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Biomedical subjects

B Föger

Publications and source records attributed to B Föger.

At least 37 records · Page 2Linked to original sources
PubMed1995

Relationship of high-density lipoprotein subfractions and cholesteryl ester transfer protein in plasma to carotid artery wall thickness.

High plasma concentrations of high-density lipoprotein (HDL) cholesterol are a powerful indicator of low vascular risk. By decreasing HDL cholesterol, cholesteryl ester transfer protein (CETP) could perhaps constitute an atherogenic protein. We measured HDL cholesterol and HDL subfractions and quantified CETP mass in fasting plasma in 21 asymptomatic probands, and related these variables to the mean intima media thickness of the extracranial carotid arteries. HDL2 cholesterol, the less dense HDL subfraction, was inversely related to carotid wall thickness (r = -0.378; P < 0.05), and CETP was directly related to carotid wall thickness (r = 0.436; P < 0.05). In plasma CETP is associated mostly with the HDL3 subfraction. We therefore calculated from our measurements the relative CETP content of HDL3, i.e., CETP/HDL3 cholesterol. This ratio was correlated with carotid wall thickness stronger than any other variable measured (r = 0.718, P < 0.001). We conclude that variation in HDL subfractions and CETP may be more closely associated with carotid intima media thickness than the accepted strong risk factor of HDL cholesterol.

Adult↗
PubMed1995

Treatment of primary mixed hyperlipidemia with etophylline clofibrate: effects on lipoprotein-modifying enzymes, postprandial lipoprotein metabolism, and lipoprotein distribution and composition.

In 17 patients with primary mixed hyperlipidemia we studied levels and composition of lipoproteins in fasting plasma, lipoprotein-modifying enzymes, and postprandial lipoprotein metabolism after an oral fat-tolerance test supplemented with vitamin A before, and 12 weeks after treatment with etophylline clofibrate. With treatment, fasting plasma cholesterol, triglycerides, and the levels of very low density lipoproteins (VLDL), intermediate density lipoproteins (IDL), and low density lipoproteins (LDL) decreased significantly; high density lipoprotein (HDL) cholesterol increased significantly. Treatment caused also an increase in the protein content of IDL, a decrease in the triglyceride content of LDL, and an increase in the size of LDL as assessed by gradient gel electrophoresis. Concentrations of triglycerides, chylomicrons, and chylomicron remnants after an oral fat load supplemented with vitamin A decreased by 33%, 30% and 6%, respectively (P < 0.005; P < 0.01; and P < 0.05). The activity of lipoprotein lipase and hepatic lipase in postheparin plasma increased by 51% and 45%, respectively (P < 0.01; P < 0.05). We found a decrease in the mass concentration of cholesteryl ester transfer protein (P < 0.05). Stepwise multiple regression analysis showed that the triglyceride content of LDL is determined primarily by fasting triglycerides (r = + 0.53, P < 0.05;baseline) and cholesteryl ester transfer protein (r = + 0.49, P < 0.05; 12 weeks); in contrast, the triglyceride content of HDL3 is determined exclusively by accumulation of postprandial triglycerides (r = + 0.67; P < 0.05; baseline) and postprandial chylomicrons (r = +0.87; P < 0.005; 12 weeks). We conclude that hypolipidemic treatment with etophylline clofibrate favorably affects the cardiovascular risk factor profile in primary mixed hyperlipidemia.

Carrier Proteins↗
PubMed1995

Exercise and postprandial lipaemia.

Postprandial hyperlipidaemia is a risk factor for atherosclerosis in multiple vascular beds, independently of high-density lipoprotein (HDL) cholesterol. An increased level of HDL cholesterol is a strong indicator of a low risk of atherosclerosis. Exercise decreases postprandial lipaemia and, in turn, increases levels of HDL cholesterol. The favourable effects of exercise on lipoprotein metabolism, particularly evident in the postprandial state, may thus help to decrease susceptibility to atherosclerosis in exercise-trained people.

Arteriosclerosis↗
PubMed1994

Effect of pancreas transplantation on lipoprotein lipase, postprandial lipemia, and HDL cholesterol.

Pancreas transplantation with systemic venous drainage of the graft causes elevated plasma levels of insulin, known to be a potent regulator of plasma lipoprotein metabolism. We studied 11 post-type I diabetic pancreas-kidney transplant recipients, 9 type I diabetic kidney transplant recipients displaying peripheral hyperinsulinemia due to subcutaneous insulin treatment, 11 nondiabetic kidney transplant recipients as controls for the effects of immunosuppressive medication, and 11 healthy control subjects, all matched for age, sex, and body mass index. We determined fasting lipids, lipoproteins and lipolytic enzymes, as well as postprandial lipid metabolism after a standardized oral fat load. High-density lipoprotein (HDL) cholesterol averaged 1.98 (0.40) mmol/L in pancreas-kidney transplant patients, clearly higher than that of kidney transplant recipients (1.52 (0.36) mmol/L, P < 0.05) or of controls (1.50 (0.38) mmol/L, P < 0.05). In pancreas-kidney transplant patients postprandial lipemia was lowest and lipoprotein lipase activity was highest (average 32% and 154%, respectively, of the mean of the controls) compared with nondiabetic kidney transplant recipients (P < 0.005, P < 0.05) and healthy controls (P < 0.001, P < 0.01). In type I diabetic kidney transplant recipients the levels of HDL cholesterol (1.88 (0.63) mmol/L), postprandial lipemia, and lipoprotein lipase activity were intermediate between pancreas-kidney transplant patients and healthy controls. The distinctly elevated HDL cholesterol in pancreas-kidney transplant patients can be readily explained by the low postprandial triglyceride levels resulting from a high activity of lipoprotein lipase. The very favorable lipid profile in post-diabetic pancreas-kidney transplant recipients could be expected to counteract the severe atherosclerotic risk of long-standing diabetes.

Adult↗
PubMed1994

Fenofibrate improves postprandial chylomicron clearance in II B hyperlipoproteinemia.

In 11 patients with IIB hyperlipoproteinemia we studied fasting lipids, lipoproteins, lipoprotein-modifying enzymes, and postprandial lipid metabolism after a standardized oral fat load supplemented with vitamin A before and 12 weeks after treatment with fenofibrate, a third-generation fibric acid derivative. Fasting plasma cholesterol, triglycerides, low-density lipoprotein cholesterol decreased significantly (P < 0.05, P < 0.01, P < 0.01), high-density lipoprotein subfraction 3 cholesterol increased significantly (P < 0.05), and high-density lipoprotein subfraction 2 cholesterol remained unchanged. Postprandial lipemia, i.e., the integrated postprandial triglyceride concentrations corrected for the fasting triglyceride level, and postprandial chylomicron concentrations, as assessed by biosynthetic labeling of chylomicrons with retinyl palmitate, decreased by 40.6% and 60.1% (P < 0.05; P < 0.05), respectively. The activity of lipoprotein lipase (LPL) increased by 33.6% (P < 0.05); the increase in LPL during fenofibrate treatment was positively correlated with the increase in high-density lipoprotein cholesterol (r = 0.84; P < 0.005). Hepatic lipase and cholesteryl ester transfer protein mass and activity remained unchanged. We conclude that lipid-lowering therapy with fenofibrate ameliorates fasting and, more profoundly, postprandial lipoprotein transport in hypertriglyceridemia by curbing postprandial triglyceride and chylomicron accumulation, at least in part, through an increase in LPL activity.

Adult↗
PubMed1994

The immunosuppressive substance 2-chloro-2-deoxyadenosine modulates lipoprotein metabolism in a murine macrophage cell line (P388 cells).

A recently developed immunosuppressive substance, 2-chloro-2-deoxyadenosine (2-CdA), was reported to inhibit monocyte functions at low concentration. Because macrophages play a key role in the formation of atherosclerotic plaques, it was of interest to study the effect of 2-CdA on cellular lipid metabolism. For this purpose we have used a macrophage cell line (P388) to perform incubation studies in the presence of acetylated low density lipoprotein (Ac-LDL) and 2-CdA. The addition of 2-CdA, in concentrations ranging from 5-20 nM, induced a dose-dependent decrease in cellular cholesterol content and in the amount of extracellular [14C]oleic acid (OA) incorporated into the cholesteryl ester (CE) fraction. The effect was maximized at 20 nM 2-CdA with an 86% reduction in cholesterol esterification compared to controls (P < 0.008). To evaluate the mechanism of interaction of 2-CdA with cellular lipid metabolism, deoxycytidine (dCyt) and 3-methoxybenzamide (3-MOB), substances known to antagonize the effect of 2-CdA in different ways, were co-administered with 2-CdA. dCyt, a competitive inhibitor of dCyt kinase, which catalyzes phosphorylation to the active metabolite, antagonized the effects of 20 nM 2-CdA, producing significantly greater incorporation of extracellular [14C]OA into the CE fraction than in the presence of 2-CdA alone (P < 0.0086). Co-incubation with 2-CdA and the poly-ADP-ribose synthetase inhibitor 3-MOB, which is known to render cells resistant to 2-CdA toxicity by preventing cellular nicotinamide adenine dinucleotide (NAD)- and adenosine triphosphase-depletion, also reversed the effect of 2-CdA on lipid accumulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylation↗
PubMed1994

Kinetics of lipids, apolipoproteins, and cholesteryl ester transfer protein in plasma after a bicycle marathon.

The short-term effects of prolonged intense exercise on plasma lipid transport parameters including cholesterol, triglycerides (TGs), low-density lipoprotein (LD) cholesterol, high-density lipoprotein (HDL) cholesterol, and its subfractions HDL2 cholesterol and HDL3 cholesterol, on apolipoproteins (apos) A-I, A-II, and B, and on mass and activity of cholesteryl ester transfer protein (CETP) were studied in eight male endurance-trained athletes over the first week after a bicycle marathon. CETP mass concentration in plasma was quantified by a newly developed immunoradiometric assay (IRMA). Plasma concentrations of cholesterol, TGs, LDL cholesterol, apo B, CETP, and cholesteryl ester transfer activity (CETA) were significantly reduced in the recovery period compared with pre-exercise values (cholesterol by 20%, P < .05; TGs by 63%, P < .05; LDL cholesterol by 32%, P < .05; apo B by 18%, P < .05; CETP mass by 29%, P < .05; and CETA by 14%, P < .05). HDL cholesterol and HDL2 cholesterol, in contrast, were significantly increased in the post-exercise period (HDL cholesterol by 12%, P < .05, and HDL2 cholesterol by 96%, P < .05), whereas HDL3 cholesterol showed a tendency to decrease in the late recovery period (by 8%, NS). Although changes in cholesterol, triglycerides, HDL cholesterol, LDL cholesterol, apo B, and CETP mass and activity were already evident in the early recovery period, HDL2 cholesterol showed a delayed response, reaching its maximum 72 hours after initiation of exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Low-density lipoproteins of the postprandial state induce cellular cholesteryl ester accumulation in macrophages.

Chemically or biologically modified low-density lipoproteins (LDL) but not native unmodified LDL lead to foam cell formation in monocyte-derived macrophages. Since the magnitude of postprandial lipemia after a challenge test seems to be associated with coronary artery disease, we tested the hypothesis that in the course of postprandial lipemia, LDL appear in plasma that are capable of leading to foam cell formation even without prior modification. We incubated the macrophage-like cell line P388 with unmodified postabsorptive and postprandial LDL from 17 healthy donors and measured the cellular cholesterol and triglyceride contents and amounts of exogenous [14C]oleic acid incorporated into the cholesteryl ester fraction. Postprandial LDL induced a significantly more pronounced cholesteryl ester accumulation than did postabsorptive LDL (477 +/- 286% versus 212 +/- 173%, respectively; P < .003). The increase in cellular total cholesterol was significantly higher as a result of cell incubation with postprandial LDL (107 +/- 61%) than with postabsorptive LDL (54 +/- 40%, P < .003), whereas no increase in triglyceride content was observed (P < .589) in either case. After CuSO4 incubation and incubation with P388 cells, postprandial LDL revealed more thiobarbituric acid-reacting substances than did postabsorptive LDL (55 +/- 10 versus 28 +/- 9 nmol/mg protein, P < .018; 28 +/- 4 versus 20 +/- 3 nmol/mg protein). The increase in cellular cholesteryl ester synthesis caused by postprandial LDL was reduced by more than 50% when lipoproteins and cells were incubated in the presence of ascorbic acid (P < .007).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

[Hypertriglyceridemia and acute pancreatitis].

Data of 26 patients suffering from severe pancreatitis, who were treated at the anesthesiologic intensive care unit during the years 1991 and 1992, were evaluated with respect to etiologic factors, especially hypertriglyceridemia, stage of the disease and clinical outcome. Hypertriglyceridemia was found in 13 cases (11 men, 2 women, mean age 42 +/- 9 years) with values between 330 mg/dl and 4000 mg/dl. Lipid electrophoresis revealed a pattern typical for type IV hyperlipidemia. Insulin dependent diabetes was present in 4 patients and 5 reported about an unusual high alcohol intake preceding pancreatitis. Beside surgical approaches, including drainage and lavage, and basic intensive care treatment plasmapheresis was performed in 8 patients with hypertriglyceridemia. 5 patients with pancreatitis and hypertriglyceridemia died out of multiorganic failure, and so the mortality rate was 38%. The group of patients with pancreatitis caused by cholelithiasis or chronic alcohol consumption showed a mortality rate of 46%. The poor outcome of pancreatitis associated with hypertriglyceridemia demonstrates the importance of the treatment of hypertriglyceridemia in order to prevent the development of pancreatitis. The determination of plasma triglyceride values should belong to the routine diagnostic procedures in acute pancreatitis.

Acute Disease↗
PubMed1994

High density lipoproteins with differing apolipoproteins: relationships to postprandial lipemia, cholesteryl ester transfer protein, and activities of lipoprotein lipase, hepatic lipase, and lecithin: cholesterol acyltransferase.

To gain insight into metabolic determinants of high density lipoproteins (HDL) containing apolipoproteins A-I and A-II (LpA-I/A-II) and those containing A-I, but devoid of A-II (LpA-I), the plasma concentration of LpA-I and LpA-I/A-II within the HDL2 and HDL3 density spectrum was measured in 14 normolipidemic male subjects on a standardized diet. Apolipoprotein plasma concentrations of HDL subspecies were compared with the magnitude of postprandial lipemia, activities of lipoprotein lipase and hepatic lipase in postheparin plasma, plasma lecithin:cholesterol acyltransferase (LCAT) activity, and cholesteryl ester transfer protein (CETP) mass. Plasma levels of LpA-I/A-II were 2.5 times higher than levels of LpA-I (123 +/- 20 vs. 48.3 +/- 22.1 mg protein/dl) and the partition of LpA-I and LpA-I/A-II between HDL2 and HDL3 differed in that the proportion of LpA-I associated with HDL2 was greater than that of LpA-I/A-II (23 +/- 19 vs. 6 +/- 6%, P < 0.002). With increasing levels of HDL2, the proportion of LpA-I in HDL2 increased (P < 0.002). Furthermore, levels of LpA-I and LpA-I/A-II were strongly correlated within the HDL2 but not within the HDL3 density region. Plasma levels of LpA-I, but not LpA-I/A-II, were inversely correlated with the magnitude of postprandial lipemia. However, activities of lipoprotein lipase and hepatic lipase tended to show stronger associations with the partition of LpA-I/A-II between HDL2 and HDL3 than with that of LpA-I. Within the HDL3, but not the HDL2 density spectrum, LpA-I/A-II exhibited a positive association with plasma LCAT activity, while LpA-I displayed an inverse association with plasma CETP mass. These results are consistent with differences in substrate properties of LpA-I and LpA-I/A-II for lipoprotein modifying enzymes and imply different, but overlapping metabolic pathways of LpA-I and LpA-I/A-II.

Adult↗
PubMed1994

[Hypertriglyceridemia].

The hypertriglyceridemias comprise a heterogenous group of lipoprotein disorders varying with respect to etiology, lipoprotein pattern, and its major clinical sequelae, i.e. pancreatitis and atherosclerosis. Therefore goals and modalities of treatment should be individualized to a large extent. Behavioral measures like diet, weight control, exercise, reduced alcohol consumption and smoking cessation form the cornerstone of medical management. Lipid lowering drugs should be considered when triglyceride levels exceed 1000 mg/dl to reduce the risk of pancreatitis and in patients at high risk for atherosclerosis, often characterized by a high total cholesterol/HDL ratio, to reduce cardiovascular endpoints.

Combined Modality Therapy↗
PubMed1993

Heterozygous lipoprotein lipase deficiency due to a missense mutation as the cause of impaired triglyceride tolerance with multiple lipoprotein abnormalities.

In 16 members of two Austrian families affected by a missense mutation at codon 188 of the lipoprotein lipase (LPL) gene (8 heterozygous and 8 normal subjects), carrier status for the mutation as determined by DNA analysis was related to LPL activity in postheparin plasma, to the magnitude of postprandial lipemia, and to concentration, composition, and size of the major lipoprotein classes of postabsorptive plasma. Carriers exhibited clearly reduced LPL activity, normal fasting triglycerides, but pronounced postprandial lipemia. The carriers' impaired triglyceride tolerance, as evident in the postprandial state of challenge only, was associated with a fasting lipoprotein constellation characterized by (a) enrichment of HDL2 with triglycerides, (b) reduced HDL2-cholesterol, (c) enrichment of VLDL and intermediate density lipoprotein (IDL) with cholesteryl esters, (d) elevated IDL levels, and (e) small-sized LDL. Within any given individual, the degrees of expression of these characteristics were quantitatively and continuously related with each other as well as with the magnitude of lipemia and with LPL activity.

Adolescent↗
PubMed1993

Polyclonal antibody-based immunoradiometric assay for quantification of cholesteryl ester transfer protein.

Cholesteryl ester transfer protein (CETP) catalyzes the transfer of neutral lipids among plasma lipoproteins and in this way plays a prominent role in cholesterol metabolic routing and, thus, probably for atherosclerosis. Studies of this important protein in various clinical settings require the ability to accurately quantify CETP in plasma. In order to gain access to such a capability, an immunoradiometric assay (IRMA) for quantification of CETP was developed. CETP was purified from human plasma to apparent homogeneity and used for raising anti-CETP antibodies in rabbits. The specificity of the polyclonal antiserum obtained was demonstrated by inhibition assays and immunoblot analysis. Before use in the CETP-IRMA, the antibodies were affinity-purified by chromatography on CETP-Sepharose. Sensitivity of the CETP-IRMA was 0.1 ng, and intra- and interassay coefficients of variation were 2.9 and 8.0%, respectively. In 30 normolipidemic healthy subjects, the mean (+/- SD) CETP concentration was 1.1 (+/- 0.22) micrograms/ml of plasma; individual values ranged from 0.644 to 1.694 micrograms CETP/ml and agreed well with measurements of CETP activity of the same samples (r = 0.85).

Antibodies↗
PubMed1991

[Development of neonatology in Tyrol 1979-1988. An epidemiologic analysis of the Innsbruck University Pediatric Clinic (in comparison with the years 1968-1978)].

From 1979-1988 5863 term and preterm infants were admitted to the Pediatric University Clinic of Innsbruck during their neonatal period. Compared to 1968-1978 the percentage of preterm infants increased from 44.8% to 47.9%. The mortality during this hospital admission decreased from 11.8% (preterms: 18.2%) to 7.8% (preterms: 10.5%). The number of patients transferred from the Gynecological University Clinic of Innsbruck and from other provinces including South-Tyrol increased, whereas the number of patients transferred from other hospitals of Tyrol decreased. Generally there was a constant trend towards an earlier point of referral (e.g. first-day-admission from the Gynecological University Clinic increased from 74.8% (1968-1978) to 92.1% (1979-1988), first-day-admission from other hospitals of Tyrol increased from 57% to 70.6%). Small-for-date-infants constituted 21.6% of hospital admissions (1979-1988) resp. 18.3% (1968-1978). Mortality of these infants was reduced from 9.2% to 5.3%. In a decade of continuously decreasing over-all-neonatal mortality especially several risk groups for perinatal complications (e.g. preterms, small-for-date-infants, twins) substantially profited from the progress of comprehensive peri- and neonatal care.

Austria↗
PubMed1991

[Trends in perinatal, neonatal and post-neonatal mortality in Austria and Tyrol, with special reference to 1979-1988].

Analysis of neonatal, perinatal and infant mortality rates is a useful basis to compare the quality of neonatal care in a country. During the last decades these parameters have been falling steadily in Austria as well as in other industrialized countries. Regarding the various provinces of Austria substantial regional differences occur. Apparently the decline in mortality rates is not only contributable to medical progress but as strongly influenced by social and economic changes. In the mid-seventies absolute and relative neonatal mortality rates in Austria definitely decreased, most probably attributable to the installation of neonatal intensive care units. During 1968-1978 the decrease in neonatal mortality was mainly due to reduced first-day-mortality, whereas during the following decade it was mainly due to reduced mortality of the 2nd until 7th day of life. Interestingly, the rate of preterm infants in Austria remained virtually constant during 1968-1988 despite improved pre- and perinatal care. Paralleling the development in full-term neonates the peri-/neo- and postneonatal mortality rates of preterm infants decreased. Predictably - as in other countries - the highest improvement was found in the low birth weight groups Nevertheless, premature births have accounted for the majority of neonatal and perinatal deaths.

Austria↗