Changes In Plasma Total Cholesterol Research Articles

Gestational cholestyramine treatment protects adult offspring of ApoE-deficient mice against maternal-hypercholesterolemia-induced atherosclerosis.

Perinatal hypercholesterolemia exacerbates the development of atherosclerotic plaques in adult offspring. Here, we aimed to study the effect of maternal treatment with cholestyramine, a lipid-lowering drug, on atherosclerosis development in adult offspring of hypercholesterolemic ApoE-deficient (ApoE-/-) mice. ApoE-/- mice were treated with 3% cholestyramine (CTY) during gestation (G). After weaning, offspring (CTY-G) were fed control diet until sacrificed at 25weeks of age. Atherosclerosis development in the aortic root of offspring was assessed after oil-red-o staining, along with some of predefined atherosclerosis regulators such as LDL and HDL by high-performance liquid chromatography (HPLC), and bile acids (BA) and trimethylamine N-oxide (TMAO) by liquid chromatography-mass spectrometry (LC-MS/MS). In pregnant dams, cholestyramine treatment resulted in significantly lower plasma total- and LDL-cholesterol as well as gallbladder total BA levels. In offspring, both males and females born to treated dams displayed reduced atherosclerotic plaques areas along with less lipid deposition in the aortic root. No significant change in plasma total cholesterol or triglycerides was measured in offspring, but CTY-G males had increased HDL-cholesterol and decreased apolipoproteins B100 to A-I ratio. This latter group also showed reduced gallbladder total and specifically tauro-conjugated bile acid pools, whereas for CTY-G females, hydrophilic plasma tauro-conjugated BA pool was significantly higher. They also benefited from lower plasma TMAO. Prenatal cholestyramine treatment reduces atherosclerosis development in adult offspring of ApoE-/- mice along with modulating the plaques' composition as well as some related biomarkers such as HDL-C, bile acids and TMAO.

Effect of Ocimum sanctum (Basil) leaf in high-fat-diet induced hyperlipidemic rat

Dyslipidemia mediated atherosclerosis is the key pathogenesis of several cardiovascular diseases. Present study aimed to evaluate the therapeutic potential of Ocimum sanctum leaf consumption against high-fat-diet induced hyperlipidemia in rat model. A total of 18 Wistar albino rats (200-215 g) were randomly divided as control, HFD (hyperlipidemic) and OS-treated groups. HFD-group received high fat diet (HFD) for 15 days, OS-treated group administered with Ocimum sanctum leaf powder (200 mg / kg of bodyweight / day) together with HFD diet for 15 days. Blood samples were analyzed for changes in plasma total cholesterol, triglyceride, high-density lipoprotein, low-density lipoprotein and very-low-density lipoprotein. Plasma atherogenic index was also calculated. HFD administration significantly increase plasma lipid levels and atherogenic index in HFD-group. Ocimum sanctum supplementation significantly reduce decrease plasma total cholesterol, triglyceride, lipoproteins and atherogenic index in OS-treated rats. 15 days Ocimum sanctum leaf (powder) supplementation at dose of 200 mg / kg of bodyweight / day effectively attenuates dyslipidemia in hyperlipidemic rats.

Effect of magnesium supplementation on lipid profile: a systematic review and meta-analysis of randomized controlled trials.

We performed a meta-analysis of randomized controlled trials (RCTs) in order to evaluate the effect of oral magnesium supplementation on lipid profile of both diabetic and non-diabetic individuals. PubMed-Medline, SCOPUS, Web of Science, and Google Scholar databases were searched (from inception to February 23, 2016) to identify RCTs evaluating the effect of magnesium on lipid concentrations. A random-effects model and generic inverse variance method were used for quantitative data synthesis. Sensitivity analysis was conducted using the leave-one-out method. A weighted random-effects meta-regression was performed to evaluate the impact of potential confounders on lipid concentrations. Magnesium treatment was not found to significantly affect plasma concentrations of any of the lipid indices including total cholesterol (WMD 0.03mmol/L, 95% CI -0.11, 0.16, p=0.671), LDL-C (WMD -0.01mmol/L, 95% CI -0.13, 0.11, p=0.903), HDL-C (WMD 0.03mmol/L, 95% CI -0.003, 0.06, p=0.076), and triglycerides concentrations (WMD -0.10mmol/L, 95% CI -0.25, 0.04, p=0.149). In a subgroup analysis comparing studies with and without diabetes, no difference was observed between subgroups in terms of changes in plasma total cholesterol (p=0.924), LDL-C (p=0.161), HDL-C (p=0.822), and triglyceride (p=0.162) concentrations. Results of the present meta-analysis indicated that magnesium supplementation showed no significant effects on the lipid profile of either diabetic or non-diabetic individuals.

Effects of acute and chronic heat stress on plasma metabolites, hormones and oxidant status in restrictedly fed broiler breeders

Heat tolerance can be improved by feed restriction in broiler chickens. It is unknown whether the same is true for broiler breeders, which are restrictedly fed. Therefore, the current study was conducted to study the effects of heat stress on plasma metabolites, hormones, and oxidative status of restricted fed broiler breeders with special emphases on the temperature and latency of heat exposure. In trial 1, 12 broiler breeders were kept either in a thermoneutral chamber (21°C, control, n = 6) or in a chamber with a step-wise increased environmental temperature from 21 to 33°C (21, 25, 29, 33°C, heat-stressed, n = 6). Changes in plasma total cholesterol, glucose, and triiodothyronine (T3) were closely related to the environmental temperature. When the temperature reached 29°C, plasma T3 (P < 0.05) was significantly decreased in acute heat-stressed birds, whereas plasma glucose (P < 0.001) and cholesterol (P = 0.002) increased only when the temperature reached 33°C. Plasma triglyceride (P = 0.026) and creatine kinase (CK, P = 0.018) were lower in heat-stressed birds than controls regardless of the temperatures applied. In Trial 2, 24 broiler breeders were divided into 2 groups and raised under 21°C and 32°C for 8 weeks, respectively. Total cholesterol was increased in chronic heat-stressed broiler breeders after 4 weeks. Plasma lactate dehydrogenase (LDH, P = 0.047) and glutamic-oxaloacetic transaminase (GOT, P = 0.036) was up-regulated after 6 weeks of thermal treatment, whereas plasma CK (P = 0.009) was increased at the end of thermal treatment. Plasma malonaldehyde, protein carbonyl content, activity of total superoxide dismutase (SOD), and corticosterone content were not altered after acute and prolonged heat challenges. Taken together, acute heat stress primarily resulted in disturbance of plasma metabolites, whereas chronic heat stress caused tissue damage reflected by increased plasma LDA, GOT, and CK. During acute heat stress, plasma metabolites were minimally disturbed in broiler breeders until the environmental temperature reached 33°C.

RHOA Is a Modulator of the Cholesterol-Lowering Effects of Statin

Although statin drugs are generally efficacious for lowering plasma LDL-cholesterol levels, there is considerable variability in response. To identify candidate genes that may contribute to this variation, we used an unbiased genome-wide filter approach that was applied to 10,149 genes expressed in immortalized lymphoblastoid cell lines (LCLs) derived from 480 participants of the Cholesterol and Pharmacogenomics (CAP) clinical trial of simvastatin. The criteria for identification of candidates included genes whose statin-induced changes in expression were correlated with change in expression of HMGCR, a key regulator of cellular cholesterol metabolism and the target of statin inhibition. This analysis yielded 45 genes, from which RHOA was selected for follow-up because it has been found to participate in mediating the pleiotropic but not the lipid-lowering effects of statin treatment. RHOA knock-down in hepatoma cell lines reduced HMGCR, LDLR, and SREBF2 mRNA expression and increased intracellular cholesterol ester content as well as apolipoprotein B (APOB) concentrations in the conditioned media. Furthermore, inter-individual variation in statin-induced RHOA mRNA expression measured in vitro in CAP LCLs was correlated with the changes in plasma total cholesterol, LDL-cholesterol, and APOB induced by simvastatin treatment (40 mg/d for 6 wk) of the individuals from whom these cell lines were derived. Moreover, the minor allele of rs11716445, a SNP located in a novel cryptic RHOA exon, dramatically increased inclusion of the exon in RHOA transcripts during splicing and was associated with a smaller LDL-cholesterol reduction in response to statin treatment in 1,886 participants from the CAP and Pravastatin Inflamation and CRP Evaluation (PRINCE; pravastatin 40 mg/d) statin clinical trials. Thus, an unbiased filter approach based on transcriptome-wide profiling identified RHOA as a gene contributing to variation in LDL-cholesterol response to statin, illustrating the power of this approach for identifying candidate genes involved in drug response phenotypes.

Adaptive changes in fatty acid profile of erythrocyte membrane in relation to plasma and red cell metabolic changes in chronic alcoholic men

Chronic alcohol consumption is a major reason for several human diseases, and alcoholism has been associated with a variety of societal problems. Changes in fatty acid metabolism in alcoholics and its effects leading to membrane damage are largely unknown. Therefore, we aimed to investigate the fatty acid composition of erythrocyte membrane phospholipids in relation with plasma lipid profile and other plasma metabolites in chronic alcoholics in comparison with controls. We systematically measured the levels of glucose, lactate and pyruvate in the blood and free amino acids, free fatty acids, mucoproteins and glycolipids, total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), very-low-density lipoprotein (VLDL) cholesterol and triglycerides (TG) in plasma of chronic alcoholics and controls. Furthermore, we measured fatty acid composition by gas chromatographic analysis. The fatty acid composition clearly revealed certain changes in chronic alcoholic erythrocyte membrane, chiefly increments in C16:0 and a decrease in C22:4 and C22:6 fatty acids besides the presence of unidentified fatty acids, probably C-24 or C-26 fatty acids. In addition, a significant increase in blood lactate, decrease in blood pyruvate and increased levels of free amino acids and free fatty acids, mucoproteins, VLDL cholesterol, TG and HDL-C in chronic alcoholics were observed with no significant change in plasma TC, LDL-C and glycolipids when compared with controls. Alcohol-induced alterations in plasma and erythrocyte membranes of chronic alcoholics in the present study might be an adaptive response to counteract the deleterious effects of alcohol. The implications of our findings warrant further investigation and needs further in-depth study to explore the mechanisms of alcohol-induced membrane changes.

High Dose trans‐10,cis‐12 CLA Increases Lean Body Mass in Hamsters, but Elevates Levels of Plasma Lipids and Liver Enzyme Biomarkers

The current study examined the efficacy of graded doses of c9,t11 and t10,c12 CLA isomers on body composition, energy expenditure, hepatic and serum lipid liver biomarkers in hamsters. Animals (n=105) were randomized to seven treatments (control, 1, 2, 3% of c9,t11; 1, 2, 3% of t10,c12) for 28days. After 28days treatment, 1-3% of t10,c12 lowered (p<0.05) body fat mass compared to the control group. The 1-3% t10,c12 and 3% c9,t11 fed groups showed higher (p<0.05) lean mass compared to other groups. We observed unfavorable changes in plasma total cholesterol and non-HDL cholesterol levels in animals fed with 3% t10,c12 CLA isomers. The 2%, 3% t10,c12 groups presented elevated (p<0.05) ALT levels. The present data suggest that a diet enriched with more than 2% t10, c12 led to liver malfunction and poses unfavorable changes on plasma lipid profiles. The 1% t10,c12 CLA lowered (p<0.05) body fat mass and increased (p<0.05) lean body mass. The c9,t11 CLA has less potent actions than t10,c12 CLA. We conclude that the actions of CLA on energy and lipid metabolism are form and dose dependent in the hamster model.

CHANGES IN LEVELS OF PLASMA TOTAL CHOLESTEROL, TRIACYLGLYCEROL AND PHOSPHOLIPID IN MICE FED ERABU SEA SNAKE (LATICAUDA SEMIFASCIATA) LIPIDS DIET

ABSTRACT The effects of dietary Erabu sea snake lipids on changes in plasma total cholesterol, triacylglycerol, and phospholipid levels of male Crlj : CD‐1 (ICR) mice was evaluated. Mice were fed three different experimental diets containing 6% lard, 6% Erabu sea snake lipid and 6% fish oil, respectively. Total cholesterol, triacylglycerol and phospholipid levels in plasma collected at weeks 0, 4, 8, 12 and 16 were measured. Levels of plasma total cholesterol and phospholipids in the sea snake dietary group were significantly reduced at weeks 8‐16 from the start of the trial, and plasma triacylglycerol was significantly reduced at week 16, while those in the lard dietary group remained unchanged and/or increased during the period of feeding trial. Plasma total cholesterol and triacylglycerol levels were significantly lower in sea snake lipids as well as fish oil dietary groups than in the lard dietary group at weeks 4–16. The results suggest that Erabu sea snake lipids rapidly induce reduction of plasma lipid levels at week 4 and reduction of plasma lipids and glucose in mice fed the sea snake lipids diet was influenced by the presence of n‐3 polyunsaturated fatty acids in the feed. PRACTICAL APPLICATIONSErabu sea snake lipids have large amounts of n‐3 polyunsaturated fatty acids, and a lowering‐effect on levels of plasma and hepatic total cholesterol, triacylglycerol, phospholipid and plasma glucose in mice similar to fish oil. The sea snake lipids may serve as a beneficial food with regard to lipid and glucose metabolism.

Change in Plasma Lutein after Egg Consumption Is Positively Associated with Plasma Cholesterol and Lipoprotein Size but Negatively Correlated with Body Size in Postmenopausal Women

We investigated associations between plasma concentrations of cholesterol and lutein after consumption of eggs. Using a crossover design, 22 postmenopausal women (50–77 y) consumed an egg treatment (640 mg/d additional cholesterol and 600 μg/d additional lutein + zeaxanthin) or a baseline treatment (no additional cholesterol or lutein + zeaxanthin) for 30 d, followed by a 3-wk washout period and the alternate diet. The increases in plasma total cholesterol and lutein due to egg consumption were related (r = 0.48, P < 0.05). There was a positive correlation between LDL size (r = 0.45, P < 0.05), HDL size (r = 0.64, P < 0.01), and plasma lutein, but no relation with the number of LDL or HDL particles. The activities of cholesterol ester transfer protein and lecithin cholesterol acyltransferase, although important in the exchange of cholesterol among lipoproteins, were not associated with changes in plasma lutein. Plasma lutein concentrations observed during the baseline period were a strong predictor of the increase in plasma lutein after egg treatment (r = 0.50 P < 0.05). There was a negative association between the change in lutein due to egg consumption and BMI (r = −0.40, P < 0.06) and waist circumference (r = −0.49, P < 0.05). This was particularly evident in individuals with BMI >29. We conclude that the increase in plasma lutein after egg consumption is associated with the change in plasma total cholesterol, but that the effect is diminished by obesity. Lipoprotein size, but not number, also affects plasma response to dietary lutein.

Lp(a) enhances coronary atherosclerosis in transgenic Watanabe heritable hyperlipidemic rabbits

Elevated plasma levels of LDL and lipoprotein (a) [Lp(a)] are associated with an increased risk of atherosclerosis and coronary heart disease. However, it is not known whether Lp(a) would enhance the atherogenic effect of LDL on coronary atherosclerosis and myocardial infarction. To address this issue, we cross-bred human Lp(a) transgenic (Tg) rabbits with Watanabe heritable hyperlipidemic (WHHL) rabbits and evaluated the long-term (at the age of 2 years) effects of Lp(a) on the development of coronary atherosclerosis. Compared to non-Tg WHHL rabbits, Tg WHHL rabbits did not show significant changes in plasma total cholesterol, triglycerides, or HDL-C. However, Tg WHHL rabbits showed significantly larger lesions in the right coronary arteries ( p < 0.05). Immunohistochemical staining revealed that the lesions of Tg WHHL rabbits were enriched in the extracellular matrix contents whereas the cellular components were not different from those in non-Tg WHHL rabbits. Increased atherosclerosis in the coronary arteries in Tg WHHL rabbit hearts was also associated with a higher incidence of chronic ischemia and myocardial infarction. These results suggest that increased plasma levels of Lp(a) enhance coronary atherosclerosis and myocardial infarction in the setting of hypercholesterolemia.

Demographic, Environmental, and Genetic Predictors of Metabolic Side Effects of Hydrochlorothiazide Treatment in Hypertensive Subjects

Thiazide diuretics are recommended for first-line treatment of hypertension. Although considered safe and effective, their use is associated with dyslipidemia, hyperglycemia, and an increased risk of developing type 2 diabetes. The aim of this study was to characterize interindividual variation in glucose and lipid responses to hydrochlorothiazide and to identify demographic, environmental, and genetic predictors associated with this variation. A community-based sample of 585 adults with essential hypertension (291 African Americans [150 women and 141 men] and 294 non-Hispanic whites [126 women and 168 men]) underwent monotherapy with hydrochlorothiazide for 4 weeks. Linear regression was used to construct prediction models for the changes in plasma total cholesterol, triglyceride, and glucose concentrations. The mean changes (+/- standard deviation) in response to hydrochlorothiazide were 6.13 +/- 22.8 mg/dL for total cholesterol, 17.21 +/- 70 mg/dL for triglycerides, and 3.5 +/- 9.5 mg/dL for plasma glucose. Ethnicity and baseline levels of the analytes were the only predictors that were significant for more than one response. Therefore, the mechanism for these metabolic effects are not entirely shared. Taken together, demographic, environmental, and genetic factors accounted for only 13% of the total variation in total cholesterol response, 17% of the variation in triglyceride response, and 11% of the variation in glucose response to hydrochlorothiazide, and less than half of this predicted variation in response was explained by measured genotypes.

The peroxisome proliferator-activated receptor α Leu162Val polymorphism influences the metabolic response to a dietary intervention altering fatty acid proportions in healthy men

Serum lipid responses to dietary modification are partly determined by genetic factors. We tested whether plasma lipoprotein and lipid responsiveness to a modification in the dietary ratio of polyunsaturated to saturated fatty acids (P:S) is influenced by the peroxisome proliferator-activated receptor alpha (PPARalpha) Leu162Val polymorphism in healthy men. Ten carriers of the V162 allele and 10 L162 homozygotes were matched according to age and body mass index (BMI). During the protocol, all subjects followed the National Cholesterol Education Program Step I diet, but intake of saturated and polyunsaturated fatty acids was adjusted to obtain a P:S of 0.3 for the first 4-wk period (low-P:S diet) and a P:S of 1.0 for the next 4-wk period (high-P:S diet). At screening, the PPARalpha Leu162Val polymorphism was not associated with anthropometric indexes or plasma lipoprotein and lipid concentrations. After the high-P:S diet, a significant gene-by-diet interaction was observed for changes in plasma total cholesterol, apolipoprotein (apo) A-I, and cholesterol concentrations in small LDL particles (P <or= 0.05). Mean differences after the high-P:S diet were observed between genotype groups for plasma apo A-I concentrations (P<0.05). Changes in BMI, waist circumference, and concentrations of triacylglycerol, phospholipid, and apo B did not differ significantly between groups. The PPARalpha Leu162Val polymorphism may contribute to interindividual variability in plasma lipoprotein and lipid response after modification of the dietary P:S ratio.

A low‐saturated‐fat, low‐cholesterol diet decreases plasma CETP activity and pre β‐HDL formation but does not affect cellular cholesterol efflux to plasma from type 1 diabetic patients

The aim of this study was to evaluate the effect of a low‐saturated‐fat, low‐cholesterol diet on plasma lipopoproteins, pre β‐high density lipoprotein (HDL) formation, lecithin:cholesterol acyltransferase (LCAT), cholesteryl ester transfer protein (CETP) and phospholipid transfer protein (PLTP) activities, as well as on the ability of plasma to stimulate cellular cholesterol efflux. Twelve male type 1 diabetic patients with plasma cholesterol >5.0 mmol/L were studied while consuming their usual diet and after 6 weeks of a low‐fat, low‐cholesterol diet. Pre β‐HDL formation was measured using crossed immuno‐electrophoresis. Plasma LCAT, CETP and PLTP activities were assayed by exogenous substrate methods. The ability of plasma to promote cellular cholesterol efflux out of Fu5AH rat hepatoma cells and out of human skin fibroblasts was also determined. Saturated fat intake was lowered (p = 0.001) due to replacement with carbohydrates, while mono‐ and polyunsaturated fat intake remained unchanged. Cholesterol intake decreased as well (p = 0.003). The changes in plasma total cholesterol, very low and low‐density lipoprotein (VLDL+LDL) cholesterol, HDL cholesterol, HDL phospholipids, apolipoprotein (apo) A‐I, plasma LCAT activity and PLTP activity were not significant. Plasma CETP activity (p = 0.008) and pre β‐HDL formation (p = 0.008) decreased. The ability of plasma to promote cholesterol efflux out of fibroblasts and Fu5AH cells remained unchanged. Reduction in dietary saturated fat and cholesterol intake does not adversely affect cellular cholesterol efflux to plasma from type 1 diabetic patients, despite a drop in pre β‐HDL formation.

Severe Hypoalphalipoproteinemia in Mice Expressing Human Hepatic Lipase Deficient in Binding to Heparan Sulfate Proteoglycan

Unlike human hepatic lipase (hHL) that is mainly cell surface-anchored via binding to heparan sulfate proteoglycans (HSPG), mouse HL (mHL) has a low affinity to HSPG and thus is largely blood-borne. The reduced HSPG binding of mHL is attributable to the C-terminal amino acids. To determine the functions of HSPG binding of hHL in vivo, we created adenovirus vectors encoding hHL or a chimeric protein (designated hHLmt) in which the C-terminal HSPG-binding sequences were replaced with the corresponding mouse sequences. Injecting hHLmt-expressing virus into C57BL/6J mice (1.8 x 10(10) virus particles/mouse) resulted in a 3-fold increase in pre-heparin HL activity, whereas infection with an identical dose of hHL virus did not change pre-heparin HL activity. In hHLmt-expressing mice, the concentration of total cholesterol and phospholipids was inversely related to the hHL activity in pre-heparin plasma in a dose- and time-dependent manner, and the decrease was mainly attributable to high density lipoproteins (HDL) cholesterol and HDL phospholipids. The expression of hHL exhibited no change in plasma total cholesterol or phospholipid levels as compared with control mice infected with luciferase or injected with saline. The reduced HDL lipids in the hHLmt-expressing mice were accompanied by markedly decreased plasma and hepatic apolipoprotein (apo) A-I. In primary hepatocytes isolated from hHLmt-expressing mice, the concentration of cell-associated and secreted apoA-I was decreased by 2-3-fold as compared with hepatocytes isolated from control mice, whereas the levels of apoB and apoE were unaltered. Infection of primary hepatocytes with hHLmt virus ex vivo also resulted in reduced apoA-I secretion but had no effect on cell-associated apoA-I. These results suggest that expression of HSPG binding-deficient hHL has a profound HDL-lowering effect.

Effects of phenanthrene on growth and basic physiological functions of the olive flounder, Paralichthys olivaceus

Flounder were exposed to waterborne phenanthrene (0.5, 1 and 2 μM) for 4 weeks to test effects of waterborne phenanthrene on growth and hematological properties of the olive flounder ( Paralichthys olivaceus). The average weight gain (WG) of flounder was significantly decreased in fish exposed to phenanthrene at 2.0 μM for 2 weeks, whereas WGs of fish treated by 1.0 and 2.0 μM phenanthrene for 4 weeks were significantly decreased. However, hepatosomatic index (HSI) and condition factor (CF) of flounder were not significantly affected by phenanthrene exposure. Red blood cell (RBC) count, hemoglobin (Hb) concentration, hematocrit (Ht), the mean corpuscular hemoglobin (MCH) and the mean corpuscular hemoglobin concentration (MCHC) mean levels were decreased with an increase in exposure time of phenanthrene to the fish, but the level of the mean corpuscular volume (MCV) was increased. Plasma bilirubin concentrations were significantly increased following exposure to waterborne phenanthrene (2.0 μM) for 2 and 4 weeks; however, there were no significant changes in plasma total cholesterol in fish of all treated groups compared to control. The phenanthrene-exposed groups (≥1.0 μM) showed significantly higher mean plasma lysozyme activity. Kidney lysozyme activity of fish exposed to phenanthrene (≥1.0 μM) was also significantly higher than that of control fish. The central finding from these data is that olive flounder exposed to waterborne phenanthrene at more than 1.0 μM are likely to experience negative impacts on fish health and basic physiological functions.

Effects of an antioxidant-rich juice (sea buckthorn) on risk factors for coronary heart disease in humans

There is increasing evidence to support the hypothesis that free radical-mediated oxidative processes contribute to atherogenesis. More recently the ability of antioxidant nutrients to affect cell response and gene expression has been reported in vitro, providing a novel mechanistic perspective for the biological activity of antioxidants. Sea buckthorn ( Hippophaë rhamnoides L.) is a rich source of antioxidants both aqueous and lipophilic, as well as polyunsaturated fatty acids. The objective of the study was to characterize the antioxidant profile of Sea buckthorn juice (SBJ) and to evaluate its effect on plasma lipids, LDL oxidation, platelet aggregation and plasma soluble cell adhesion protein concentration. Twenty healthy male volunteers were given either a placebo or SBJ for 8 weeks. Additional daily intakes of vitamin C, α-tocopherol, β-carotene and flavonoids through SBJ supplementation were 462, 3.2, 1.0 and 355 mg respectively. There were no significant changes in plasma total cholesterol, LDL-C, platelet aggregation or plasma intercellular cell adhesion molecule 1 (ICAM-1) levels between treatment groups. Although not significant, a 20% and 17% increase in plasma HDL-C and triacylglycerol (TAG) concentrations were observed. SBJ supplementation also resulted in a moderate decrease in the susceptibility of LDL to oxidation.

Beneficial effects of increasing monounsaturated fat intake in adolescents with type 1 diabetes

This study aimed to increase the monounsaturated fat content in the diet of outpatient adolescents with type 1 diabetes and to examine the metabolic effects after 12 weeks. Twenty-three adolescents were randomly allocated to either a high monounsaturated fat diet or a control diet. Their mean age was 16.9 (S.D. 2.1) years and median HbA 1c was 9.1% [IQR 7.9–10.4%]. Dietary targets were not reached judged by their 4-day food diaries. However, the whole study group had a significant increase in monounsaturated fat as indexed by red cell phospholipid fatty acids (RCFAs), with an increase of n-9 RCFAs from 14.9% [IQR: 14.5–21.7%] to 21.7% [IQR: 18.8–25.6%] ( P=0.002). Changes in n-9 RCFAs were inversely related to changes in HbA 1c ( R 2=0.26, P=0.02), such that a 10% increase in n-9 RCFAs corresponded to a 0.64% improvement (decrease) in HbA 1c. Changes in n-9 RCFAs were also inversely related to changes in plasma total cholesterol ( R 2=0.38, P=0.002) and plasma LDL cholesterol ( R 2=0.21, P=0.03). These changes were not associated with changes in insulin dose, body weight or physical activity. Overall, the results demonstrate that a modest increase in the monounsaturated fat content of an adolescent diet has the potential to improve glycaemic control and lipid profile.

Cardiovascular Diseases Risk Factors During The First Year of Life 519

The pattern of change in plasma total cholesterol (TC) and blood pressure(SBP and DBP) over time and their relations to anthropometric measurements were observed longitudinally. In 40 infants who were seen at a pediatric clinic in The Woodlands, Texas, TC (by the Reflotron), SBP, DBP (by the Dinamap), weight and body length were measured at ages 0.5, 2, 4, 6, 9 and 12 months. For TC, in males, the greatest increment in median values, from 114 to 134 mg/dl, occurred between ages 0.5 and 2.0 months. For females, the greatest increment in TC, from 131 to 141 mg/dl, occurred between ages 9 and 12 months. There were strong tracking correlations between paired TC measurements taken as early as age 0.5 months with later measurements. These correlations were stronger and more often significant for males than for females. The associations of body measurements with TC were modest at most, and somewhat stronger for females than for males. Infants who received breast milk had mean TC values 47 mg/dl higher than infants receiving formula only during the period of breast feeding. This difference disappeared by age 12 months. For both SBP and DBP, for males and females togather, the greatest increment (10 mmHg) occurred between ages 0.5 and 2.0 months. DBP continued to increase to age 4 months. Tracking correlations of SBP and DBP were generallyweak and not significant for either gender. The correlations between DBP, but not SBP, and body measurements were significant only for females at age 12 months. Maternal history of CVD risk factors was significantly related to SBP in females but not males. For DBP, neither maternal nor paternal history was related. This study further documents changes in TC and blood pressure measurements during infancy with gender differences in behavior of these measurements at this early age.

Replacement of linoleic acid with α-linolenic acid does not alter blood lipids in normolipidaemic men

The effect of partial dietary replacement of linoleic acid (18:2n-6; linoleic acid-rich diet) with alpha-linolenic acid (18:3n-3; alpha-linolenic acid-rich diet) on plasma lipids was investigated in twenty-nine healthy young men. After a 2-week stabilization period subjects were randomly assigned to either the alpha-linolenic acid-rich diet group (n 15), receiving a mean of 10.1 g of alpha-linolenic acid and 12.1 g of linoleic acid/d, or the linoleic acid-rich diet group (n 14), receiving a mean of 1.0 g of alpha-linolenic acid and 21.0 g of linoleic acid/d, for a 6-week test period. Blood samples were taken at the commencement of the stabilization period and at the start (week 0), midpoint (week 3) and endpoint (week 6) of the test period and plasma lipids analysed. The changes occurring on the linoleic acid-rich diet and alpha-linolenic acid-rich diet were compared but no significant differences in the changes in plasma total cholesterol, LDL-cholesterol, HDL-cholesterol, the subfractions HDL2 and HDL3 or triacylglycerols were found. These results indicate that dietary replacement of linoleic acid with alpha-linolenic acid in the diet of healthy male subjects offers similar cardioprotective benefits with respect to lipid metabolism.

Magnesium pyridoxal-5′-phosphate glutamate, "A vitamin B 6 derivative", does not affect lipoprotein levels in patients with familial hypercholesterolaemia

In this double-blind, randomized, placebo-controlled, dose-finding study we assessed the short-term efficacy and safety of increasing dosages of magnesium pyridoxal-5'-phosphate glutamate (MPPG) compared to placebo in patients with familial hypercholesterolaemia (FH). Twenty-three patients of either sex, over the age of 18 years and suffering from heterozygous FH, were treated with MPPG for a period of 16 weeks. Baseline characteristics and lipoprotein profiles of the patients were comparable in the two treatment groups. Overall compliance was 90%. Neither after the first 8 weeks treatment period with 450 mg MPPG daily nor after the second 8 weeks treatment period with 600 mg MPPG daily were statistically significant changes in plasma total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol or triglyceride levels observed between the treatment and placebo groups. Plasma levels of lipoprotein (Lp)(a), apolipoprotein (apo) A1, apo B100, very low density lipoprotein (VLDL) cholesterol and VLDL triglyceride also did not change. Although it has been demonstrated that MPPG improves lipoprotein levels in patients with different forms of dyslipidaemia, MPPG is not effective for the treatment of FH patients.