Electronic Structure of Heterocyclic Ring Chain Polymers

The band gaps, ionization potentials and electron affinities of conjugated chain polymers comprising heterocyclic aromatic rings are studied systematically as a function of atomic substitutions with N, O and S using first principles density functional calculations

Hepatic fatty acid oxidation : activity, localization and function of some enzymes involved

Fatty acid oxidation is an important pathway for energy production in mammals and birds. In animal tissues the enzymes of fatty acid oxidation are located in the mitochondrion. Recent reports suggest that this is not the case in Castor bean endosperm. In this tissue the enzymes of B-oxidation are localized in a very fragile cell organelle, called the glyoxysomes . Fatty acids are transported in the blood complexed to albumin, or in esterified form as triglycerides and phospholipids, complexed to protein (lipoproteins). Lipoproteins are synthesized in the liverand in the intestinal epithelium (chylomicrons). Before entering the cell these triglycerides are generally hydrolyzed by lipoprotein lipase, an enzyme activated by heparin and probably present in the endothelial cells of the capillary wall. From the foregoing it is evident that fatty acid presented to the cell for further metabolism is in the form of "free" fatty acid. Fatty acids cannot participate in any reaction of intermediary metabolism, before they have been "activated" to their thioester with CoA. This reaction is necessary for triglyceride and phospholipid biosynthesis, for acyl interchange between complex lipids, for chain-elongation reactions and also for oxidative degradation of fatty acids

Characterization of human high-density lipoprotein subclasses LP A-I and LP A-I/A-II and binding to HepG2 cells

Abstract Plasma HDL can be classified according to their apolipoprotein content into at least two types of lipoprotein particles: lipoproteins containing both apo A-I and apo A-II (LP A-I/A-II) and lipoproteins with apo A-I but without apo A-II (LP A-I). LP A-I and LP A-I/A-II were isolated by immuno-affinity chromatography. LP A-I has a higher cholesterol content and less protein compared to LP A-I/A-II. The average particle mass of LP A-I is higher (379 kDa) than the average particle weight of LP A-I/A-II (269 kDa). The binding of 125I-LP A-I to HepG2 cells at 4°C, as well as the uptake of [3H]cholesteryl ether-labelled LP A-I by HepG2 cells at 37° C, was significantly higher than the binding and uptake of LP A-I/A-II. It is likely that both binding and uptake are mediated by apo A-I. Our results do not provide evidence in favor of a specific role for apo A-II in the binding and uptake of HDL by HepG2 cells

Insulin decreases plasma cholesteryl ester transfer but not cholesterol esterification in healthy subjects as well as in normotriglyceridaemic patients with type 2 diabetes

Background. Plasma cholesterol esterification (EST) and subsequent cholesteryl ester transfer (CET) from high-density lipoproteins (HDLs) towards apolipoprotein (apo) B-containing lipoproteins are key steps in HDL metabolism. Materials and methods. The effects of exogenous hyperinsulinaemia on plasma CET and EST, measured with isotope methods, were evaluated in 10 male normotriglyceridaemic (plasma triglycerides < 2.0 mmol L-1) patients with type 2 diabetes and 10 individually matched healthy subjects during a two-step hyperinsulinaemic euglycaemic clamp over 6-7 h. Results. No between-group differences in baseline plasma lipid parameters were observed, but the HDL cholesteryl ester content was lower (P < 0.02) and the HDL triglyceride content was higher (P < 0.05) in diabetic patients. Baseline CET and EST were similar in the groups. In both groups, hyperinsulinaemia decreased plasma triglycerides (P < 0.01) and the HDL triglyceride content (P < 0.01) compared with saline infusion in healthy subjects, whereas the HDL cholesteryl ester content increased (P < 0.05 vs. saline infusion) in diabetic patients. CET was similarly decreased by hyperinsulinaemia in both groups (P < 0.01 vs. saline infusion). In contrast, the change in EST in either group was not different from that during saline administration. In the combined group, baseline CET was positively correlated with plasma triglycerides (R(s) = 0.68, P < 0.01). The HDL cholesteryl ester content was negatively (R(s) = -0.48, P < 0.05) and the HDL triglyceride content was positively (R(s) = 0.64, P < 0.01) correlated with CET. Conclusion. Insulin infusion decreases plasma CET in conjunction with a fall in triglycerides but does not decrease cholesterol esterification in healthy and type 2 diabetic subjects, indicating that acute hyperinsulinaemia has a different effect on these processes involved in HDL metabolism. Despite unaltered fasting plasma CET, HDL core lipid composition was abnormal in diabetic patients, suggesting-that additional mechanisms may contribute to changes in HDL metabolism in diabetes mellitus

Effect of dietary elaidic versus vaccenic acid on blood and liver lipids in the hamster

Male hamsters (30 per group) were fed five different semi-purified diets ad libitum. The diets, containing 30% of energy (en%) as fat, differed in their dietary fat composition (specified fatty acids exchanged at 10 en%) and were fed for 4 weeks. The five fatty acids compared in mixed triglycerides were elaidic acid (C18:1 9t), vaccenic acid (C18:1 11t), their cis-counterpart oleic acid (C18:1 9c), medium-chain fatty acids (MCFA; C8:0 and C10:0), and palmitic acid (C16:0). Compared with oleic acid, dietary MCFA and palmitic acid tended to increase blood cholesterol levels in the hamsters. The effect of elaidic and vaccenic acid on blood cholesterol did not differ from that of oleic acid. When elaidic acid and vaccenic acids were compared directly, the ratio of LDL/HDL-cholesterol in plasma was significantly higher in hamsters fed vaccenic acid than in those fed elaidic acid, and elaidic acid was incorporated at low levels, but more efficiently than vaccenic acid at the sn-2 position of platelet phospholipids. Biological consequences of this low incorporation are considered unlikely as levels of arachidonic acid (C20:4 n-6) and docosohexaenoic acid (C22:6 n-3) in the platelet phospholipids of all dietary groups did not differ. With respect to the effect on the LDL/HDL-cholesterol ratio, elaidic acid may be preferable to vaccenic acid. We conclude that this animal study does not provide evidence for the suggestion, based on epidemiological observations, that elaidic acid would be more detrimental to cardiovascular risk than vaccenic acid

Dialysis of isolated low density lipoprotein induces a loss of lipophilic antioxidants and increases the susceptibility to oxidation in vitro

We determined the effects of different dialysis conditions on the antioxidant content, duration of the lag phase and oxidation rate of LDL. Dialysis for 22 h resulted in a 56%–66% reduction in the concentrations of β-carotene, lycopene and α-tocopherol. The lag phase of copper-induced oxidation of freshly isolated LDL was considerably longer than that of LDL dialysed for 22 or 44 h. Our data show that dialysis may result in LDL preparations with antioxidant compositions that are not truly representative of freshly isolated lipoproteins

Dietary trans fatty acids increase serum cholesterylester transfer protein activity in man

The average diet may provide some 8–10 g/day of unsaturated fatty acids with a trans double bond. Previous studies showed that dietary trans fatty acids may simultaneously raise low-density lipoprotein (LDL) cholesterol and reduce high-density lipoprotein (HDL) cholesterol. Human plasma contains a protein (CETP) which transfers cholesterylesters from HDL to lipoproteins of lower density. We hypothesized that CETP could play a role in the effect of trans fatty acids on lipoproteins and measured the activity levels of CETP in serum samples from a 9-week study in which 55 volunteers were fed three controlled diets with different fatty acid profiles. Mean activity was 114 (% of reference serum) after consumption of a high trans fatty acid diet, as opposed to 96 after linoleic acid and 97 after stearic acid (P < 0.02). We conclude that the increased activity of CETP may contribute to the rise in LDL cholesterol and the fall in HDL cholesterol seen on diets with high contents of trans fatty acids