Changes in the serum lipoprotein pattern induced by two low-fat diets with a different vegetable content in hypercholesterolemic patients.

Thirty-two hypercholesterolemic outpatients were treated by a conventional low-fat diet (carbohydrate 56%; fat 25%; vegetable proteins 7%; animal proteins 12% of energy; P/S ratio 1.0). After 1 month T-C decreased by 11%, VLDL-C by 32%, LDL-C by 8%, HDLt-C by 10% and HDL2-C by 11%. Thirty-two comparable patients were treated by a different low-fat diet which provided 69% of energy as carbohydrate, 19% as fat, 7% as vegetable proteins and 5% as animal proteins; P/S ratio was 1.3. After 1 month T-C decreased by 9% and LDL-C by 12%. VLDL-C, HDL2-C and HDL3-C did not change significantly. A cross-over study on 24 patients confirmed that both diets have lowering effects on T-C and LDL-C levels, but only the conventional low-fat diet decreases VLDL-C and HDL2-C.

Solid-phase microextraction gas chromatography/mass spectrometric analysis of volatile organic compounds in water

In this work, a solid-phase microextraction (SPME) method for the extraction of volatile organic compounds (VOCs) from water samples has been developed. Fifty-five volatile compounds (from the sixty listed in EPA method no. 524.2) were extracted from aqueous solutions using an SPME fiber coated with Carboxen-polydimethylsiloxane (Carboxen-PDMS), 75 &mgr;m film thickness. Time of sampling and chromatographic separation conditions were optimised. Standard solutions of VOC mixtures with concentrations as low as 0.05 ppb were analysed and their signal/noise ratios measured. Linearity of response for each component of the mixture was tested and mass spectral quality evaluated. A comparison with purge and trap analysis of VOCs was made. The method was applied to real-world samples of drinking, surface and leaching waters. Copyright 1999 John Wiley & Sons, Ltd.

Long-term effects of bezafibrate and of a bezafibrate and cholestyramine combination on lipids and lipoprotein lipids in type IIa hypercholesterolaemic patients.

Eighteen hypercholesterolaemic patients have been treated for four months with bezafibrate 200 mg thrice daily. After one month of therapy, total cholesterol (T-C) decreased on the average by 19%, total triglycerides (T-TG) by 28%, very low density lipoprotein-TG by 47%, LDL-C by 25% and HDL3-C increased by 16%. At the fourth month of therapy the lipoprotein pattern was unchanged as compared to the one observed at the first month. In 12 patients T-C was normalized by bezafibrate and the patients continued the treatment for one year without experiencing further changes in lipoprotein pattern. Six patients with severe hypercholesterolaemia (mean baseline T-C of 11.51 +/- 0.63 mmoles/l) failed to adequately respond to bezafibrate treatment and were put on the combined bezafibrate 600 mg/day and cholestyramine 16g/day therapy. During bezafibrate their T-C decreased on the average by 21% and LDL-C by 23% and during the combined therapy by 33% and by 37% respectively, as compared to the baseline values. Combined bezafibrate and cholestyramine treatment seems then to be more effective than bezafibrate alone in decreasing serum cholesterol and may be useful in patients with severe hypercholesterolaemia.

[Serum lipoproteins and coronary disease in diabetes. Changes in the lipoprotein pattern in relation to the type of antidiabetic therapy]. / Lipoproteine sieriche e malattia coronarica nel diabete. Modificazione del quadro lipoproteico in relazione al tipo della terapia antidiabetica.

One hundred and fifty seven maturity-onset diabetics (77 males and 80 females) with coronary heart disease (CHD) were compared with 130 non-CHD diabetic patients (62 males and 68 females) of the same age-range. Integrated mean blood pressure, duration of diabetes, serum triglycerides, beta and prebeta-lipoproteins were significantly higher and alpha lipoproteins significantly lower in CHD than in non-CHD patients. Alpha lipoproteins, duration of diabetes and beta lipoproteins were the variables of highest weight in discriminating CHD from non-CHD patients. Alpha lipoprotein had a greater discriminating power than beta lipoprotein in man, while in women the opposite occurred. In patients on insulin and on sulfonylurea therapy, both with and without CHD, the concentration of alpha lipoproteins, but not of other lipoproteins, was higher than in the corresponding subgroups of the diet-treated patients. However, within each treatment group, patients with CHD had lower alpha lipoproteins.

Effects of acetylsalicylic acid on plasma lipids and on post-heparin lipase activities.

Acetylsalicylic acid (ASA) was administered orally at the dose of 3 g a day for 2 days to healthy subjects. Plasma free fatty acids, serum triglycerides and prebetalipoproteins were significantly decreased, while cholesterol, beta and alpha 1 lipoproteins did not change. The two fractions (protamine-resistant and protamine-inactivated) of plasma post-heparin lipoprotein lipase activity (PHLA) significantly fell after ASA. PHLA diminution was reproduced by direct addition of ASA or sodium salicylate or of plasma from individuals under treatment with ASA to post-heparin plasma of untreated subjects and is, therefore, explained by a direct inactivation. The inhibition of PHLA was not followed by a significant impairment of the removal of circulating triglycerides.

Influence of two non-steroidal anti-inflammatory drugs on lipolysis and on plasma post-heparin lipoprotein lipase activity in normal man.

Indomethacin 50 mg i.v. or p.o. and diclofenac sodium 50 mg p.o. produced a prompt and significant increase in plasma free fatty acid concentration. In 10 subjects who took indomethacin 150 mg/d p.o. for 3 days, plasma post-heparin lipoprotein lipase activity was also significantly increased. The same effect occurred in 9 subjects treated for 3 days with diclofenac sodium 50 mg t.d.s. Since both indomethacin and diclofenac sodium are potent inhibitors of prostaglandin synthetase, these findings are consistent with the hypothesis tht prostaglandins are involved in the feed-back regulation of lipolysis, and mediate the inhibitory effect of lipolysis on lipoprotein lipase activity.

Evidence of an effect of inhaled disodium cromoglycate on lipid metabolism in man: enhanced lipolysis and decreased plasma post-heparin lipase activities.

Inhalation of therapeutic doses of disodium cromoglycate (DSCG) was followed by a prompt increase of plasma free fatty acids (FFA). After treatment with DSCG for 3 days both hepatic and non-hepatic (lipoprotein lipase sensu strictiori) plasma post-heparin lipoprotein lipase activities were significantly depressed. No significant change was induced on serum lipids and lipoproteins, nor on the fat tolerance curve, though a trend to an elevation of this last parameter was noted. Our results show that the inhalation of DSCG produces systemic metabolic effects, being in accord with the view that this drug raises intracellular cyclic adenosine monophosphate. Furthermore, they support the contention that lipoprotein lipase activity is controlled by intracellular concentration of FFA and/or cyclic adenosine monophosphate.

Probucol and cholestyramine combination in the treatment of severe hypercholesterolemia.

This study was carried out to evaluate the effect of the combined probucol and cholestyramine treatment on the lipoprotein pattern of hypercholesterolemic patients. Probucol was given in the dose of 1 g and cholestyramine in the dose of 16 g per day in 3 different sequences: Probucol, Cholestyramine, Probucol + Cholestyramine; Probucol + Cholestyramine, Probucol, Cholestyramine; Cholestyramine, Probucol + Cholestyramine, Probucol. After a period of dietary stabilization, 12 patients were randomly allocated to one of the treatment sequences to be followed for 9 months. Each treatment period lasted 3 months. During the cholestyramine period serum cholesterol decreased on the average by 18% and LDL cholesterol by 26%; during probucol, the mean decrease was 13% and 14%, and during the combined therapy 26% and 32%, respectively. Serum triglycerides and VLDL cholesterol showed a trend toward an increase during the cholestyramine period. HDL2 cholesterol significantly decreased during probucol treatment. Variation in both VLDL and HDL2 cholesterol observed when the drugs were given singly were no longer seen during the combination therapy.

Changes in serum lipoprotein pattern following bezafibrate. Differential effects in type IIa and in type IIb hyperlipoproteinemic patients.

Sixteen type IIb and 26 type IIa hyperlipoproteinemic patients were treated with bezafibrate 200 mg t.i.d. After 1 month VLDL-TG decreased by 54% in type IIb and by 43% in type IIa; LDL-C decreased by 13% in type IIb and by 23% in type IIa patients. HDL3-C rose in both group of patients, while HDL2-C significantly increased (52%) only in patients with phenotype IIb. The change in LDL-C and in HDL2-C concentrations resulted to be related to the pretreatment VLDL lipid concentration and to its change during the treatment. Twenty patients were treated with bezafibrate for 4 months. On the average, the changes in lipoprotein lipid concentration attained at the end of the first month of therapy remained substantially constant in the following 3 months.

Serum lipoprotein subfractions before and during low-calorie diet in obese women.

Twenty-five obese women were put on low-calorie diet for one month. The mean weight loss was 2.7 kg and was accompanied by a 9% decrease of LDL-cholesterol. LDL-apolipoprotein B (in 13 subjects) showed a 16% fall and LDL-triglyceride levels did not change. The results suggest both a decrease of LDL concentration and a relative increase of triglyceride-rich particles in the density range of 1.006-1.063. HDL2-cholesterol showed a 17% decrease and HDL3-cholesterol a 16% increase. Total and lipoprotein triglycerides were not modified. The changes of lipoprotein pattern suggest a sluggish VLDL catabolism by lipoprotein lipase. In 10 women followed for 6 months the decrease of LDL-cholesterol seen after one month of diet was no more present at the 6th month, while the decrease of HDL2-cholesterol and the increase of HDL3-cholesterol were still evident. At the end of the 6th month a slight but significant decrease of total and VLDL-triglycerides also occurred.

Increase in lipolysis and decrease in plasma-heparin lipoprotein lipase activity and alpha 1 lipoprotein level after aminophylline in man.

Intravenous aminophylline 0.48 g produced a sharp increase in plasma free fatty acids. After three days of treatment with aminophylline 0.96 g/day i.v., plasma post-heparin lipoprotein lipase was significantly reduced, and post-heparin hepatic triglyceridase remained unchanged. alpha 1 lipoprotein was reduced by treatment, in parallel with lipoprotein lipase, while other lipoprotein fractions, serum cholesterol and triglycerides were unaffected.

Interrelationships between body mass and lipid and lipoprotein triglycerides and cholesterol in obese women.

In 72 obese women body mass index positively correlated with age and both showed multiple correlations with serum lipids and lipoprotein lipids. After adjustment for age (partial correlation procedure), body mass index resulted to be positively correlated with serum triglycerides, VLDL lipids, HDL-triglycerides and negatively correlated with HDL-cholesterol. The decrease in HDL-cholesterol concentration along with the increase in body weight was due to the reduction of cholesterol in HDL2 subfraction, while HDL3-cholesterol did not show any significant correlation with body mass index. The negative correlation between HDL2-cholesterol and body mass index was independent of other lipoprotein variables and in particular of VLDL lipid levels that were, as expected, inversely related to HDL2-cholesterol. HDL2-cholesterol is believed to be a strong protective factor against atherosclerosis, while doubts exist on the meaning of VLDL lipids as risk factors. Thus, the decrease in HDL2-cholesterol concentration, rather than the increase in VLDL lipids, might give a rational basis to the high incidence rate of vascular disease in obese subjects.

Long-term effects of fenofibrate on serum lipids and on lipoprotein cholesterol in type II hyperlipoproteinemic patients.

Twenty two patients with primary type II hyperlipoproteinemia (13 phenotype IIa and 9 phenotype IIb) were treated with fenofibrate 300 mg a day for 4-12 months. Serum total cholesterol decreased, on the average, by 22 per cent and LDL cholesterol by 24 per cent. In the patients with familial hypercholesterolemia, total cholesterol decreased by 28 per cent and LDL cholesterol by 31 per cent. One patient with homozygous familial hypercholesterolemia showed the greatest fall of total and LDL cholesterol (44 and 48 per cent respectively) and this was accompanied by a nearly complete disappearance of xanthelasmas and xanthomas.

Fenofibrate therapy of hypertriglyceridaemia. Differential effects on LDL cholesterol level in type IV and in type IIb primary hyperlipoproteinaemia.

Twenty five hypertriglyceridaemic patients (16 Type IV and 9 Type IIb) were treated with fenofibrate 300 mg/d. In Type IV patients serum triglycerides and VLDL cholesterol decreased, while LDL and HDL cholesterol rose significantly. In Type IIb patients, triglycerides and total, VLDL, IDL and LDL cholesterol were significantly reduced by the treatment. The correction of hypertriglyceridaemia by fenofibrate seems, therefore, to induce different changes in lipoproteins in Type IIb and in Type IV hyperlipoproteinaemic patients. The practical implications of these results are discussed.

Serum lipoproteins in diabetes: relation of alpha-lipoprotein level to therapy.

Three hundred and sixty diabetic patients (125 on insulin, 109 on sulfonylureas and 126 on diet alone) were selected to investigate the effect of the type of treatment and of the degree of metabolic control on serum lipoproteins. Prebeta-lipoprotein concentration was higher than normal in all treatment groups. Beta-lipoproteins were significantly higher in diabetic women than in controls. No difference in beta- and prebeta-lipoprotein concentration existed between the 3 treatment groups. Alpha-lipoproteins were significantly higher in insulin-treated than in diet-treated patients irrespective of the degree of metabolic control. The daily dose of insulin and, in patients on diet or sulfonylureas, serum IRI were positively correlated to alpha-lipoprotein concentration while this lipoprotein fraction was not significantly correlated to fasting blood sugar. Alpha-lipoprotein concentration, then, appears to be markedly influenced by exogenous and endogenous insulin, independently of the degree of metabolic control.

Relationship of serum triglyceride concentration to lipoprotein composition and concentration in normolipidemic and hyperlipidemic subjects.

In a series of 438 subjects (184 normolipidemics and 254 hyperlipidemics) the relationship among serum concentration of triglycerides, lipoprotein lipids and apoproteins A-I and B has been evaluated. The results show that as serum triglyceride level increases, VLDL rise and become enriched in triglycerides. The increase of VLDL is associated with a reduction of serum levels of LDL and HDL which appear to be rich in triglycerides and poor in cholesterol. The decrease in serum HDL level is mainly due to a reduction in serum concentration of the HDL2 subfraction. The triglyceride content of HDL2 and HDL3 rises with increasing serum triglycerides. The increase in serum triglyceride concentration seems then to be associated with a complex metabolic derangement which involves all the lipoprotein fractions.