Increase In High-density Lipoprotein Concentration Research Articles

Дія мелатоніну та кверцетину на запалення i метаболізм за умов цілодобового освітлення та висококалорійної вуглеводно-ліпідної дієти

The study is aimed at investigating the impact of exogenous melatonin and quercetin on indices of systemic inflammatory response and indicators of carbohydrate and lipid metabolism in the blood serum of male rats exposed to round-the-clock lighting (RCL) with 1500 lx intensity during the last 30 days of being kept on a 60 day high-calorie carbohydrate-lipid diet (HCCLD, 20% fructose solution and the proper chow). The study has demonstrated that the restoration of serum melatonin concentration in rats by its exogenous administration during the RCL exposure and keeping them on HCCLD did not fully correct the indicators of the systemic inflammatory response such as the content of tumor necrosis factor α (TNF-α) and C-reactive protein (CRP), as well as indices of carbohydrate and lipid metabolism such as concentration of insulin, highdensity lipoprotein (HDL), very low-density lipoprotein (VLDL) and triglycerides, HOMA-IR insulin resistance index. The administration of quercetin under the experimental conditions was accompanied by a significant increase in the serum melatonin concentration (by 85.9%), a decrease in the content of TNF-α (by 53.9%), CRP (by 54.4%), glucose (by 49.2%), insulin (by 49.6%), VLDL (by 49, 2%) and triglycerides (by 49.3%), and an increase in HDL concentration (by twofold), but these indicators (with the exception of the HOMA-IR index, which decreased by 62.4%) did not reach the values of the intact group. The combined effect of melatonin and quercetin under RCL exposure and HLLD significantly improved the indicators of systemic inflammatory response, carbohydrate and lipid metabolism that is confirmed by a more significant decrease in serum levels of TNF-α, CRP, insulin, VLDL and triglycerides, an increase in HDL concentration, and a decrease in the HOMA-IR index compared with the separate use of melatonin and quercetin.

Resveratrol ameliorates oxidative stress, inflammatory response and lipid metabolism in common carp (Cyprinus carpio) fed with high-fat diet

High-fat diet is regarded as crucial inducers of oxidative stress, inflammation, and metabolic imbalance. In order to investigate the ameliorative potential of resveratrol against the progression of liver injury towards steatohepatitis, common carp (Cyprinus carpio) were distributed into six experimental groups and were fed with a normal-fat diet, a high-fat diet, and supplemented with resveratrol (0.8, 1.6, 2.4, and 3.2 g/kg diet) for 8 weeks. The high-fat diet decreased the antioxidant capacities, as well as causing the inflammatory response and lipid deposition of common carp. Resveratrol induced a marked elevation in the final body weight, weight gain rate, condition factor and significant decrease in the feed conversion ratio. Moreover, dietary resveratrol showed a significant decrease in the alanine aminotransferase, aspartate aminotransferase, triglyceride and low-density lipoprotein levels, which was accompanied by an increase in high-density lipoprotein concentration in serum. A significant elevation in total superoxide dismutase, catalase, glutathione peroxidase and a decreased malondialdehyde content were observed, along with a substantial elevation in antioxidant activities were found. Additionally, fish fed with resveratrol had an up-regulation of hepatic catalase, copper, zinc superoxide dismutase, glutathione peroxidase 1a, and glutathione peroxidase 1b gene expression via Nrf2 signaling pathway. Expectedly, our results also demonstrated that resveratrol regulates hepatic lipid metabolism in fish by inhibiting the expression of hepatic lipogenesis genes (acetyl-CoA carboxylase 1, fatty acid synthase, and sterol regulatory element binding protein 1), fatty acid uptake-related genes of lipoprotein lipase, and β-oxidation-related genes via PPAR-γ signaling pathway. Furthermore, dietary resveratrol reduced inflammation, as evident by down-regulating the interleukin-1β, interleukin-6, interleukin-8, and tumor necrosis factor-α expression levels and upregulating the interleukin-10 and transforming growth factor-β2 expression levels via NF-κB signaling pathway. As a whole, our results demonstrated that resveratrol defensed the impacts against high-fat diet on the serum biochemical, hepatic antioxidants, inflammation, and lipid metabolism.

The effects of cranberry on cardiovascular metabolic risk factors: A systematic review and meta-analysis

The impetus for the current study was to evaluate the efficacy of cranberry supplementation on cardiovascular disease metabolic risk factors in adult populations. A systematic review was conducted on PubMed, Scopus, Web of Science and Google Scholar up to June 2018, to identify randomized controlled trials investigating the effect of cranberry supplementation on cardiovascular metabolic risk factors. The results of the pooled effect size indicated that cranberry administration significantly reduced systolic blood pressure and body mass index. No statistically significant change was observed in triacylglycerol, total cholesterol, low-density lipoprotein, high-density lipoprotein, fasting plasma glucose, fasting insulin, homeostasis model assessment of insulin resistance, diastolic blood pressure, waist circumference, C-reactive protein, and intercellular adhesion molecule. Stratified analysis showed that SBP reduction was more pronounced in studies with ≥50 mean age participants. Also, subgroup analysis suggested a significant increase in high-density lipoprotein concentrations in subgroups with subjects <50 mean age, and triacylglycerol levels in subsets with cranberry administered in juice form. This systematic review and meta-analysis suggests cranberry supplementation may be effective in managing systolic blood pressure, body mass index and high-density lipoprotein in younger adults. Further high-quality studies are needed to confirm these results.

Hypolipidaemic and renoprotective effects of Glycine max (Soy bean) against lipid profile and renal biochemical alterations in hypercholesterolemic rat

Background : Hyperlipidemia can be defined as concentration of lipids in the blood of a fasted (>12hrs) patient that exceeds the upper range of normal for that species. Studies have showed that rats with hypercholesterolemia are prompt to the development of cardiovascular diseases (CVD). Methods: Twenty-four (24) male albino Wister rats were used in this study. The rats weighed between 180-190g and were randomly divided into four (4) groups (A-D) with six (6) rats per group. For hypercholesterolemia induction, rats in group B, C and D were administered with HCD (2000mg/kg) once daily in the presence of carbimazole (1.35mg/kg) for 14days. Group B (test group) were treated with soymilk (2000mg/kg) and group C (positive control) with atorvastatin (20mg/kg) for 14 days. Group A (normal control) received water and vital feed only. At the end, fasting blood specimens were collected from all the animals in all the groups for estimation of lipid profile and renal biochemical parameters. The biochemical parameters of lipid profile: Total Cholesterol (TC), High density lipoprotein (HDL), Low density lipoprotein (LDL), Very low density lipoprotein (VLDL) and Triglycerides (TG) were assayed. Results : Results showed that the test group (soymilk) showed a non-significant decrease in TC, TG, LDL, VLDL and a non-significant increase in HDL concentrations but not as much as group C (Atorvastatin) which showed a significant decrease in TC and LDL (p<0.01), TG (p<0.05), VLDL and also a significant increase in HDL concentrations (p<0.05) when compared to the negative control group (HCD alone).Renal injury was assessed by measuring serum Na + , K + , Cl - , HCO 3 - , creatinine and urea levels. The HCD treatment resulted in marked elevation of: K + (8.670.77mmol/l); creatinine (2.070.23mg/dl); and urea (89.0014.42mg/dl) and caused deranged renal functions which were significantly improved by soymilk treatment: K + (6.510.34mmol/l); creatinine (1.030.24mg/dl); and urea (46.676.89mg/dl) with [P<0.05 or p<0.01]. Conclusion: Arguably, the phytochemicals in soy prevented dyslipidaemia and protected the kidney against the oxidative stress and the resultant renal dysfunction produced by hypercholesterolemia.

Randomized, double-blind, placebo-controlled, clinical study on the effect of Diabetinol&amp;reg; on glycemic control of subjects with impaired fasting glucose

BackgroundThis study investigated the efficacy of Diabetinol® in people with diabetes on medication but not meeting the American Association of Clinical Endocrinologists and American Diabetes Association glycemic, blood pressure, and lipid targets.Subjects and methodsFifty subjects, aged 18–75 years, with fasting blood glucose ≤15.4 mmol/L, hemoglobin A1c levels ≤12%, and a body mass index between 25 and 40 kg/m2, were enrolled in a 24-week, randomized, double-blind, placebo-controlled, parallel study. Diabetinol® or placebo was administered as 2×525 mg capsules/day.ResultsIn the Diabetinol® group, 14.3% versus 0% in the placebo group, 33.3% versus 15.4% in placebo, 20.0% versus 12.5% in placebo, and 83.3% versus 60% in placebo achieved the American Association of Clinical Endocrinologists and American Diabetes Association targets for hemoglobin A1c, low-density lipoprotein, total cholesterol, and systolic blood pressure, respectively. There was no difference in the maximum concentration (Cmax) of serum glucose or area under the curve (AUC)0–240 minutes. The time to Cmax was longer for participants on Diabetinol® than placebo group at week 12 (P=0.01). Fasting blood glucose increased from baseline to week 24 in both groups; however, this increase was 14.3 mg/dL lower in the Diabetinol® group versus placebo. The Diabetinol® group showed an increase of 5.53 mg/dL in fasting insulin at week 12 (P=0.09) and 3.2 mg/dL at week 24 (P=0.41) over and above the placebo group. A decrease of 1.5% in total cholesterol, 5.8% in low-density lipoprotein, and a 1.6% increase in high-density lipoprotein concentrations were seen in the Diabetinol® group. Diabetinol® improved 6-month oral glucose tolerance test and 2-hour postprandial glucose profiles in participants between 40 and 60 years of age.ConclusionThe current study suggests a role for Diabetinol® as an adjunctive therapy for glycemic maintenance and for decreasing the risk of diabetes-associated comorbidities in type 2 diabetic patients on conventional therapies.

Body Composition, Lipid Profile, Adipokine Concentration, and Antioxidant Capacity Changes during Interventions to Treat Overweight with Exercise Programme and Whole-Body Cryostimulation.

The aim of this study was to determine the effect of six-month-long physical exercise programme with a two-time exposure to whole-body cryostimulation (WBC) in 20 sessions on antioxidant enzyme activities, lipid profile, and body composition changes in obese people (30 adult subjects; BMI = 30.39 ± 4.31 kg/m2). Blood samples were taken before the programme, one month following the exercise programme, before and after the first WBC treatment, six months following the exercise programme, after the second WBC treatment, and finally one month after the intervention. Six months of moderate aerobic activity combined with WBC did not change body mass or fat and lean body mass percentages, or circulating adiponectin, leptin, and resistin concentrations. In response to intervention a significant decrease in the level of low-density lipoprotein and triglycerides was observed, with a slight increase in high-density lipoprotein concentration. The nature of changes in the activity of respective antioxidant enzymes was not identical. After one month of increased physical activity, a significant decrease in superoxide dismutase, catalase, and glutathione reductase activities was observed (13%, 8%, and 70%, resp.). The SOD activity increased significantly after successive whole-body cryostimulation sessions. As regards catalase, a significant progressive decrease in its activity was observed.

Changes in Lipidemia during Chronic Care Treatment of Childhood Obesity

Childhood obesity and related co-morbidities are increasing. This intervention study assessed the associations between weight changes and lipidemia in obese children and adolescents. A total of 240 obese children and adolescents (median age, 11.3 years; range, 3.9-20.9) were enrolled in a best-practice multidisciplinary chronic care treatment program. The concentrations of total cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), and triglycerides (TGs) and anthropometric data comprising height and weight were collected at baseline and after up to 39 months of continuous treatment. The BMI standard deviation score (SDS) decreased in 51% of patients and maintained unchanged in 32% of patients during the treatment. At baseline, 65 (27.1%) of the patients exhibited dyslipidemia defined as increased concentrations of total cholesterol (>200 mg/dL), LDL (>130 mg/dL), or TGs (>150 mg/dL), or decreased HDL concentration (<35 mg/dL). Dyslipidemia improved with weight loss; the odds ratio (OR) was 0.37 per BMI SDS (p = 0.014) after adjusting for age, sex, and baseline BMI SDS. Baseline TG concentration correlated positively and HDL concentration correlated negatively with baseline BMI SDS. Weight loss was associated with a decrease in the concentrations of total cholesterol (p = 0.0005), LDL (p < 0.0001), non-HDL (p < 0.0001), and TGs (p < 0.0001), and with an increase in HDL concentration (p < 0.0001). High lipid concentrations were associated with childhood obesity. The lipid profile improved during weight loss independently of the baseline BMI SDS and baseline lipid concentration.

Effects on Plasma Lipids during Long Term Antihypertensive Treatment with Felodipine

A total of 130 patients with mild to moderate hypertension were recruited to an open study and treated with the vascular selective calcium antagonist felodipine (10 to 40mg once daily) for 1 year. For patients completing the study, median lipid concentrations (mmol/L) at baseline were: total cholesterol 6.50, triglycerides 1.44, low density lipoprotein (LDL) 4.20, and high density lipoprotein (HDL) 1.40. Plasma concentrations of total cholesterol, triglycerides and LDL were essentially unchanged during the study, while there was a statistically significant increase in HDL concentration which reflected in a significant decrease in the LDL/HDL ratio; these changes were about 5% in magnitude. Blood pressure was well controlled during treatment and adverse effects were principally related to vasodilation. In total 13 patients were withdrawn during the study, 10 of these due to adverse events. In conclusion, long term antihypertensive treatment with felodipine does not adversely affect plasma lipids. In fact, there was a slight increase in HDL, indicating a possible favourable action.

Pharmacotherapy of disorders of plasma lipoprotein metabolism

Pharmacologic intervention for altering plasma lipoproteins is aimed principally at reducing atherogenesis and thereby preventing coronary artery disease. These drugs should be prescribed only after nonpharmacologic interventions (reduction of saturated fat and cholesterol consumption, weight reduction, aerobic exercise, cessation of cigarette smoking) have failed to achieve an adequate effect. The plasma concentration of the atherogenic low-density lipoprotein (LDL) may be reduced in hypercholesterolemic patients by increasing hepatic LDL receptor synthesis (bile acid sequestering resins, 3-hydroxy-3-methyl-glutaryl coenzyme A reductase inhibitors) or by reducing hepatic very low density lipoprotein synthesis (gemfibrozil, nicotinic acid). LDL concentration may also be reduced by treatment with one of the fibrates (e.g., fenofibrate). Several classes of lipid-lowering drugs also increase the plasma high-density lipoprotein (HDL) cholesterol concentration. In the case of the fibrates, this appears to be principally mediated through an increase in lipoprotein lipase activity. Gemfibrozil additionally stimulates apolipoprotein AI synthesis. The increase in HDL cholesterol produced by nicotinic acid is due primarily to decreased clearance of HDL particles from the circulation. The increase in HDL concentration produced by gemfibrozil was shown in the Helsinki Heart Study to make a major contribution to a reduced incidence of coronary artery disease, independently of that made by the decrease in LDL. The Cholesterol-Lowering Atherosclerosis Study demonstrated that combined therapy with a resin (colestipol) and nicotinic acid can reduce the progression of coronary atherosclerosis and the development of graft lesions in patients who have undergone coronary artery bypass graft surgery.

The influence of cellular and lipoprotein cholesterol contents on the flux of cholesterol between fibroblasts and high density lipoprotein.

Previous studies indicate that free cholesterol moves passively between high density lipoprotein (HDL) and cell plasma membranes by uncatalyzed diffusion of cholesterol molecules in the extracellular aqueous phase. By this mechanism, the rate constants for free cholesterol influx (Cli) and efflux (ke) should not be very sensitive to the free cholesterol content of cells or HDL. Thus, at a given HDL concentration, the unidirectional influx and efflux of cholesterol mass (Fi, Fe) should be proportional to the cholesterol content of HDL and cells, respectively, and net efflux of cholesterol mass (Fe-Fi greater than 0) should occur when either cells are enriched with cholesterol or HDL is depleted of cholesterol. We have examined the influence of cell and HDL free cholesterol contents on the bidirectional flux of free cholesterol between HDL and human fibroblasts and also attempted to detect some dependence of flux on the binding of HDL to the cells. In the range of HDL concentrations from 1 to 1000 micrograms of protein/ml, ke for cell free cholesterol approximately doubled for every 10-fold increase in HDL concentration, reaching 0.04 h-1 at 1000 micrograms of HDL/ml. ke and Cli were not influenced by the doubling of fibroblast free cholesterol content (from 31 +/- 5 to 62 +/- 13 micrograms of cholesterol/mg of protein). There was an approximate exchange of cholesterol between HDL and the unenriched fibroblasts (e.g. at [HDL] = 100 micrograms/ml, Fe and Fi = 3.2 and 3.0 micrograms of cholesterol/[4 h.mg of cell protein], respectively). In contrast, there was substantial net efflux from the enriched cells (at [HDL] = 100 micrograms/ml, Fe and Fi = 5.5 and 3.1 micrograms of cholesterol/[4 h.mg of cell protein], respectively). The rate constants for cholesterol flux were not influenced by changing the free cholesterol content of HDL, so that there was net efflux of cell cholesterol in the presence of cholesterol-depleted HDL and net influx from cholesterol-rich HDL. The Kd of HDL binding to fibroblasts was reduced from 1.7 to 0.9 micrograms/ml by the enrichment of the cells with free cholesterol; this increase in affinity for HDL was not reflected in enhanced rate constants for cholesterol flux. The inhibition of specific HDL binding by treatment of the lipoprotein with dimethyl suberimidate did not affect cholesterol flux using either control or cholesterol-rich cells at any HDL concentration in the range 1-1000 micrograms/ml. The above results are consistent with the concept that net movement of free cholesterol between cells and HDL occurs by passive, mass-action effects.(ABSTRACT TRUNCATED AT 400 WORDS)

Increase in plasma high-density lipoprotein concentration following complete androgen blockage in men with prostatic carcinoma

There is evidence that endogenous estrogens have a positive effect on plasma high density lipoprotein (HDL) concentration, whereas the relation between HDL and male sex hormones is unclear, since both positive and negative effects have been reported. This study examined the effects of LHRH agonist in combination with an antiandrogen on plasma lipids and lipoproteins in 17 elderly men with prostatic carcinoma. Subjects were examined prior to and after therapy at 4-week intervals up to 16 weeks. Prior to therapy, their lipid and lipoprotein profiles were not significantly different from a control group composed of individuals of similar age and living in the same community area. Following therapy plasma levels of testosterone and dihydrotestosterone were markedly decreased (above 90%) and their residual activity neutralized through effective use of an antiandrogen. Plasma estradiol decreased between 65% and 85% and the concentration of cortisol was unaffected. The very low density lipoprotein (VLDL) apo-B decreased and low density lipoprotein (LDL) apo-B increased; thus, no change was observed in the total plasma apo-B levels. Total plasma cholesterol increased by 6% (baseline v peak values, mg/dL, mean ± SEM; 219 ± 9 v 233 ± 9, P < 0.05) due to a significant rise in HDL cholesterol concentration (45.5 ± 2.8 v 56.5 ± 3.6, P < 0.01). Both VLDL and LDL cholesterol levels remained unchanged. The mean elevation of 21% in HDL cholesterol was accompanied by a significant rise in HDL apo-A concentration (161 ± 6 v 193 ± 10, P < 0.01), thus suggesting an increase in HDL mass and/or particle number. The opposite changes in the concentration of apo-B in the VLDL and LDL fractions, together with a corresponding increase in HDL concentration, are suggestive of stimulation in VLDL hydrolysis. The favorable effect of this antihormonal therapy on plasma lipoprotein profile is indicated by decrease in the atherogenic index ratios. Finally, the data suggests that suppression of endogenous androgens in men increases HDL concentration and hence, it may be concluded that the low levels of HDL in men (relative to women) might be the result of the metabolic actions of androgens.