Fig 5. Lipg deficiency delays TRL lipolysis in mice.

A.³H oleate plasma clearance curves from EL WT vs. Lipg^-/- mice administered ³H-triolein labeled human TRLs. Mice were administered radiolabeled TRLs and plasma ³H levels were measured over 15 minutes and normalized to the 1 minute timepoint. B. Clearance of ¹²⁵I tyramine cellobiose labeled human TRLs in EL WT vs. Lipg^-/- mice fed a high fat diet for 12 weeks. Plasma clearance of ¹²⁵I-TRL apolipoprotein B (apoB) after intravenous TRL administration was measured over 15 minutes. C. ³H-triolein-labeled TRL clearance in WT mice treated with AAV Null vector, Lipg^-/- mice treated with AAV Null, or Lipg^-/- mice treated with AAV expressing murine Lipg and all fed a high-fat diet for 12 weeks and then treated with radiolabeled TRLs as described in (A). D. Uptake of ³H-oleate into the indicated tissues after 15 min of administration of ³H-triolein labeled TRLs in the mice from (A). ³H activity in a fixed amount of tissue was normalized to the 1 minute plasma ³H activity for each mouse. Normalized tissue ³H activity is expressed for each tissue relative to the mean of the WT group. E. Hepatic mRNA expression of Lpl and Lipc in mice from (A). Quantitative real-time PCR cycle number for each gene was normalized to that of β-actin. F. Immunoblots of LPL and HL from liver lysates of mice in (A). Immunoblots of the proteins from the lysates for β-actin are shown as a loading control. A, C: *P<0.05, ****P<0.0001, repeated factor 2-way ANOVA. D & E: *P<0.05, **P<0.01, ****P<0.0001, student’s unpaired T-test. Data is expressed as mean ± S.E.M.