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. 2015 Feb;91(2):1-9.
doi: 10.1093/femsec/fiu002. Epub 2014 Dec 5.

Altered gut microbial energy and metabolism in children with non-alcoholic fatty liver disease

Sonia Michail  1 , Malinda Lin  2 , Mark R Frey  2 , Rob Fanter  3 , Oleg Paliy  4 , Brian Hilbush  5 , Nicholas V Reo  4
Affiliations

Altered gut microbial energy and metabolism in children with non-alcoholic fatty liver disease

Sonia Michail et al. FEMS Microbiol Ecol. 2015 Feb.

Abstract

Obesity is becoming the new pediatric epidemic. Non-alcoholic fatty liver disease (NAFLD) is frequently associated with obesity and has become the most common cause of pediatric liver disease. The gut microbiome is the major metabolic organ and determines how calories are processed, serving as a caloric gate and contributing towards the pathogenesis of NAFLD. The goal of this study is to examine gut microbial profiles in children with NAFLD using phylogenetic, metabolomic, metagenomic and proteomic approaches. Fecal samples were obtained from obese children with or without NAFLD and healthy lean children. Stool specimens were subjected to 16S rRNA gene microarray, shotgun sequencing, mass spectroscopy for proteomics and NMR spectroscopy for metabolite analysis. Children with NAFLD had more abundant Gammaproteobacteria and Prevotella and significantly higher levels of ethanol, with differential effects on short chain fatty acids. This group also had increased genomic and protein abundance for energy production with a reduction in carbohydrate and amino acid metabolism and urea cycle and urea transport systems. The metaproteome and metagenome showed similar findings. The gut microbiome in pediatric NAFLD is distinct from lean healthy children with more alcohol production and pathways allocated to energy metabolism over carbohydrate and amino acid metabolism, which would contribute to development of disease.

Keywords: NASH; carbohydrate; energy metabolism; gut microbiome; obesity.

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Figures

None
This study describes the gut microbial profile of obese children with and without fatty liver and identifies several key metabolites that have potential to contribute to the pathophysiology of this common disease.
Figure 1.
Figure 1.
Distribution of COG functional categories in healthy children and obese children with NAFLD.
Figure 2.
Figure 2.
Total assigned MS/MS spectra for COG-catalogued proteins that were found to be differentially expressed by a factor of at least three. C: energy production and conversion; CQ: COG functional categories C and Q (secondary metabolites biosynthesis, transport and catabolism); E: amino acid transport and metabolism; ET: COG functional categories E and T (signal transduction mechanisms); G: carbohydrate transport and metabolism; H: coenzyme transport and metabolism; J: translation, ribosomal structure and biogenesis; O: post translational modifications, protein turnover, chaperones; U: intracellular trafficking, secretion and vesicular support.
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