Plasma delipidation process induces rapid regression of atherosclerosis and mobilisation of adipose tissue

Abstract

Cholesterol is a major component of atherosclerotic plaques. Cholesterol accumulation within the arterial intima and atherosclerotic plaques is determined by the difference of cellular cholesterol synthesis and/or influx from apo B-containing lipoproteins and cholesterol efflux. In humans, apo A-1 Milano infusion has led to rapid regression of atherosclerosis in coronary arteries. We hypothesised that a multifunctional plasma delipidation process (PDP) would lead to rapid regression of experimental atherosclerosis and probably impact on adipose tissue lipids. In hyperlipidemic animals, the plasma concentrations of cholesterol, triglyceride and phospholipid were, respectively, 6-, 157-, and 18-fold higher than control animals, which consequently resulted in atherosclerosis. PDP consisted of delipidation of plasma with a mixture of butanol-diisopropyl ether (DIPE). PDP removed considerably more lipid from the hyperlipidemic animals than in normolipidemic animals. PDP treatment of hyperlipidemic animals markedly reduced intensity of lipid staining materials in the arterial wall and led to dramatic reduction of lipid in the adipose tissue. Five PDP treatments increased apolipoprotein A1 concentrations in all animals. Biochemical and hematological parameters were unaffected during PDP treatment. These results show that five PDP treatments led to marked reduction in avian atherosclerosis and removal of lipid from adipose tissue. PDP is a highly effective method for rapid regression of atherosclerosis.

Detergent-Mediated Phospholipidation of Plasma Lipoproteins Increases HDL Cholesterophilicity and Cholesterol Efflux via SR-BI

“…Although lipid-free apo A-I induces cholesterol and phospholipid efflux via the ABCA1 transporter (15,37), the PC component of HDL is directly involved in efflux via SR-BI (10,38), ABCG1 (39), and spontaneous transfer (40)(41)(42). Although short-chained PCs spontaneously associate with and enrich plasma lipoproteins (8)(9)(10)(43)(44)(45), naturally occurring PCs are resistant to spontaneous incorporation into lipoproteins (Figure 1). Moreover, the short plasma lifetime of short-chained PCs (46), such as dimyristoyl-PC, which is frequently used to prepare reassembled (r)HDL, makes them unlikely candidates for therapeutic use.…”

Not All “BAD” Cholesterol Carriers Are Necessarily Bad and Not All “GOOD” Cholesterol Carriers Are as Good as Can Be: Plasma Delipidation, a Non-Pharmacological Treatment for Atherosclerosis

“…Batch LA-treatments on five consecutive days corresponding to treatments of 1.25 of body plasma volume, resulted in markedly reduced lipid in the arterial wall as well as marked increases in the lumen diameter [20].…”

Intravascular infusion of autologous delipidated plasma induces antiatherogenic lipoproteins and causes regression of atherosclerosis <br>—Studies in non-primates, monkeys and humans

“…Five LA treatments in normolipidemic and hyperlipidemic animals with increased concentration of plasma cholesterol, triglycerides and phospholipids resulted in the removal of considerably more lipid from hyperlipidemic animals than in normolipidemic animals. LA treatments of hyperlipidemic animals markedly reduced atherosclerosis in the arterial wall and also led to dramatic reduction of lipid in the adipose tissue [38,42]. Five LA treatments also increased the concentrations of ApoA1 in both normolipidemic and hyperlipidemic animals [42,43].…”

“…LA treatments of hyperlipidemic animals markedly reduced atherosclerosis in the arterial wall and also led to dramatic reduction of lipid in the adipose tissue [38,42]. Five LA treatments also increased the concentrations of ApoA1 in both normolipidemic and hyperlipidemic animals [42,43]. It is not known whether these increases were due to increased synthesis or decreased catabolism.…”