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At least 469 records · Page 26Linked to original sources
PubMed1986

Apolipoprotein B metabolism in subjects with deficiency of apolipoproteins CIII and AI. Evidence that apolipoprotein CIII inhibits catabolism of triglyceride-rich lipoproteins by lipoprotein lipase in vivo.

Previous data suggest that apolipoprotein (apo) CIII may inhibit both triglyceride hydrolysis by lipoprotein lipase (LPL) and apo E-mediated uptake of triglyceride-rich lipoproteins by the liver. We studied apo B metabolism in very low density (VLDL), intermediate density (IDL), and low density lipoproteins (LDL) in two sisters with apo CIII-apo AI deficiency. The subjects had reduced levels of VLDL triglyceride, normal LDL cholesterol, and near absence of high density lipoprotein (HDL) cholesterol. Compartmental analysis of the kinetics of apo B metabolism after injection of 125I-VLDL and 131I-LDL revealed fractional catabolic rates (FCR) for VLDL apo B that were six to seven times faster than normal. Simultaneous injection of [3H]glycerol demonstrated rapid catabolism of VLDL triglyceride. VLDL apo B was rapidly and efficiently converted to IDL and LDL. The FCR for LDL apo B was normal. In vitro experiments indicated that, although sera from the apo CIII-apo-AI deficient patients were able to normally activate purified LPL, increasing volumes of these sera did not result in the progressive inhibition of LPL activity demonstrable with normal sera. Addition of purified apo CIII to the deficient sera resulted in 20-50% reductions in maximal LPL activity compared with levels of activity attained with the same volumes of the native, deficient sera. These in vitro studies, together with the in vivo results, indicate that in normal subjects apo CIII can inhibit the catabolism of triglyceride-rich lipoproteins by lipoprotein lipase.

Adult↗
PubMed1992

Three types of naturally occurring modified lipoproteins induce intracellular lipid accumulation in human aortic intimal cells--the role of lipoprotein aggregation.

Blood monocytes or intimal smooth muscle cells from normal aorta were incubated with low density lipoprotein (LDL) from patients with coronary atherosclerosis, or with LDL from diabetic patients, or with lipoprotein(a) (Lp(a)). In each case there was a 2- to 4-fold rise in the intracellular cholesteryl ester content. LDL from healthy subjects failed to induce intracellular lipid accumulation in these cells. LDL from patients with coronary atherosclerosis, LDL from diabetic patients, and Lp(a) form aggregates under cell culture conditions. The ability of these lipoproteins to increase the cholesteryl ester content of cultured cells is directly correlated to the degree of lipoprotein aggregation. When aggregates were removed from the lipoprotein preparations by filtration, the latter became less effective in promoting intracellular lipid accumulation. Incubation of cells with lipoprotein aggregates, isolated by gel filtration, induced a 3- to 5-fold elevation of the cellular cholesteryl ester content. These results suggest that LDL from atherosclerotic patients, or LDL from diabetic patients, or Lp(a) have a tendency to form aggregates and that these aggregates are avidly taken up by intimal smooth muscle cells followed by lipid accumulation. This aggregation tendency may play a role in atherogenesis.

Aorta↗
PubMed1993

Effects of pregnancy and lactation on plasma lipid and lipoprotein concentrations, lipoprotein composition and post-heparin lipase activities in Shetland pony mares.

The incidence of hyperlipaemia in ponies is highest in mares in late gestation and then early in lactation. Plasma lipid and lipoprotein concentrations were measured to establish the metabolic basis for this and the lipoprotein composition of six healthy Shetland ponies was analysed before pregnancy, in the last six weeks of gestation and one month after foaling. In the pregnant ponies, the concentrations of cholesterol and triglyceride were significantly increased (both P < 0.05) because of increased concentrations of high density lipoproteins (HDL) and very low density lipoproteins (VLDL), respectively (both P < 0.05). The VLDL were significantly enriched in triglyceride and depleted of protein (P < 0.05 in each case), with the majority of cholesterol in the free rather than esterified form. These changes appeared to reflect increased hepatic triglyceride synthesis and VLDL secretion because the activities of lipoprotein lipase and hepatic lipase, the enzymes responsible for the catabolism of VLDL and their remnants, were unaltered. After foaling, the concentrations of triglyceride and VLDL decreased significantly (both P < 0.05) because of increased lipoprotein lipase activity consistent with the induction of the enzyme in mammary tissue to provide for milk fat synthesis. Plasma cholesterol and HDL concentrations remained high and non-esterified fatty acid concentrations were significantly increased (P < 0.05). The VLDL remained enriched in triglyceride but had normal cholesterol and protein compositions, although the mass of phospholipids was reduced. The changes in plasma VLDL concentration and composition found in the pregnant ponies mimicked those previously reported in ponies with hyperlipaemia and suggested a metabolic basis for the incidence of the disease in late gestation.

Animals↗
PubMed1977

Interaction of canine and swine lipoproteins with the low density lipoprotein receptor of fibroblasts as correlated with heparin/manganese precipitability.

Canine HDL1 and canine and swine HDLc were fractionated into several lipoprotein subpopulations by heparin/manganese precipitation. The ability of the various subfractions of HDL1 or HDLc to compete with 125I-labeled low density lipoproteins (LDL) for binding and degradation by human fibroblasts was compared. The HDL1 or HDLc which precipitated at the lowest concentration of heparin (a concentration which precipitates LDL) were the most effective in competing with 125I-LDL for binding, internalization, and degradation. A striking characteristic of these lipoproteins was the occurrence of a prominence of the arginine-rich apoprotein. The HDL1 or HDLc subfractions which were not precipitated by heparin/managanese lacked detectable arginine-rich apoprotein and did not compete significantly with the 125I-LDL for binding and degradation. Furthermore, the lipid to protein ratio differed in the precipitable and nonprecipitable lipoproteins, with those which were most efficiently bound and degraded containing more cholesterol. Specific lipoprotein interaction with heparin and with the cell surface receptors may occur by a common mechanism; namely, through a positively charged region on the lipoprotein surface which may reside with the B and arginine-rich apoproteins.

Animals↗
PubMed1972

Very low density lipoproteins and lipoprotein lipase in serum of rats deficient in essential fatty acids.

Rats fed a diet deficient in essential fatty acids have a low level of serum very low density lipoproteins (VLDL). It was found that after intraperitoneal injection of heparin, deficient rats had a higher level of lipoprotein lipase activity in their plasma than did normal rats. VLDL isolated from serum of normal and deficient rats were compared as substrates for postheparin lipase of rat plasma. There was no significant difference in V(max) between the two preparations of lipoproteins, but the apparent K(m) for lipoproteins from deficient animals was significantly less than that for normal animals. These observations suggest that the low concentration of VLDL in deficient rats may be explained (a) by an increased activity of lipoprotein lipase in the tissues of these animals and (b) by the VLDL of deficient rats being more rapidly hydrolyzed at low concentrations by lipoprotein lipase than VLDL from normal rats.

Animals↗
PubMed1994

Overfeeding increases very low density lipoprotein diameter and causes the appearance of a unique lipoprotein particle in association with failed yolk deposition.

Structurally specific very low density lipoprotein (VLDL) particles are presumed to redirect VLDL uptake during yolk deposition. Egg production is an energy intensive process, but energy excess negatively affects egg production. This study sought to determine whether overfeeding changed hen lipoprotein profiles, and if so, whether changes were related to egg production. Overfeeding caused 33% of hens to stop yolk deposition and reabsorb unovulated follicles (involute). VLDL of control hens possessed characteristic small particle size (30 nm) and composition indicative of limited intravascular metabolism. Overfeeding generally increased VLDL diameter, the effect being slight (+6.6 nm) in overfed laying hens when compared to overfed-involuted hens (+51.2 nm). Changes in composition indicated that increased intravascular metabolism of VLDL parallelled increases in particle diameter. Overfed-involuted hens showed significant elevations of plasma low density lipoprotein, VLDL cholesteryl ester, and high density lipoprotein (HDL) triacylglycerol content. Overfeeding increased plasma HDL, and in association with involution, caused redistribution of HDL particle sizes, including the appearance of novel HDL approximately 20 nm in diameter, termed HDLR, and a 97 kDa protein within the HDL fraction. The overfed hen model may provide new insight into the role of lipoprotein physical properties in determining the metabolism of triacylglycerol-rich lipoprotein, and the process of reverse lipid transport. Overfeeding generally increases VLDL size and plasma HDL levels suggesting that increased peripheral metabolism, and perhaps mechanical exclusion of enlarged VLDL by the granulosa basal lamina, contribute to the obesity and impaired yolk deposition observed in hens with excessive energy intakes. Temporal definition of massive VLDL enlargement relative to follicular collapse remains to be established.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗
PubMed1996

Longitudinal study on lipoprotein profile, high density lipoprotein subclass, and postheparin lipases during gestation in women.

To understand the mechanism responsible for maternal hyperlipidemia, 25 healthy pregnant women were studied longitudinally during the three trimesters of gestation and at post-partum, and 11 were studied again at post-lactation. Triglyceride and cholesterol levels increased with gestation in all the lipoprotein fractions. However, the greatest change appeared in low density (LDL) and high density (HDL) lipoproteins, both of which showed an increase in their triglyceride/cholesterol ratio. The proportional distribution of HDL subfractions showed that the HDL2b fraction was the only one that increased with gestation, whereas both HDL3a and HDL3b had the greatest decrease. Cholesteryl ester transfer protein activity increased during the second trimester of gestation. While postheparin lipoprotein lipase activity decreased during the third trimester, postheparin hepatic lipase activity progressively decreased from the first trimester. The 17 beta-estradiol, progesterone, and prolactin hormones progressively increased from the first trimester of gestation. The lipoprotein-triglyceride values correlated linearly and negatively with the logarithm of either postheparin lipase activities, HDL-triglycerides showing the highest correlation coefficient when plotted against the hepatic lipase values (r = -0.757). It appeared that the highest correlation between any of the HDL subclasses and the activity of the enzymes was for hepatic lipase activity versus HDL2b (r = 0.456) or HDL3a (r = 0.519). A significant lineal correlation also appeared between the postheparin hepatic lipase activity and the logarithm of any of the sex hormones studied, the highest value corresponding to estradiol (r = -0.783). Therefore, during gestation, the effect of estrogen in enhancing very low density lipoprotein (VLDL) production and decreasing hepatic lipase activity plays a key role in the accumulation of triglycerides in lipoproteins of density higher than VLDL.

Adult↗
PubMed1996

[Very low density lipoproteins and subclasses of intermediate density lipoproteins in postmenopausal women].

Post menopausal women present an increase of cardiovascular risk associated with the atherogenic plasma lipoproteins IDL and LDL. Our purpose was to study the composition of VLDL, IDL and the subfractions IDL-1 and IDL-2, and the Lipoprotein Lipase and Hepatic Lipase activities in a group of twelve healthy post menopausal women as compared with eleven fertile controls. The mean values of total cholesterol and LDL cholesterol were significantly increased in the post menopausal group compared to the controls (p < 0.005 and p < 0.001 respectively). The contribution of the HDL-cholesterol plasma concentration to total cholesterol was lower in the postmenopausal women (p < 0.02) although no one had HDL-cholesterol lower than 35 mg/dl and the mean value was 50 mg/dl. Postmenopausal women had increased concentrations of VLDL, total IDL and IDL-2 compared to controls (p < 0.05, p < 0.005 and p < 0.001 respectively). Plasma concentrations of total IDL was increased in postmenopausal women (33.6 +/- 3.4 vs 22.6 +/- 0.8 mg/dl, p < 0.005). The increase in total IDL was due to IDL-2 (19.9 +/- 1.7 vs 11.5 +/- 0.8 mg/dl, p < 0.001, in postmenopausal women vs controls). The IDL-2 subfraction was 60 +/- 2.6% of total IDL in postmenopausal women and 51 +/- 2.0% in controls (p < 0.02). In postmenopausal women and in controls the ratio triglyceride/protein (which indicates particles size) was significantly higher in IDL-1 than in IDL-2 (p < 0.005 and p < 0.01 respectively), but this ratio did not show differences when VLDL, total IDL and IDL-2 were compared between postmenopausal and control women. Then, the increased plasma concentration of these lipoproteins would show an increased number of particles in the postmenopausal women vs controls. There were no differences in the Lipoprotein Lipase and Hepatic Lipase activities between both groups. Lipoprotein Lipase vs total IDL-triglycerides and IDL-2-triglycerides showed a significant inverse correlation in controls (p < 0.05) but not in postmenopausal women. We conclude that the qualitative and quantitative study of the lipoproteins shows a more atherogenic profile in the postmenopausal group, with an increase in the concentration and number of particles of VLDL, total IDL and IDL-2.

Cholesterol, HDL↗
PubMed1988

Lipoprotein pattern and plasma lipoprotein lipase activities in patients with primary biliary cirrhosis. Relationship with increase of HDL2 fraction in Lp-X-positive and Lp-X-negative subjects.

Plasma lipids, apoprotein A-I and B in serum and in lipoprotein fractions (VLDL + LDL, HDL2, and HDL3) obtained by preparative ultracentrifugation, as well as postheparin lipoprotein lipase activity (H-TGL and LPL) were evaluated in 17 subjects with primary biliary cirrhosis (stage II and III) subdivided into two groups according to the presence or absence of lipoprotein X (Lp-X). A reduction in total lipoprotein lipase activity was observed in both patient groups, compared to controls (P less than 0.01); the hepatic lipoprotein lipase was significantly reduced (P less than 0.01) only in the Lp-X-positive group. The lipid (477.8 +/- 154.3 vs 239.6 +/- 51.1; P less than 0.01) and protein (147.4 +/- 37.1 vs 83.3 +/- 19.7; P less than 0.01) masses in the VLDL + LDL fraction of the Lp-X-positive group were increased compared to controls. In the same group, the HDL2 fraction also showed an increase in lipid (186.6 +/- 80.0 vs 77.9 +/- 21.6; P less than 0.01) and protein (133.9 +/- 60.0 vs 67.9 +/- 16.5; P less than 0.01) masses; in addition, the HDL2 percent lipid composition was different in the two patient groups, showing a decrease in esterified cholesterol (20.4 +/- 3.6 vs 25.7 +/- 2.2; P less than 0.01) and an increase in phospholipids (59.2 +/- 2.9 vs 54.8 +/- 2.6; p less than 0.01) in the Lp-X-positive group.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoproteins B↗
PubMed1985

Serum low-density lipoprotein and high-density lipoprotein cholesterol, and liver size in subjects on drugs inducing hepatic microsomal enzymes.

Serum low-density lipoprotein cholesterol and high-density lipoprotein cholesterol concentration and the ratio between them, major risk factors of coronary heart disease, and liver size were investigated in 18 subjects who were on enzyme-inducing anticonvulsants, phenytoin alone or in combination with phenobarbital and/or carbamazepine. The subjects with a high liver cytochrome P-450, indicating hepatic microsomal enzyme induction, who showed an increase in liver size, had an elevated high-density lipoprotein concentration and high-density lipoprotein cholesterol/total cholesterol ratio, and a reduced low/high-density lipoprotein cholesterol ratio. The high-density lipoprotein cholesterol concentration and its ratio to total cholesterol were directly and related to the ratio between low and high-density lipoprotein cholesterol were inversely related to the extent of liver enlargement. The serum cholesterol distribution profile associated with an increase in liver size was typical of subjects with a low risk of coronary heart disease. The results suggest that enzyme-inducers, such as phenytoin and phenobarbital, induce structural and functional changes in hepatocellular membranes associated with liver enlargement and cholesterol distribution characteristic of low susceptibility to atherosclerotic vascular disease.

Adult↗
PubMed2002

Relationship between smoking habits and low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, and triglycerides in a hypercholesterolemic adult cohort, in relation to gender and age.

Elevated total cholesterol, the related low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, triglycerides, and smoking habits are risk factors for cardiovascular disease. The objective of this study was to investigate the influence of habitual smoking on these parameters in 492 hypercholesterolemic men and women, aged between 26 and 66 years. Relative differences between smokers and non-smokers in the mean values of total cholesterol, low-density and hig-density lipoprotein-cholesterol, and triglycerides were 2.2%, 5.5%, -8.1%, and 13.7%, respectively. These differences were statistically significant (P<0.04). Over the entire cohort, including men and women, age did not affect the mean values significantly, except for total cholesterol and triglyceride values in smoking women, which were significantly higher in women over 50 years than in the younger women (P=0.011 and P=0.004). In both men and women, regardless of smoking habits, 43%-59% of subjects exceeded the upper reference range value for low-density lipoprotein-cholesterol (4.9 mmol/l), while 38%-59% exceeded the upper reference range value for triglycerides (2.0 mmol/l) and 82%-91% had values below the lower reference range value for high-density lipoprotein-cholesterol (0.9 mmol/l for men, 1.2 mmol/l for women). Smoking habits hardly influenced the extent to which reference values were exceeded, except for low-density lipoprotein-cholesterol in all subjects (higher percentage for smokers, P=0.041). Similar results were obtained for age, except for triglycerides in smoking women, wich showed high values in 26% of women <50 years versus 50% of women > or = 50 years (P=0.026). In conclusion, smoking has an adverse effect on low-density and high-density lipoprotein-cholesterol, and triglycerides in a hypercholesterolemic population of men and women, regardless of age.

Adult↗
PubMed1987

Serum cholesterol (total, low-density lipoprotein, and high-density lipoprotein cholesterol), triglyceride levels, and fat consumption among Jerusalem Arab and Jewish schoolchildren.

As part of initial health screening for the "Know Your Body" Program-based comprehensive health education program, 841 Jerusalem first- and second-grade schoolchildren were tested for total serum cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triglycerides. The same population, which included 643 Jewish (76.5%) and 198 Arab children (23.5%), had their nutritional habits evaluated by means of a parent-completed food-frequency questionnaire. Arab schoolchildren had significantly lower total, high-density lipoprotein, and low-density lipoprotein cholesterol levels and higher triglyceride levels than the Jewish children studied (total cholesterol: Arab mean, 153.1 mg/dl, Jewish mean, 170.3 mg/dl; high-density lipoprotein cholesterol: Arab mean, 46.4 mg/dl, Jewish mean, 48.5 mg/dl; low-density lipoprotein cholesterol: Arab mean, 90.7 mg/dl, Jewish mean, 108.5 mg/dl; triglycerides: Arab mean, 77.9 mg/dl, Jewish mean, 66.3 mg/dl). No significant differences in consumption level of foods high in saturated fats and/or cholesterol were found between populations, although the Arab children showed a tendency to eat more of these foods. Significant differences in total cholesterol values were also found among Jewish children of different origins, but no significant differences were found in consumption levels of saturated fats and cholesterol. Further studies are needed to determine the reasons for the differences in total cholesterol and lipoprotein levels found between Jewish and Arab schoolchildren.

Child↗
PubMed1989

Arterial blood derived low density lipoprotein increases platelet aggregation and macrophage cholesterol content in comparison to lipoprotein derived from veinous blood.

We studied the biochemical and biological properties of plasma lipoproteins taken from blood derived from either the aorta or femoral vein of patients with normal coronary arteriography. There were no significant differences in concentrations of cholesterol, triglycerides, apoprotein A-1 and apoprotein B derived from either source. The cholesterol content of very low density lipoprotein (VLDL) and high density lipoprotein (HDL) was similar in both aortic and venous blood. The low density lipoprotein (LDL) concentration, however, was significantly higher in the aortic blood sample. Arterial LDL significantly enhanced in vitro platelet aggregation when compared to venous LDL. (p less than 0.02). When incubated with mouse peritoneal macrophages (MPM) arterial LDL and VLDL caused an increased cholesterol accumulation and enhanced cholesterol esterification within these macrophages. The venous lipoproteins had little effect. The differences noted in the arterial lipoproteins in composition and biological function when compared to venous lipoproteins might be related to the much higher incidence of atherosclerosis found in the arterial tree.

Adult↗
PubMed1988

Genetics of the quantitative Lp(a) lipoprotein trait. I. Relation of LP(a) glycoprotein phenotypes to Lp(a) lipoprotein concentrations in plasma.

The Lp(a) lipoprotein is a complex particle composed of a low density lipoprotein (LDL)-like lipoprotein and the disulfide bonded Lp(a) glycoprotein. The complex represents a quantitative genetic trait. SDS gel electrophoresis under reducing conditions of sera followed by immunoblotting with affinity-purified polyclonal anti-Lp(a) demonstrated inter- and intra-individual size heterogeneity of the glycoprotein with apparent Mr in the range 400-700kDa. According to their relative mobilities compared to apo B-100 the Lp(a) patterns were categorized into phenotypes F, B, S1, S2, S3 und S4 and into the respective double-band phenotypes. This size heterogeneity seems to be controlled by multiple alleles designated LpF, LpB, LpS1, LpS2, LpS3, LpS4 and a null allele (LpO) at a single locus. Phenotype frequencies observed in 441 unrelated subjects were in good agreement with those expected from the genetic hypothesis. Comparison of Lp(a) lipoprotein concentrations in the different phenotypes revealed a highly significant association of phenotypes B, S1 and S2 with high, and phenotypes S3 und S4 with intermediate Lp(a) concentrations. A third mode is represented by the null phenotype were no Lp(a) band is detected upon immunoblotting and Lp(a) lipoprotein is low or absent. We conclude that the same gene locus is involved in determining Lp(a) glycoprotein phenotype and Lp(a) lipoprotein concentrations in plasma. This major gene seems to be the Lp(a) glycoprotein structural gene locus.

Alleles↗
PubMed1996

Lipoprotein composition in NIDDM: effects of dietary oleic acid on the composition, oxidisability and function of low and high density lipoproteins.

Oxidation of low density lipoprotein (LDL) plays an important role in the pathogenesis of atherosclerosis and is related to the fatty acid composition which is altered in diabetes mellitus. This study examines the relationship between the fatty acid composition of LDL and high density lipoprotein (HDL) and lipoprotein oxidation. A group of nine non-insulin-dependent diabetic (NIDDM) patients were compared to seven healthy control subjects before and after a high monounsaturated diet. Lipoproteins were isolated and oxidisability was measured by conjugated diene formation and lipid peroxide analysis. Serum HDL cholesterol was significantly lower in the diabetic patients. LDL cholesteryl ester linoleic acid in the diabetic patients was significantly higher at baseline and decreased after diet (p < 0.05) while oleic acid increased in both diabetic and non-diabetic subjects (p < 0.05). HDL cholesteryl ester oleic acid was lower in the diabetic patients compared with control subjects (p < 0.05) before diet and it increased significantly after diet (p < 0.05). LDL lipid peroxides and conjugated diene formation were related to LDL glycation (r = 0.46, p < 0.05 and r = 0.49, p < 0.05, respectively). Both decreased following diet (lipid peroxides for diabetic patients from 476 +/- 30 to 390 +/- 20 nmol/mg protein p < 0.05 and for control subjects from 350 +/- 36 to 198 +/- 30 nmol/mg protein p < 0.05). HDL conjugated diene formation decreased in both groups after diet but only significantly in the control group (55.4 +/- 7.5 to 53.2 +/- 6.7 nmol/mg protein for diabetic patients and 45.8 +/- 6.4 to 31.6 +/- 4.8 nmol/mg protein p < 0.05 for control subjects). There was a positive correlation between LDL lipid peroxide formation and percentage of cholesteryl ester linoleic acid in LDL from diabetic patients (r = 0.61, p < 0.05) and control subjects (r = 0.91, p < 0.01). Fatty acid composition of LDL was reflected in the composition of HDL. In the presence of HDL lipoprotein peroxidation decreased. This decrease in lipoprotein peroxidation was positively related to the percentage of linoleic acid in LDL (r = 0.71, p < 0.05). This study confirms the close relationship between the fatty acid composition of LDL and HDL and demonstrates the importance of the fatty acid composition of the cholesteryl ester fraction in relation to LDL oxidation in diabetes. Linoleic acid in HDL appears to be a protecting factor against oxidation.

Adult↗
PubMed1984

Glucose tolerance, plasma lipoproteins and tissue lipoprotein lipase activities in body builders.

Oral glucose tolerance, insulin binding to erythrocyte receptors, serum lipids, and lipoproteins, and lipoprotein lipase activities of adipose tissue and skeletal muscle were measured in nine body builders (relative body weight (RBW) 118 +/- 4%), eight weight-matched (RBW 120 +/- 5%) and seven normal-weight controls (RBW 111 +/- 3%). The body builders had 50% higher relative muscle mass of body weight (% muscle) and 50% smaller relative body fat content (% fat) than the two other groups (P less than 0.005). Maximal aerobic power was comparable in the three groups. In the oral glucose tolerance test (OGTT), blood glucose levels, and plasma insulin levels were lower (P less than 0.05) in the body builders than in weight-matched controls. Insulin binding to erythrocytes was similar in each group. On the basis of multiple linear regression analysis, 87% of the variation in plasma insulin response could be explained by body composition (% muscle and % fat) and VO2max. Plasma total cholesterol, low-density lipoprotein (LDL) cholesterol, and very low-density lipoprotein (VLDL) triglyceride concentrations were significantly lower in the body builders than in weight-matched controls. In comparison with the normal-weight group, the body builders had a lower total cholesterol level. High density lipoprotein (HDL) cholesterol, its subfractions (HDL2 and HDL3 cholesterol) and lipoprotein lipase (LPL) activities of adipose tissue and skeletal muscle were comparable in all three groups. Partial correlation analysis showed a positive relationship between plasma total triglyceride, total cholesterol and LDL cholesterol on the other hand and the % fat on the other.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1983

[Lipoproteins and lipoprotein receptors and their significance for the pathogenesis of arteriosclerosis].

Plasma lipoproteins are macromolecular complexes which serve as vehicles for the transport of lipids in the blood in a soluble form. The protein components of lipoproteins are referred to as apoproteins. They apparently direct each lipoprotein to its site of metabolism. It is now evident that lipoprotein receptors on the surface of cells in the liver, extrahepatic tissues and perhaps in the RES mediate the uptake of lipoproteins by these tissues. Understanding the mechanisms of the uptake of atherogenic lipoproteins by the cells will lead to further insights of the etiology of atherosclerosis.

Apoproteins↗
PubMed1985

Plasma lipoproteins and lipoprotein lipase in young diabetics with and without ketonuria.

Plasma lipoprotein and lipoprotein lipase activity have been evaluated in young diabetics with and without ketonuria and in healthy controls of the same age. Fifteen (age range 7-23 years) newly detected diabetics (8 with ketonuria, 7 non ketonuric) have been examined before starting the treatment. Five healthy medical students (age range 19-21 years) have also been studied. Both ketotic and non ketotic patients showed an impaired insulin and C-peptide response to the glucose load in comparison to controls. Ketotic patients had low lipoprotein lipase activity (p less than 0.01) and high density lipoprotein (p less than 0.01); total plasma Triglycerides and VLDL Triglyceride and Cholesterol were higher than in controls. Plasma Triglyceride and VLDL Triglyceride and Cholesterol were inversely related to lipoprotein lipase activity. Low lipoprotein lipase activity, from adipose tissue and muscle, has been found to be associated with hypertriglyceridemia and reduced HDL Cholesterol in young diabetic patients with ketonuria.

Adolescent↗