Ethanol Production by Selected Intestinal Microorganisms and Lactic Acid Bacteria Growing under Different Nutritional Conditions

Abstract

To gain some specific insight into the roles microorganisms might play in non-alcoholic fatty liver disease (NAFLD), some intestinal and lactic acid bacteria and one yeast (Anaerostipes caccae, Bacteroides thetaiotaomicron, Bifidobacterium longum, Enterococcus fecalis, Escherichia coli, Lactobacillus acidophilus, Lactobacillus fermentum, Lactobacillus plantarum, Weissella confusa, Saccharomyces cerevisiae) were characterized by high performance liquid chromatography for production of ethanol when grown on different carbohydrates: hexoses (glucose and fructose), pentoses (arabinose and ribose), disaccharides (lactose and lactulose), and inulin. Highest amounts of ethanol were produced by S. cerevisiae, L. fermentum, and W. confusa on glucose and by S. cerevisiae and W. confusa on fructose. Due to mannitol-dehydrogenase expressed in L. fermentum, ethanol production on fructose was significantly (P < 0.05) reduced. Pyruvate and citrate, two potential electron acceptors for regeneration of NAD+/NADP+, drastically reduced ethanol production with acetate produced instead in L. fermentum grown on glucose and W. confusa grown on glucose and fructose, respectively. In fecal slurries prepared from feces of four overweight volunteers, ethanol was found to be produced upon addition of fructose. Addition of A. caccae, L. acidophilus, L. fermentum, as well as citrate and pyruvate, respectively, abolished ethanol production. However, addition of W. confusa resulted in significantly (P < 0.05) increased production of ethanol. These results indicate that microorganisms like W. confusa, a hetero-fermentative, mannitol-dehydrogenase negative lactic acid bacterium, may promote NAFLD through ethanol produced from sugar fermentation, while other intestinal bacteria and homo- and hetero-fermentative but mannitol-dehydrogenase positive lactic acid bacteria may not promote NAFLD. Also, our studies indicate that dietary factors interfering with gastrointestinal microbiota and microbial metabolism may be important in preventing or promoting NAFLD.

An Intestinal Microbiota–Farnesoid X Receptor Axis Modulates Metabolic Disease

“…Bacteria community analysis, based on 16S rRNA gene sequencing, has revealed stark differences between metabolically-normal individuals and those with NAFLD and NASH. Broad phyla level (noted shifts in Bacteroidetes, Firmicutes, and Proteobacteria) changes have been reported and some have attempted to implicate specific bacterial strains with disease, although these observations remain preliminary 16–18 . Interestingly, stool bacterial community profiles of children with NAFLD are unique compared with adults with NAFLD, but this inconsistency might be expected given observations from others 19 .…”

Gut Microbial Metabolism and Nonalcoholic Fatty Liver Disease

“…A number of studies have demonstrated that children and adolescents with NAFLD have increased serum ethanol levels, although this finding is not consistent across all studies . The gut microbiome can generate ethanol from dietary precursors, and manipulation of the gut microbiome is known to alter endogenous ethanol production . A common finding in NAFL and NASH is enrichment in Escherichia and/or Lactobacillus genera , which have the capability to produce ethanol.…”

“…(69) The gut microbiome can generate ethanol from dietary precursors, and manipulation of the gut microbiome is known to alter endogenous ethanol production. (128) A common finding in NAFL and NASH is enrichment in Escherichia and/ or Lactobacillus genera, (65,(68)(69)(70)(71)74,75,(77)(78)(79) which have the capability to produce ethanol. These findings suggest that increased endogenous ethanol production by the gut microbiome could contribute to the pathogenesis of NAFLD.…”

Anti-Contamination Strategies for Yeast Fermentations

“…fermentum produces lactate, acetate, and mannitol from the mixture of glucose and fructose in sugarcane juice. The acidic products cause a decrease in sugar consumption, growth inhibition of S. cerevisiae, and a decrease in ethanol production [64]. If S. cerevisiae is contaminated by L. fermentum, flocculation (co-aggregation) of S. cerevisiae with L. fermentum can occur [65][66][67].…”