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Biomedical subjects

J R Patsch

Publications and source records attributed to J R Patsch.

At least 109 records · Page 6Linked to original sources
PubMed1990

Effect of alcohol dose on plasma lipoprotein subfractions and lipolytic enzyme activity in active and inactive men.

Controversy as to which lipoprotein subfraction of high-density lipoprotein (HDL) increases during alcohol consumption prompted the current study of the effects of two alcohol doses over varying time intervals on plasma lipoproteins and lipolytic enzymes. Measurements were made in 49 healthy men before and after three weeks of abstinence from alcohol and after consumption of one or three 12-ounce cans of beer per day. We found that HDL (10%), HDL2 (14%), and HDL3 (9%) cholesterol, and apolipoprotein A-I (7%) decreased with abstinence from alcohol and then increased with its consumption. These increases were not significant until after 3 weeks of daily alcohol intake, but they were significant in both the one-can and three-cans of beer per day groups. In the 23 inactive subjects HDL and HDL2 cholesterol decreased with abstinence but did not increase significantly with alcohol intake. Lipolytic enzymes were not changed by alcohol manipulation, but the level of lipoprotein lipase was higher and that of hepatic lipase was lower at each measurement point in the 26 habitually active versus the 23 inactive subjects. Adjustment for weight or skinfold thickness did not affect lipoprotein changes over time within groups but did eliminate many of the differences between activity groups. Alcohol consumption seems to be related to possibly beneficial influences on plasma HDL and HDL2 cholesterol, and may thus impact the risk of heart disease.

Adult↗
PubMed1990

Effect of blood collection and processing on radioimmunoassay results for apolipoprotein B in plasma.

We studied the effects of different blood collection and processing procedures on quantification of apolipoprotein (apo) B by radioimmunoassay. High-density lipoprotein subfractions HDL3 and HDL2 and isolated apoA-I did not cross-react in the assay. Analytical recovery of apoB at different doses of very-low- and low-density lipoproteins were complete. Inter- and intra-assay coefficients of variation (CVs) averaged 7.4% and 6.0%, respectively. Blood from 20 subjects was collected into tubes containing EDTA alone or EDTA with antiproteolytic and antioxidant agents; one half of each plasma was separated immediately, half after 3 h at 4 degrees C. Regardless of the addition of protective agents or the time difference in separating plasma from other blood elements, freezing plasma at -70 degrees C decreased apoB content a similar amount, an average of 6.8%. This loss of apoB immunoreactivity was not related to apoB content in fresh plasma. Analysis of variance showed no differential effect on apoB content by the various additions to whole blood or plasma. No additional apoB content was lost in once-frozen aliquots of three human plasma pools during storage at -70 degrees C for up to 18 months. We conclude that concentrations of apoB in human plasma can be measured reliably after long-term storage, although the absolute value may decrease slightly as a result of freezing.

Analysis of Variance↗
PubMed1990

[The effect of hyperlipoproteinemia on serum fructosamine].

In 127 patients, we investigated the influence of hyperlipemia on observed fructosamine values. An in vitro influence of the lipids on the fructosamine reading could be excluded for cholesterol, HDL-cholesterol and triglycerides. However, in patients with type I diabetes, both, cholesterol and triglycerides significantly (p less than 0.05) correlated with fructosamine. This may be explained by in vivo effects of hyperglycemia on lipids or lipoproteins. For a given level of hyperglycemia, fructosamine is slightly more sensitive than HbA1c.

Blood Proteins↗
PubMed1989

The hyperlipoproteinemias.

The association of disturbances of plasma lipid transport and atherogenesis has been recognized, and scientific data continue to accumulate to explain this association from a mechanistic viewpoint. A number of recent clinical trials have shown that cholesterol-lowering therapy can prevent the complications of atherosclerosis. Consequently, the attention of physicians to therapeutic intervention has increased and public awareness to plasma cholesterol levels has been heightened. This article summarizes current knowledge of how plasma lipid transport is regulated. The classical primary hyperlipoproteinemias are considered and hyperlipoproteinemias occurring secondary to other diseases are discussed. Standard methods to diagnose the defined genetic hyperlipidemias are outlined, and new approaches to assess risk of atherosclerosis are examined. Finally, the role of dietary measures and drugs in lowering blood lipids and reducing risk of coronary heart disease is delineated.

Apoproteins↗
PubMed1989

Risk factors for coronary artery disease: a study comparing hypercholesterolaemia and hypertriglyceridaemia in angiographically characterized patients.

Fifty-two male patients undergoing coronary angiography were allocated to four groups each consisting of 13 subjects: group I had normal coronary arteries and patients in groups II-IV exhibited coronary artery disease. In group II, plasma cholesterol was below 250 mg dl-1 and triglycerides below 160 mg dl-1; in group III, cholesterol was above 270 mg dl-1 and triglycerides under 160 mg dl-1; and in group IV, cholesterol was under 270 mg dl-1 and triglycerides above 180 mg dl-1. The hypertriglyceridaemic group IV had the highest coronary score. In addition, it had lowest lipoprotein lipase activity, lowest HDL-cholesterol and lowest high-density lipoproteins-2 (HDL-2) levels, suggesting that this type of hypertriglyceridaemia is caused--at least in part--by lipoprotein lipase deficiency with impaired removal of the triglyceride-rich lipoproteins and increased catabolism of HDL-2. Our findings point towards a type of hypertriglyceridaemia strongly associated with coronary artery disease which should therefore be treated accordingly.

Adult↗
PubMed1989

[Pathophysiology of lipid transport in plasma].

Atherosclerosis of coronary and peripheral arteries is a major cause of death and disability in civilizations outside the third world. Disturbances of the lipid transport in plasma are a major cause for atherogenesis. The transport of exogenous and endogenous lipids in plasma is facilitated by lipoproteins. The concentration of the various lipoprotein families is subject to complex regulation such as secretion by intestine and liver, intravascular metabolism and clearance by hepatic and extrahepatic receptors of high and low affinity. To understand the pathophysiology of lipid transport and the role of certain lipoproteins as risk factors for atherosclerosis it is important to understand the regulatory mechanisms governing lipoprotein concentrations. Elevated concentrations of certain lipoproteins such as low-density-lipoproteins (LDL) constitute an increased risk for atherosclerosis. This elevation of LDL in plasma can be caused by increased production and/or reduced catabolism. With a better understanding of the pathophysiology of the lipid transport system more rational and precise modalities of both treatment and prevention of atherosclerosis can be expected.

Animals↗
PubMed1989

A dual-precipitation method evaluated for measurement of cholesterol in high-density lipoprotein subfractions HDL2 and HDL3 in human plasma.

The dual-precipitation method for measurement of cholesterol in high-density lipoprotein subfractions HDL2 and HDL3 (Warnick et al., Clin Chem 1982;28:1574) was compared with quantification of cholesterol in HDL2 and HDL3 by zonal ultracentrifugation (Patsch et al., J Lipid Res 1974;15:356-66). For 39 plasma specimens differing widely in their HDL subfraction cholesterol concentration, the coefficient of correlation between the two methods was 0.94 for HDL2-cholesterol, 0.82 for HDL3-cholesterol. Storage of plasma specimens at -70 degrees C decreased the apparent content of HDL3-cholesterol by 5%; no significant changes in HDL2-cholesterol were observed. In frozen plasma, interference by apoB-containing lipoproteins and by lipoprotein(a) was negligible. Mean weight ratios of apoA-I to cholesterol were twice as high for HDL3 as for HDL2, reflecting the increased cholesterol content of HDL2. The study suggests that quantification of HDL2 and HDL3 cholesterol by precipitation is appropriate for use in epidemiological studies.

Apolipoproteins A↗
PubMed1988

Effects of biosynthetic human proinsulin on plasma lipids in type 2 diabetes mellitus.

Plasma cholesterol, triglycerides, HDL2-cholesterol, and HDL3-cholesterol were studied in 18 patients with Type 2 diabetes. Prior to entering the clinical trial, the study subjects were in stable control under a fixed mixture of 20% regular and 80% NPH (isophane) biosynthetic human insulin twice daily. The patients were randomized to treatment with either biosynthetic human proinsulin or biosynthetic human NPH insulin (controls) twice daily. Glucose control was kept constant in both groups throughout the study. Of the nine patients treated with proinsulin, eight exhibited a decrease of plasma triglycerides (median decrease by 0.13 mmol/l). In contrast, all nine controls showed a rise (median increase by 0.69 mmol/l) of plasma triglycerides (p less than 0.001). In keeping with the fall of plasma triglycerides, HDL2-cholesterol rose in all but one proinsulin-treated patients. Both treatment modalities reduced HDL3-cholesterol with a median decrease of 0.20 mmol/l (p less than 0.01) with proinsulin and 0.26 mmol/l with NPH insulin (p less than 0.05). We conclude that human proinsulin is able to reduce plasma triglycerides and to increase HDL2-cholesterol in the majority of patients with Type 2 diabetes and thus appears to alter favourably risk factors for coronary heart disease.

Aged↗
PubMed1988

[Effects of intensified insulin therapy on fat metabolism in type 1 diabetes mellitus].

The effect on fat metabolism of an intensified insulin treatment regimen was tested in 23 type I diabetics and compared with that of conventional insulin treatment. Definite improvement in blood glucose levels was found after a one-year intensified treatment schedule (HbA1 of 8.1% under intensified treatment, compared with 10.6% under conventional treatment). The intensified treatment schedule also resulted in a significant reduction in plasma triglycerides from an average of 114 mg/dl to 94 mg/dl (p less than 0.05), at the same time the plasma HDL-cholesterol levels increased. Plasma concentrations of total cholesterol and LDL-cholesterol remained unchanged. Thus intensified insulin treatment was shown to improve glucose metabolism, lower HDL-cholesterol and in this way improve the risk profile for macroangiopathy.

Adolescent↗
PubMed1988

[Normalization of perinatal morbidity in gestational diabetes by strict metabolic adjustment].

A prospective study compared the perinatal morbidity of 141 normal pregnancies (group I) with that of 108 pregnancies in whom gestational diabetes had been treated early (group II) and 35 with unsatisfactorily treated gestational diabetes (group III). The therapeutic goal in gestational diabetes was to have a postprandial blood-glucose level of less than 130 mg/100 ml. If this was not achievable through diet alone, insulin was injected once daily. Neonatal macrosomia, dystrophy, acidosis, hyperbilirubinaemia, hypoglycaemia and hypocalcaemia had a normal incidence in group II, but in group III macrosomia was twice as frequent as in group II (P less than 0.02), and acidosis (pH less than 7.20) twice as frequent (P less than 0.05). The results indicate that strict metabolic control in gestational pregnancy will achieve a normal rate of perinatal morbidity.

Apgar Score↗
PubMed1987

High density lipoprotein2. Relationship of the plasma levels of this lipoprotein species to its composition, to the magnitude of postprandial lipemia, and to the activities of lipoprotein lipase and hepatic lipase.

Lipoprotein lipase (LPL) activity in postheparin plasma of 38 normolipidemic volunteers was related to the magnitude of postprandial lipemia after a fat meal, to triglyceride content of high density lipoprotein2 (HDL2), to hepatic lipase (HL) activity, and to HDL2 levels. LPL activity correlated indirectly with lipemia, triglyceride content of HDL2, HL activity, and levels of HDL2 but not of HDL3. HL activity correlated directly with lipemia and indirectly with HDL2 levels. Triglyceride content of HDL2 correlated directly with lipemia and indirectly with HDL2 levels. In HDL2, abundance of apolipoprotein (apo) A-II and the apoA-I/apoA-II ratio varied widely. The latter correlated positively with LPL activity and HDL2 levels, and, inversely, with HL activity, lipemia, and triglyceride content of HDL2. The study suggests that HDL-cholesterol is not an independent parameter of lipid transport, but is strongly affected by triglyceride metabolism through lipolytic enzymes, as exemplified by postprandial lipemia that affect both composition and plasma levels of HDL2.

Apolipoproteins A↗
PubMed1987

Measurement of glycated protein by a rapid and specific method for absolute quantification of lysine-bound glucose.

We modified the liquid-chromatographic assay of Schleicher and Wieland (J Clin Chem Clin Biochem 1981; 19:81-7) for measuring lysine-bound glucose in serum proteins, increasing its performance and practicality. After precipitating serum proteins from 10- to 50-microL samples with ethanol (700 mL/L) and hydrolyzing these in 6 mol/L HCl, we inject 20 microL of the diluted hydrolysate directly into the chromatograph, which consists of an acid-resistant C18 precolumn combined with a high-resolution C18 main column. The eluent is 3.5 mmol/L H3PO4 solution containing 30 mL of acetonitrile per liter. These modifications increase sensitivity, provide excellent resolution and longevity of stationary phases, shorten assay times to 15 to 20 min, and are suited for automation. The assay is highly sensitive and highly specific, quantifying nanomoles of lysine-bound glucose per milligram of protein. A precision (CV) of 5.1% is achievable at physiological and supra-physiological glucose concentrations, and analytical recovery is 99%. This inexpensive method has been applied to serum albumin, bulk serum proteins, and preparations of low-density lipoproteins and immunoglobulins.

Blood Proteins↗
PubMed1986

Effects of insulin on lipoprotein secretion in rat hepatocyte cultures. The role of the insulin receptor.

Insulin inhibits the secretion of lipoprotein components such as triglyceride, phospholipid, and apolipoproteins B and E in primary rat hepatocyte cultures. The aim of this study was to determine whether these hormonal effects are related to the interaction of insulin with its receptor on the surface of cultured hepatocytes. Half-maximal inhibition of secretion of apolipoprotein E and triglyceride occurred at 6 ng/ml porcine insulin, equivalent to a 20% receptor occupancy. When compared to porcine insulin, both guinea pig insulin and desoctapeptide insulin were 60 times less inhibitory on triglyceride and apolipoprotein secretion. These analogs were also 60 times less effective in competing with porcine 125I-insulin for receptor binding. Anti-insulin receptor IgG inhibited binding of porcine insulin to cells in a dose-dependent fashion. However, similar to the hormone itself, it reduced the secretion of triglyceride and apolipoproteins E and B. Preincubation of cells with 200 ng/ml porcine insulin for 15 h caused a 2.5-fold reduction of surface receptor number. These cells were less sensitive to the inhibitory effect of porcine insulin on secretion of triglyceride and apolipoproteins B and E. We conclude that the effects of insulin on lipoprotein processing by hepatocytes in culture are receptor-mediated, can be imitated by antibodies, to the insulin receptor, and are subject to control by receptor down-regulation.

Affinity Labels↗