{
"METABOLOMICS WORKBENCH":{"STUDY_ID":"ST000907","ANALYSIS_ID":"AN001474","VERSION":"1","CREATED_ON":"December 1, 2017, 11:09 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.(Urine)","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":"urine"},

"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":"hippurate","C1":"250.6731656","C2":"202.6968613","C3":"196.6267142","C4":"216.9695819","C5":"179.4161928","C6":"239.9963858","T1":"198.7595936","T2":"203.3415659","T3":"167.9743074","T4":"142.8332548","T5":"172.679867","T6":"189.3842227"},{"Metabolite":"PAG","C1":"509.5759996","C2":"444.5828599","C3":"421.1258148","C4":"448.7129039","C5":"607.7959892","C6":"494.2317124","T1":"524.3036306","T2":"507.2351136","T3":"400.9022055","T4":"380.950891","T5":"447.2819154","T6":"447.7920189"},{"Metabolite":"IS","C1":"281.3477471","C2":"170.3647059","C3":"209.6309101","C4":"198.8115116","C5":"266.6106797","C6":"217.3031097","T1":"311.5927087","T2":"283.605262","T3":"287.2129253","T4":"172.141199","T5":"230.6551593","T6":"223.5808028"},{"Metabolite":"4-HPA","C1":"294.9234518","C2":"265.3563264","C3":"232.230322","C4":"242.3776327","C5":"447.1892373","C6":"270.7525755","T1":"209.6754708","T2":"294.7596491","T3":"186.6210147","T4":"236.8927987","T5":"245.4384213","T6":"201.2817186"},{"Metabolite":"TMAO","C1":"7.886985229","C2":"6.370776033","C3":"6.760731579","C4":"7.859306449","C5":"7.065138793","C6":"7.948923333","T1":"8.031412518","T2":"9.267394979","T3":"8.06568439","T4":"7.2022188","T5":"7.789678872","T6":"6.889986525"}],

"Metabolites":[{"metabolite_name":"hippurate"},{"metabolite_name":"PAG"},{"metabolite_name":"IS"},{"metabolite_name":"4-HPA"},{"metabolite_name":"TMAO"}]
}

}