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  • 1
    Keywords: INHIBITION ; MODEL ; GENE ; GENE-EXPRESSION ; METABOLISM ; MICE ; OBESITY ; inflammation ; MOUSE MODELS ; COACTIVATOR PGC-1 ; INSULIN-RESISTANCE ; TECHNOLOGY ; NUCLEAR RECEPTORS ; Hepatic expression of transcriptional cofactor TBL1 is impaired in fatty livers ; Hepatic deficiency in TBL1 promotes liver steatosis and hypertriglyceridemia ; Hepatic TBL1 acts in concert with TBLR1 and nuclear receptor PPARα ; NONALCOHOLIC FATTY LIVER ; STIMULATED LIPOPROTEIN RECEPTOR
    Abstract: The aberrant accumulation of lipids in the liver ("fatty liver") is tightly associated with several components of the metabolic syndrome, including type 2 diabetes, coronary heart disease, and atherosclerosis. Here we show that the impaired hepatic expression of transcriptional cofactor transducin beta-like (TBL) 1 represents a common feature of mono- and multigenic fatty liver mouse models. Indeed, the liver-specific ablation of TBL1 gene expression in healthy mice promoted hypertriglyceridemia and hepatic steatosis under both normal and high-fat dietary conditions. TBL1 deficiency resulted in inhibition of fatty acid oxidation due to impaired functional cooperation with its heterodimerization partner TBL-related (TBLR) 1 and the nuclear receptor peroxisome proliferator-activated receptor (PPAR) alpha. As TBL1 expression levels were found to also inversely correlate with liver fat content in human patients, the lack of hepatic TBL1/TBLR1 cofactor activity may represent a molecular rationale for hepatic steatosis in subjects with obesity and the metabolic syndrome.
    Type of Publication: Journal article published
    PubMed ID: 21459324
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  • 2
    ISSN: 1432-2013
    Keywords: Key words Conductance scanning ; Epithelial barrier ; Epithelial transport ; Impedance ; Intestinal biopsy specimens ; Secretion ; Tissue distension ; Ussing chamber
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Ussing chamber experiments with human intestinal tissue are impeded by the small size of forceps biopsy specimens. Therefore, a miniaturized container insert featuring low edge damage was designed with an exposure area of only 0.05 cm2. It allows measurement of short-circuit current (I SC) and transmural resistance (R t) on endoscopically obtained biopsy specimens, as well as alternating current impedance analysis and conductance scanning. Comparison with larger specimens mounted in a conventional Ussing chamber without the insert (exposure area 0.54 cm2) was made using rat jejunum and rectum. No differences in I SC, R t, or secretory response were found, indicating proper sealing and prevention of edge damage, as well as tissue viability in the container system. If biopsy samples obtained from human rectum were mounted in the insert, the local resistance near the edge was almost the same as the overall resistance (52.3 Ω·cm2). Epithelial and subepithelial resistances of human rectum were 43±1 Ω·cm2 and 10±1 Ω·cm2, respectively. In conclusion, we present a tool that allows reliable Ussing-type, impedance, and conductance scanning measurements to be made from intestinal biopsy specimens.
    Type of Medium: Electronic Resource
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