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To test the hypothesis that the gut microbiota of patients with nonalcoholic fatty liver disease (NAFLD) produces enough ethanol to be a driver of the development and progression of this complex disease, we conducted a prospective clinical study and an intervention study
.
Ethanol
was measured 120 min after the fasting and mixed meal test (MMT) in 146 individuals.
In a subset of 37 people and an external validation cohort, ethanol
in the blood of the portal vein was measured.
In one intervention study, 10 patients with NAFLD and 10 overweight but healthy controls were injected with a selective alcohol dehydrogenase (ADH) inhibitor
before MMT.
Compared with fasting peripheral blood, the median portal ethanol concentration was 187 times (IQR, 17-516) and increased from 2.
1 mM in non-steatosis individuals and 21.
0 mM
in nonalcoholic steatohepatitis with disease progression.
Inhibition of ADH increases the concentration of peripheral blood ethanol in patients with NAFLD by 15 times (IQR, 1.
6-20 times), although this effect is eliminated
after antibiotic therapy.
Specifically, Lactobacidae was associated with postprandial peripheral ethanol concentrations (Spearman ratio, 0.
42; P < 10?5).
Our data show that, for the first time, endogenous ethanol production levels are masked by effects, suggesting that microbial ethanol can be considered the pathogenesis of this highly endemic liver disease
.
.
Ethanol
was measured 120 min after the fasting and mixed meal test (MMT) in 146 individuals.
In a subset of 37 people and an external validation cohort, ethanol
in the blood of the portal vein was measured.
In one intervention study, 10 patients with NAFLD and 10 overweight but healthy controls were injected with a selective alcohol dehydrogenase (ADH) inhibitor
before MMT.
Compared with fasting peripheral blood, the median portal ethanol concentration was 187 times (IQR, 17-516) and increased from 2.
1 mM in non-steatosis individuals and 21.
0 mM
in nonalcoholic steatohepatitis with disease progression.
Inhibition of ADH increases the concentration of peripheral blood ethanol in patients with NAFLD by 15 times (IQR, 1.
6-20 times), although this effect is eliminated
after antibiotic therapy.
Specifically, Lactobacidae was associated with postprandial peripheral ethanol concentrations (Spearman ratio, 0.
42; P < 10?5).
Our data show that, for the first time, endogenous ethanol production levels are masked by effects, suggesting that microbial ethanol can be considered the pathogenesis of this highly endemic liver disease
.
