This increase in VLDLR was accompanied by the presence of hepatic steatosis in Pparβ/δ −/− mice compared to wild-type littermates, as demonstrated by ORO and hematoxylin-eosin staining and hepatic triglyceride quantification ( Figure 1 C and D), whereas differences in plasma triglyceride levels did not reach statistical significance (data not shown).
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Hepatic regulation of VLDL receptor by PPARβ/δ and FGF21 modulates non-alcoholic fatty liver disease.
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