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In vitro studies suggest that liver fatty acid binding protein (L-FABP) and sterol carrier protein-2/sterol carrier protein-x (SCP2/SCPx) gene products facilitate uptake and metabolism and detoxification of dietary-derived phytol in mammals. However, concomitant upregulation of L-FABP in SCP2/SCPx null mice complicates interpretation of their physiological phenotype. Therefore, the impact of ablating both the L-FABP gene and SCP2/SCPx gene (L-FABP/SCP2/SCPx null or TKO) was examined in phytol-fed female wild-type (WT) and TKO mice. TKO increased hepatic total lipid accumulation, primarily phospholipid, by mechanisms involving increased hepatic levels of proteins in the phospholipid synthetic pathway. Concomitantly, TKO reduced expression of proteins in targeting fatty acids towards the triacylglycerol synthetic pathway. Increased hepatic lipid accumulation was not associated with any concomitant upregulation of membrane fatty acid transport/translocase proteins involved in fatty acid uptake (FATP2, FATP4, FATP5 or GOT) or cytosolic proteins involved in fatty acid intracellular targeting (ACBP). In addition, TKO exacerbated dietary phytol-induced whole body weight loss, especially lean tissue mass. Since individually ablating SCPx or SCP2/SCPx elicited concomitant upregulation of L-FABP, these findings with TKO mice help to resolve the contributions of SCP2/SCPx gene ablation on dietary phytol-induced whole body and hepatic lipid phenotype independent of concomitant upregulation of L-FABP.
Pubmed ID: 27940000 RIS Download
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Database enables integration of genomic and phenomic data by providing access to primary experimental data, data collection protocols and analysis tools. Data represent behavioral, morphological and physiological disease-related characteristics in naive mice and those exposed to drugs, environmental agents or other treatments. Collaborative standardized collection of measured data on laboratory mouse strains to characterize them in order to facilitate translational discoveries and to assist in selection of strains for experimental studies. Includes baseline phenotype data sets as well as studies of drug, diet, disease and aging effect., protocols, projects and publications, and SNP, variation and gene expression studies. Provides tools for online analysis. Data sets are voluntarily contributed by researchers from variety of institutions and settings, or retrieved by MPD staff from open public sources. MPD has three major types of strain-centric data sets: phenotype strain surveys, SNP and variation data, and gene expression strain surveys. MPD collects data on classical inbred strains as well as any fixed-genotype strains and derivatives that are openly acquirable by the research community. New panels include Collaborative Cross (CC) lines and Diversity Outbred (DO) populations. Phenotype data include measurements of behavior, hematology, bone mineral density, cholesterol levels, endocrine function, aging processes, addiction, neurosensory functions, and other biomedically relevant areas. Genotype data are primarily in the form of single-nucleotide polymorphisms (SNPs). MPD curates data into a common framework by standardizing mouse strain nomenclature, standardizing units (SI where feasible), evaluating data (completeness, statistical power, quality), categorizing phenotype data and linking to ontologies, conforming to internal style guides for titles, tags, and descriptions, and creating comprehensive protocol documentation including environmental parameters of the test animals. These elements are critical for experimental reproducibility.
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