Apolipoproteins C-II and C-III metabolism in hypertriglyceridemic patients Effect of a drastic triglyceride reduction by combined diet restriction and fenofibrate administration

Kinetics of plasma apolipoprotein C-III as a determinant of diet-induced changes in plasma triglyceride levels

“…Studies have demonstrated that the hypotriglyceridemic effect of fibrates was mediated in part via the peroxisome proliferator-activated receptors (PPAR)-a through the inhibition of apoC-III gene transcription and the upregulation of the LPL gene (Schoonjans et al, 1996). This may explain part of the results obtained by Malmendier et al (1989). Although data concerning the modulating impact of dietary factors on gene expression are still scarce, they are the focus of increasing interest.…”

“…Our results concur with these data in that the lack of change in plasma TG and apoC-III concentrations with the ad libitum consumption of the low-fat control diet mirrored the absence of change in apoCIII metabolism. Malmendier et al (1989) investigated the effect of a combined treatment comprising a restricted hypocaloric diet limited in fat and 300 mg fenofibrate daily on the kinetics of 131 I-apoC-III in four hypertriglyceridemic men. After 1 month of treatment, reductions in plasma TG and apoC-III levels (À56 and À48%, respectively) were observed, which were associated with an increase in apoC-III catabolism and a decrease in apoC-III production.…”

“…After 1 month of treatment, reductions in plasma TG and apoC-III levels (À56 and À48%, respectively) were observed, which were associated with an increase in apoC-III catabolism and a decrease in apoC-III production. Because a combined treatment was used, the authors were not able to differentiate which of the diet and the fenofibrate treatment was responsible for the observed effects (Malmendier et al, 1989). Studies have demonstrated that the hypotriglyceridemic effect of fibrates was mediated in part via the peroxisome proliferator-activated receptors (PPAR)-a through the inhibition of apoC-III gene transcription and the upregulation of the LPL gene (Schoonjans et al, 1996).…”

“…Only a limited number of studies have investigated the impact of nonpharmacological treatments such as diet on plasma apoC-III metabolism and concentration (Huff and Nestel, 1982;Malmendier et al, 1989). We have recently shown that when consumed under ad libitum conditions, a high-fat diet rich in monounsaturated fatty acid (MUFA) significantly reduced plasma TG and apoC-III levels, whereas a low-fat control diet had no significant impact on these variables (Archer et al, 2003a(Archer et al, , 2005.…”

Isotretinoin and fenofibrate induce adiposity with distinct effect on metabolic profile in a rat model of the insulin resistance syndrome

“…Both fibratesFagonists of peroxisome proliferator-activated receptor alpha (PPARa)Fand retinoidsFpanagonists of the retinoic acid receptors RAR and RXRFwere commonly shown to influence triglyceridemia through changing the expression of apolipoprotein C-III (ApoC-III) gene. 6,7 This gene alone as well as the whole ApoA-I/C-III/A-IV cluster (and most recently its new member, ApoA-V) were associated with dyslipidemia in human populations and animal models 3,8 and were also suggested as putative candidates for hypertriglyceridemia in a genetic model of insulin resistance syndrome, polydactylous (PD/Cub) rat strain [9][10][11][12][13][14] (http:// www.img.cas.cz/fb/, Table 1). Therefore, we examined the effect of fenofibrate and isotretinoin administration on metabolic profile, insulin sensitivity and lipolysis in tissues and the expression of ApoC-III and one of its proposed upstream regulatory genes, hepatocyte nuclear factor-4 (Hnf-4), in the PD/Cub rat strain.…”