables were evaluated in addition to the presence of NAFLD on abdominal imaging. Results: Of the 372 eligible patients, 141 (37.9%) were tested positive for SIBO (study group) and 231 (62.1%) were negative for it (control group). NAFLD occurred in 45.4% (64/141) of the study group compared to 17.3% (40/231) of the control group (p<0.001). Patients in the study group were found to have higher rates of elevated aspartate aminotransferase (AST) (20.6% vs. 11.3%; p=0.034) and alanine aminotransferase (ALT) levels (56.0% vs. 40.7%; p= 0.039), type 2 diabetes (23.4% vs. 13.9%; p=0.041), hypertension (54.6% vs. 40.3%; p=0.046) and metabolic syndrome (78.0% vs. 60.2%; p=0.020). In the multivariate analysis, SIBO (odds ratio [OR]: 1.95; 95% confidence interval [CI]: 1.14-3.31; p=0.014), type 2 DM (OR: 3.04; 95%CI: 1.57-5.90; p=0.001) and obesity (OR: 3.58; 95%CI: 1.70-7.54; p=0.001) remained associated with NAFLD.Conclusion: Patients with SIBO have an increased risk for hepatic steatosis and may benefit from aggressive control of the risk factors for NAFLD including metabolic syndrome. Abbreviations: ALT: alanine aminotransferase; AST: aspartate aminotransferase; BMI: body mass index; CTE: computed tomography enterography; DM: diabetes mellitus; ETOH: ethanol; IL: interleukin; LPS: lipopolysaccharide; NAFLD: non-alcoholic fatty liver disease; NASH: non-alcoholic steatohepatitis; PPI: proton pump inhibitor; SIBO: small intestinal bacterial overgrowth; TLR-4: toll-like receptor 4; TMAO: trimethylamine-N-oxide (TMAO); TNF-α: tumor necrosis factor alpha.

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Increased Orocecal Transit Time in Patients with Nonalcoholic Fatty Liver Disease

Cited by 49 publications

References 20 publications

Is a leaky gut involved in the pathogenesis of intrahepatic cholestasis of pregnancy?

Is a leaky gut involved in the pathogenesis of intrahepatic cholestasis of pregnancy?

Small intestinal bacteria overgrowth decreases small intestinal motility in the NASH rats

Small Intestinal Bacterial Overgrowth Is Associated with Non- Alcoholic Fatty Liver Disease

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