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Increased plasma triglyceride concentrations are an independent risk factor for cardiovascular disease.
There was no correlation between changes in plasma triglyceride levels and tHcy levels.
Dietary cholesterol significantly increased plasma and liver cholesterol, and plasma triglyceride concentrations.
Plasma triglyceride (TG) levels in T254I heterozygotes were similar to those in subjects without mutation.
There were no significant changes in plasma triglyceride or HDL cholesterol concentrations after the administration of FM-VP4.
No differences in plasma triglyceride or high-density lipoprotein-cholesterol were observed among groups in the non-fasting state.
In response to bezafibrate therapy, plasma triglyceride and apoC-III levels decreased by 69 and 42%, respectively.
Pre-treatment with UASG inhibited the elevated plasma triglyceride level after the oral administration of the lipid emulsion to rats.
A high dietary protein CHO ratio reduced plasma FGF21 concentration, and increased liver PCK1 protein content and plasma triglyceride concentration.
All samples then underwent assay for plasma amitriptyline by high-performance gas chromatography with the mass selection method and plasma triglyceride estimation by a commercial laboratory.
Consistent with the plasma triglyceride data, hepatic triglyceride concentrations were comparable between the groups (Table 1).
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