<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Chen P</submitter><funding>BLRD VA</funding><funding>NIDDK NIH HHS</funding><funding>NIAAA NIH HHS</funding><pagination>203-214.e16</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4274236</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>148(1)</volume><pubmed_abstract>&lt;h4>Background &amp; aims&lt;/h4>Alcoholic liver disease is a leading cause of mortality. Chronic alcohol consumption is accompanied by intestinal dysbiosis, and development of alcoholic liver disease requires gut-derived bacterial products. However, little is known about how alterations to the microbiome contribute to pathogenesis of alcoholic liver disease.&lt;h4>Methods&lt;/h4>We used the Tsukamoto-French mouse model, which involves continuous intragastric feeding of isocaloric diet or alcohol for 3 weeks. Bacterial DNA from the cecum was extracted for deep metagenomic sequencing. Targeted metabolomics assessed concentrations of saturated fatty acids in cecal contents. To maintain intestinal metabolic homeostasis, diets of ethanol-fed and control mice were supplemented with saturated long-chain fatt</pubmed_abstract><journal>Gastroenterology</journal><pubmed_title>Supplementation of saturated long-chain fatty acids maintains intestinal eubiosis and reduces ethanol-induced liver injury in mice.</pubmed_title><pmcid>PMC4274236</pmcid><funding_grant_id>R01 AA020216</funding_grant_id><funding_grant_id>K23 DK090303</funding_grant_id><funding_grant_id>R01 AA020203</funding_grant_id><funding_grant_id>I01 BX002213</funding_grant_id><funding_grant_id>K08 DK081830</funding_grant_id><funding_grant_id>U24 DK097153</funding_grant_id><funding_grant_id>P50 AA011999</funding_grant_id><funding_grant_id>RC2 AA019405</funding_grant_id><funding_grant_id>U01 AA021856</funding_grant_id><funding_grant_id>R01 AA020703</funding_grant_id><pubmed_authors>Starkel P</pubmed_authors><pubmed_authors>Nelson KE</pubmed_authors><pubmed_authors>van Pijkeren JP</pubmed_authors><pubmed_authors>Ho SB</pubmed_authors><pubmed_authors>Chen P</pubmed_authors><pubmed_authors>Torralba M</pubmed_authors><pubmed_authors>Tan J</pubmed_authors><pubmed_authors>Bajaj JS</pubmed_authors><pubmed_authors>Mutlu EA</pubmed_authors><pubmed_authors>Embree M</pubmed_authors><pubmed_authors>Tsukamoto H</pubmed_authors><pubmed_authors>Keshavarzian A</pubmed_authors><pubmed_authors>Schnabl B</pubmed_authors><pubmed_authors>Fouts DE</pubmed_authors><pubmed_authors>DePew J</pubmed_authors><pubmed_authors>Loomba R</pubmed_authors><pubmed_authors>Zengler K</pubmed_authors></additional><is_claimable>false</is_claimable><name>Supplementation of saturated long-chain fatty acids maintains intestinal eubiosis and reduces ethanol-induced liver injury in mice.</name><description>&lt;h4>Background &amp; aims&lt;/h4>Alcoholic liver disease is a leading cause of mortality. Chronic alcohol consumption is accompanied by intestinal dysbiosis, and development of alcoholic liver disease requires gut-derived bacterial products. However, little is known about how alterations to the microbiome contribute to pathogenesis of alcoholic liver disease.&lt;h4>Methods&lt;/h4>We used the Tsukamoto-French mouse model, which involves continuous intragastric feeding of isocaloric diet or alcohol for 3 weeks. Bacterial DNA from the cecum was extracted for deep metagenomic sequencing. Targeted metabolomics assessed concentrations of saturated fatty acids in cecal contents. To maintain intestinal metabolic homeostasis, diets of ethanol-fed and control mice were supplemented with saturated long-chain fatt</description><dates><release>2015-01-01T00:00:00Z</release><publication>2015 Jan</publication><modification>2026-06-04T00:39:33.502Z</modification><creation>2019-03-27T01:42:13Z</creation></dates><accession>S-EPMC4274236</accession><cross_references><pubmed>25239591</pubmed><doi>10.1053/j.gastro.2014.09.014</doi></cross_references></HashMap>