{
"METABOLOMICS WORKBENCH":{"STUDY_ID":"ST000908","ANALYSIS_ID":"AN001475","VERSION":"1","CREATED_ON":"December 1, 2017, 11:19 am"},

"PROJECT":{"PROJECT_TITLE":"Murine vitamin A deficiency results in a hypermetabolic state and alterations in bacterial community structure and metabolism","PROJECT_SUMMARY":"Vitamin A deficiency (A-) is a significant public health problem. To better understand how vitamin A status influences gut microbiota and host metabolism, we systematically analyzed urine, cecum, serum, and liver samples from vitamin A sufficient (A+) and A- mice using 1H NMR-based metabolomics, quantitative (q)PCR, and 16S rRNA gene sequencing coupled with multivariate data analysis. The microbiota in the cecum of A- mice showed compositional as well as functional shifts compared to the microbiota from A+ mice. Targeted 1H NMR analyses revealed significant changes in microbial metabolite concentrations including higher butyrate and hippurate and decreased acetate and 4-hydroxyphenylacetate in A+ relative to A- mice. Bacterial butyrate-producing genes including butyryl-CoA:acetate CoA-transferase and butyrate kinase were significantly higher in bacteria from A+ versus bacteria from A- mice. A - mice had disturbances in multiple metabolic pathways including alterations in energy metabolism (hyperglycemia, glycogenesis, TCA cycle, and lipoprotein biosynthesis) and the A- host showed metabolites indicative of a hypermetabolic state (higher levels of amino acids and nucleic acids). A- mice had hyperglycemia, liver dysfunction, changes in bacterial metabolism, and altered gut microbial communities. Moreover, integrative analyses indicated a strong correlation between gut microbiota and host energy metabolism pathways in the liver. Vitamin A regulates the microbiota, bacterial metabolism and the effects of vitamin A on the microbiota results in alterations to host metabolism.","INSTITUTE":"The Pennsylvania State University (Penn State)","LAST_NAME":"Nichols","FIRST_NAME":"Robert","ADDRESS":"101 Life science building, University Park, State college, PA, 16803","EMAIL":"rgn5011@psu.edu","PHONE":"7247662694"},

"STUDY":{"STUDY_TITLE":"Murine vitamin A deficiency results in a hypermetabolic state and alterations in bacterial community structure and metabolism. (Cecal contents)","STUDY_SUMMARY":"Vitamin A deficiency (A-) is a significant public health problem. To better understand how vitamin A status influences gut microbiota and host metabolism, we systematically analyzed urine, cecum, serum, and liver samples from vitamin A sufficient (A+) and A- mice using 1H NMR-based metabolomics, quantitative (q)PCR, and 16S rRNA gene sequencing coupled with multivariate data analysis. The microbiota in the cecum of A- mice showed compositional as well as functional shifts compared to the microbiota from A+ mice. Targeted 1H NMR analyses revealed significant changes in microbial metabolite concentrations including higher butyrate and hippurate and decreased acetate and 4-hydroxyphenylacetate in A+ relative to A- mice. Bacterial butyrate-producing genes including butyryl-CoA:acetate CoA-transferase and butyrate kinase were significantly higher in bacteria from A+ versus bacteria from A- mice. A - mice had disturbances in multiple metabolic pathways including alterations in energy metabolism (hyperglycemia, glycogenesis, TCA cycle, and lipoprotein biosynthesis) and the A- host showed metabolites indicative of a hypermetabolic state (higher levels of amino acids and nucleic acids). A- mice had hyperglycemia, liver dysfunction, changes in bacterial metabolism, and altered gut microbial communities. Moreover, integrative analyses indicated a strong correlation between gut microbiota and host energy metabolism pathways in the liver. Vitamin A regulates the microbiota, bacterial metabolism and the effects of vitamin A on the microbiota results in alterations to host metabolism.","INSTITUTE":"Pennsylvania State University","LAST_NAME":"Nichols","FIRST_NAME":"Robert","ADDRESS":"101 Life science building, University park, PA, 16803","EMAIL":"rgn5011@psu.edu","PHONE":"17247662694"},

"SUBJECT":{"SUBJECT_TYPE":"mouse","SUBJECT_SPECIES":"Mus musculus","TAXONOMY_ID":"10090"},
"SUBJECT_SAMPLE_FACTORS":[
{
"Subject ID":"Vit A sufficient",
"Sample ID":"C1",
"Factors":{"Treatment":"Control"},
"Additional sample data":{"Genotype":"Wild-Type"}
},
{
"Subject ID":"Vit A sufficient",
"Sample ID":"C2",
"Factors":{"Treatment":"Control"},
"Additional sample data":{"Genotype":"Wild-Type"}
},
{
"Subject ID":"Vit A sufficient",
"Sample ID":"C3",
"Factors":{"Treatment":"Control"},
"Additional sample data":{"Genotype":"Wild-Type"}
},
{
"Subject ID":"Vit A sufficient",
"Sample ID":"C4",
"Factors":{"Treatment":"Control"},
"Additional sample data":{"Genotype":"Wild-Type"}
},
{
"Subject ID":"Vit A sufficient",
"Sample ID":"C5",
"Factors":{"Treatment":"Control"},
"Additional sample data":{"Genotype":"Wild-Type"}
},
{
"Subject ID":"Vit A sufficient",
"Sample ID":"C6",
"Factors":{"Treatment":"Control"},
"Additional sample data":{"Genotype":"Wild-Type"}
},
{
"Subject ID":"Vit A deficient",
"Sample ID":"T1",
"Factors":{"Treatment":"Vit-A deficient food"},
"Additional sample data":{"Genotype":"Wild-Type"}
},
{
"Subject ID":"Vit A deficient",
"Sample ID":"T2",
"Factors":{"Treatment":"Vit-A deficient food"},
"Additional sample data":{"Genotype":"Wild-Type"}
},
{
"Subject ID":"Vit A deficient",
"Sample ID":"T3",
"Factors":{"Treatment":"Vit-A deficient food"},
"Additional sample data":{"Genotype":"Wild-Type"}
},
{
"Subject ID":"Vit A deficient",
"Sample ID":"T4",
"Factors":{"Treatment":"Vit-A deficient food"},
"Additional sample data":{"Genotype":"Wild-Type"}
},
{
"Subject ID":"Vit A deficient",
"Sample ID":"T5",
"Factors":{"Treatment":"Vit-A deficient food"},
"Additional sample data":{"Genotype":"Wild-Type"}
},
{
"Subject ID":"Vit A deficient",
"Sample ID":"T6",
"Factors":{"Treatment":"Vit-A deficient food"},
"Additional sample data":{"Genotype":"Wild-Type"}
}
],
"COLLECTION":{"COLLECTION_SUMMARY":"Cecal Contents"},

"TREATMENT":{"TREATMENT_SUMMARY":"Twelve male litters were weaned at 3 wks and continuously fed the vitamin A sufficient diet, vitamin A deficient diet, or the vitamin A deficient diet, supplemented with retenoic acid until the end of the experiment."},

"SAMPLEPREP":{"SAMPLEPREP_SUMMARY":"The NMR sample prep for the urine, liver, cecal contents and serum are attached."},

"CHROMATOGRAPHY":{"CHROMATOGRAPHY_TYPE":"-","INSTRUMENT_NAME":"-","COLUMN_NAME":"-"},

"ANALYSIS":{"ANALYSIS_TYPE":"NMR"},

"NM":{"INSTRUMENT_NAME":"Bruker Avance III","INSTRUMENT_TYPE":"FT-NMR","NMR_EXPERIMENT_TYPE":"1D-1H","SPECTROMETER_FREQUENCY":"600 Mhz"},

"NMR_METABOLITE_DATA":{
"Units":"total peak intensity per metabolite",

"Data":[{"Metabolite":"acetate","C1":"35902067.08","C2":"21964262.56","C3":"23959580.48","C4":"4046677.596","C5":"26173025.25","C6":"26868998.41","T1":"33166725.77","T2":"35864804.84","T3":"34445827.99","T4":"27918223.86","T5":"26221084.11","T6":"24380303.54"},{"Metabolite":"propionate","C1":"14420383.85","C2":"10585431.8","C3":"11088992.02","C4":"2039701.981","C5":"10596926.38","C6":"13436571.27","T1":"13981771.55","T2":"14107908.09","T3":"12550751.96","T4":"11722249.3","T5":"9931552.314","T6":"10796258.23"},{"Metabolite":"Butyrate","C1":"12673516.55","C2":"8270391.494","C3":"8635433.809","C4":"1603244.003","C5":"8050290.328","C6":"7895843.467","T1":"10632083.58","T2":"9713683.712","T3":"10146527.99","T4":"8794033.087","T5":"6785268.375","T6":"6605754.46"}],

"Metabolites":[{"metabolite_name":"acetate"},{"metabolite_name":"propionate"},{"metabolite_name":"Butyrate"}]
}

}