Ptprd deficiency promotes a phenotype of metabolic disease. (IMAGE)
Caption
(a) Ptprd-deficient liver disease mouse model. Male Ptprd+/+ (n=22) and Ptprd+/− (n=13) mice aged 8 weeks received 16 weeks of CDA-HFD, followed by 8 weeks of normal diet before sacrifice. (b) Ptprd±mice show a similar incremental weight gain as compared with Ptprd+/+ mice following CDA-HFD during the 16-week period. (c) Ptprd+/− mice present significantly (T-test) higher levels of fasting blood glucose compared with Ptprd+/+ mice after 8 weeks of CDA-HFD. (d-e) Ptprd+/− mice (n=6) present significantly (U-test) higher hepatic lipid levels following CDA-HFD, as compared with Ptprd+/+ mice (n=10). Microscopy analysis with Oil red O staining. Bar represents 500 µm. (f–h) Ptprd-deficient mice present a dysregulated hepatic lipid profile. Ptprd+/− mice (n=6) show a significant alteration (U-test) in the intrahepatic levels of palmitic, oleic and γ-linoleic acids, as compared with Ptprd+/+ mice (n=10) following CDA-HFD. Data are represented as µmol/L normalised to total protein concentration. CDA-HFD, choline-deficient, L-amino acid defined, high-fat diet; n.s., not significant; Ptprd, protein tyrosine phosphatase delta. *P<0.05, **p<0.01, ***p<0.001, ****p<0.0001.
Credit
By Armando Andres Roca Suarez, Frank Jühling, Julien Moehlin et al.
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