Retraction: Nassef, Y. et al. The Impact of Aerobic Exercise and Badminton on HDL Cholesterol Levels in Adult Taiwanese. Nutrients 2019, 11, 515

Elevated levels of high-density lipoprotein cholesterol (HDL-C) have been associated with a decreased risk of coronary heart disease (CHD). An active lifestyle is necessary to improve HDL-C, including (but not limited to) physical exercise. Research on the association between badminton, an intermittent exercise, and HDL-C is limited. We investigated the impact of aerobic exercise and badminton on HDL-C levels in Taiwanese adults. The sociodemographic data of 7543 participants, comprising 3472 men and 4071 women aged between 30 and 70 years, were retrieved from the Taiwan Biobank. The participants were grouped into three exercise categories—no exercise, aerobic exercise, and badminton exercise. The HDL-C levels were compared using an analysis of variance (ANOVA). Multivariate linear regression models were used to determine the associations between HDL and exercise. Comparing the other two groups to the no-exercise group, the individuals who were engaged in aerobic and badminton exercise were significantly associated with higher HDL-C levels (β = 1.4077; p < 0.0001 and β = 5.6052; p = 0.0079, respectively). Aerobic exercise and badminton were also associated with higher HDL-C levels among carriers of the lipoprotein lipase (LPL) rs328 genotypes. Aerobic exercise and regular badminton were associated with higher levels of HDL-C, with the badminton group being more significant.

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The Impact of Aerobic Exercise and Badminton on HDL Cholesterol Levels in Adult Taiwanese

Nutrients ◽

10.3390/nu11030515 ◽

2019 ◽

Vol 11 (3) ◽

pp. 515 ◽

Cited By ~ 5

Author(s):

Yasser Nassef ◽

Kuan-Jung Lee ◽

Oswald Nfor ◽

Disline Tantoh ◽

Ming-Chih Chou ◽

...

Keyword(s):

Aerobic Exercise ◽

Regression Models ◽

Intermittent Exercise ◽

Density Lipoprotein ◽

Hdl Cholesterol ◽

Exercise Group ◽

Linear Regression Models ◽

Active Lifestyle ◽

Cholesterol Levels ◽

The Impact

Elevated levels of high-density lipoprotein cholesterol (HDL-C) have been associated with a decreased risk of coronary heart disease (CHD). An active lifestyle is necessary in order to improve lipid HDL-C, including (but not limited to) physical exercise. Research on the association between badminton, an intermittent exercise, and HDL-C is limited. We investigated the impact of aerobic exercise and badminton on HDL-C levels in Taiwanese adults. The sociodemographic data of 7797 participants comprising 3559 men and 4238 women aged between 30 to 70 years were retrieved from the Taiwan Biobank. The participants were grouped into three exercise categories—no exercise, aerobic exercise, and badminton exercise. The HDL-C levels were compared using an analysis of variance (ANOVA). The multivariate linear regression models were used to determine the associations between HDL and exercise. Comparing the other two groups to the no-exercise group, the individuals who were engaged in aerobic and badminton exercise were significantly associated with a higher HDL-C (β =1.3154; p <0.0001 and β = 6.5954; p = 0.0027, respectively). Aerobic exercise and badminton were also associated with higher HDL-C levels among carriers of the lipoprotein lipase (LPL) rs328 genotypes. Aerobic exercise and regular badminton were associated with higher levels of HDL-C, with the badminton group being more significant.

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Abstract P291: Effects of a Multidisciplinary Lifestyle Intervention on HDL Cholesterol Efflux Capacities in Adolescents With Obesity

Circulation ◽

10.1161/circ.141.suppl_1.p291 ◽

2020 ◽

Vol 141 (Suppl_1) ◽

Author(s):

Katherine Gagnon ◽

Marjorie Boyer ◽

Benoit J. Arsenault ◽

Dominique Desrosiers ◽

Johanne Harvey ◽

...

Keyword(s):

Cholesterol Efflux ◽

Intervention Program ◽

Lifestyle Modification ◽

Hdl Cholesterol ◽

Activity Levels ◽

Cholesterol Levels ◽

Increased Risk ◽

Lifestyle Modification Program ◽

Induced Changes ◽

The Impact

Studies have suggested that a reduced HDL cholesterol efflux capacities (CECs) may be associated with an increased risk of coronary heart disease. However, only few studies have evaluated the impact of a lifestyle modification program on HDL-CEC in adolescents with obesity. The objective of this study was to determine if a 16-week lifestyle modification program would improve HDL-CECs in adolescents with obesity. Twenty-nine adolescents with obesity (16 boys and 13 girls) from 11 to 16 years of age (14.0 ± 1.6 years) were selected to participate in this study. The aim of the lifestyle modification program was to improve eating habits and physical activity levels. During the study, each adolescent was followed by a multidisciplinary team and trained three sessions per week for 16 weeks. The exercise program focused on endurance type activities and all training sessions were supervised and performed in groups. Anthropometric data, metabolic variables and HDL-CECs were measured at baseline and at the end of the intervention. HDL-CECs were measured using ( 3 H)cholesterol-labeled J774 macrophages and HepG2 hepatocytes. Body mass index (33.6 to 32.7 kg/m 2 , p<0.0001) and waist circumference (102.4 to 100.5 cm, p=0.001) were significantly reduced after the 16-week intervention program. We also found a significant decrease in triglyceride concentrations (1.28 to 1.04 mmol/L, p=0.02) as well as in total cholesterol/HDL cholesterol ratio (4.42 to 3.91, p=0.0007) whereas HDL cholesterol levels increased (1.03 to 1.14 mmol/L, p=0.002). J774-HDL-CECs and HepG2-HDL-CECs were not significantly modified after the intervention. In order to further explore the impact of intervention-induced changes in HDL cholesterol levels on exercise-induced changes in HDL-CECs, adolescents were divided into two groups according to their changes in HDL cholesterol levels during the study (low or high intervention-induced changes in HDL cholesterol levels). Adolescents with low HDL cholesterol levels intervention-induced changes did not show an increased in HepG2-HDL-CECs. However, a significant improvement in HepG2-HDL-CEC after the intervention was observed among adolescents characterized by the highest intervention-induced changes in HDL cholesterol levels (p=0.03). Intervention-induced changes in HDL cholesterol levels were also significantly associated with changes in HepG2-HDL-CEC (r=0.55; p=0.002). No association was found between changes in HDL cholesterol levels and changes in J774-HDL-CECs. In conclusion, we found that a structured lifestyle modification program leads to significant improvements in cardiometabolic risk profile and in HepG2-HDL-CEC in obese adolescents.

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Evaluation of the gene–age interactions in HDL cholesterol, LDL cholesterol, and triglyceride levels: The impact of the SORT1 polymorphism on LDL cholesterol levels is age dependent

Atherosclerosis ◽

10.1016/j.atherosclerosis.2011.03.008 ◽

2011 ◽

Vol 217 (1) ◽

pp. 139-141 ◽

Cited By ~ 20

Author(s):

Brian H. Shirts ◽

Sandra J. Hasstedt ◽

Paul N. Hopkins ◽

Steven C. Hunt

Keyword(s):

Ldl Cholesterol ◽

Hdl Cholesterol ◽

Cholesterol Levels ◽

Age Dependent ◽

The Impact ◽

Gene Age

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Dapagliflozin reduces thrombin generation and platelet activation: implications for cardiovascular risk reduction in type 2 diabetes mellitus

Diabetologia ◽

10.1007/s00125-021-05498-0 ◽

2021 ◽

Author(s):

Christina Kohlmorgen ◽

Stephen Gerfer ◽

Kathrin Feldmann ◽

Sören Twarock ◽

Sonja Hartwig ◽

...

Keyword(s):

Type 2 Diabetes ◽

Cardiovascular Risk ◽

Blood Glucose ◽

Platelet Activation ◽

Thrombin Generation ◽

Atherosclerotic Lesion ◽

Hdl Cholesterol ◽

Cholesterol Levels ◽

The Impact

Abstract Aims/hypothesis People with diabetes have an increased cardiovascular risk with an accelerated development of atherosclerosis and an elevated mortality rate after myocardial infarction. Therefore, cardioprotective effects of glucose-lowering therapies are of major importance for the pharmacotherapy of individuals with type 2 diabetes. For sodium–glucose cotransporter 2 inhibitors (SGLT2is), in addition to a reduction in blood glucose, beneficial effects on atherosclerosis, obesity, renal function and blood pressure have been observed. Recent results showed a reduced risk of worsening heart failure and cardiovascular deaths under dapagliflozin treatment irrespective of the diabetic state. However, the underlying mechanisms are yet unknown. Platelets are known drivers of atherosclerosis and atherothrombosis and disturbed platelet activation has also been suggested to occur in type 2 diabetes. Therefore, the present study investigates the impact of the SGLT2i dapagliflozin on the interplay between platelets and inflammation in atherogenesis. Methods Male, 8-week-old LDL-receptor-deficient (Ldlr−/−) mice received a high-fat, high-sucrose diabetogenic diet supplemented without (control) or with dapagliflozin (5 mg/kg body weight per day) for two time periods: 8 and 25 weeks. In a first translational approach, eight healthy volunteers received 10 mg dapagliflozin/day for 4 weeks. Results Dapagliflozin treatment ameliorated atherosclerotic lesion development, reduced circulating platelet–leucocyte aggregates (glycoprotein [GP]Ib+CD45+: 29.40 ± 5.94 vs 17.00 ± 5.69 cells, p < 0.01; GPIb+lymphocyte antigen 6 complex, locus G+ (Ly6G): 8.00 ± 2.45 vs 4.33 ± 1.75 cells, p < 0.05) and decreased aortic macrophage infiltration (1.31 ± 0.62 vs 0.70 ± 0.58 ×103 cells/aorta, p < 0.01). Deeper analysis revealed that dapagliflozin decreased activated CD62P-positive platelets in Ldlr−/− mice fed a diabetogenic diet (3.78 ± 1.20% vs 2.83 ± 1.06%, p < 0.01) without affecting bleeding time (85.29 ± 37.27 vs 89.25 ± 16.26 s, p = 0.78). While blood glucose was only moderately affected, dapagliflozin further reduced endogenous thrombin generation (581.4 ± 194.6 nmol/l × min) × 10−9 thrombin vs 254.1 ± 106.4 (nmol/l × min) × 10−9 thrombin), thereby decreasing one of the most important platelet activators. We observed a direct inhibitory effect of dapagliflozin on isolated platelets. In addition, dapagliflozin increased HDL-cholesterol levels. Importantly, higher HDL-cholesterol levels (1.70 ± 0.58 vs 3.15 ± 1.67 mmol/l, p < 0.01) likely contribute to dapagliflozin-mediated inhibition of platelet activation and thrombin generation. Accordingly, in line with the results in mice, treatment with dapagliflozin lowered CD62P-positive platelet counts in humans after stimulation by collagen-related peptide (CRP; 88.13 ± 5.37% of platelets vs 77.59 ± 10.70%, p < 0.05) or thrombin receptor activator peptide-6 (TRAP-6; 44.23 ± 15.54% vs 28.96 ± 11.41%, p < 0.01) without affecting haemostasis. Conclusions/interpretation We demonstrate that dapagliflozin-mediated atheroprotection in mice is driven by elevated HDL-cholesterol and ameliorated thrombin–platelet-mediated inflammation without interfering with haemostasis. This glucose-independent mechanism likely contributes to dapagliflozin’s beneficial cardiovascular risk profile. Graphical abstract

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What multiple Mendelian randomization approaches reveal about obesity and gout

10.1101/2021.03.26.21254420 ◽

2021 ◽

Author(s):

Charleen D. Adams ◽

Brian Boutwell

Keyword(s):

Observational Studies ◽

Mendelian Randomization ◽

Association Studies ◽

Hdl Cholesterol ◽

P Value ◽

Genome Wide Association Studies ◽

Cholesterol Levels ◽

Genome Wide ◽

The Impact ◽

Apparent Ability

Background/Objectives: Gout is a painful arthritic disease. A robust canon of observational literature suggests strong relationships between obesity, high urate levels, and gout. But findings from observational studies can be fraught with confounding and reverse causation. They can conflict with findings from Mendelian randomization (MR), designed to tackle these biases. We aimed to determine whether the relationships between obesity, higher urate levels, and gout were causal using multiple MR approaches, including an investigation of how other closely related traits, LDL, HDL cholesterol, and triglyceride levels fit into the picture. Subjects/Methods: Summary results from genome-wide association studies of the five above-mentioned traits were extracted and used to perform two-sample (univariable, multivariable, and two-step) MR and MR mediation analysis. Results Obesity increased urate (beta=0.127; 95% CI=0.098, 0.157; P-value=1.2E-17) and triglyceride levels (beta=0.082; 95% CI=0.065, 0.099; P-value=1.2E-21) and decreased HDL cholesterol levels (beta=-0.083; 95% CI=-0.101, -0.065; P-value=2.5E-19). Higher triglyceride levels increased urate levels (beta=0.198; 95% CI=0.146, 0.251; P-value=8.9E-14) and higher HDL levels decreased them (beta=-0.109; 95% CI=-0.148, -0.071; P-value=2.7E-08). Higher urate levels (OR=1.030; 95% CI=1.028, 1.032; P-value=1.1E-130) and obesity caused gout (OR=1.003; 95% CI=1.001, 1.004; P-value=1.3E-04). The mediation MR of obesity on gout with urate levels as a mediator revealed, however, that essentially all of the effect of obesity on gout is mediated through urate. The impact of obesity on LDL cholesterol was null (beta=-0.011; 95% CI=-0.030, 0.008; P-value=2.6E-01), thus it was not included in the multivariable MR. The multivariable MR of obesity, HDL cholesterol, and triglycerides on urate levels revealed that obesity has an effect on urate levels even when accounting for HDL cholesterol and triglyceride levels. Conclusions: Obesity impacts gout indirectly by influencing urate levels and possibly other traits, such as triglycerides, that increase urate levels. Obesity's impact on urate is exacerbated by its apparent ability to decrease HDL cholesterol.

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The Effects of L-Carnitine Supplementation on Serum Lipids: A Systematic Review and Meta-Analysis of Randomized Controlled Trials

Current Pharmaceutical Design ◽

10.2174/1381612825666190830154336 ◽

2019 ◽

Vol 25 (30) ◽

pp. 3266-3281 ◽

Cited By ~ 1

Author(s):

Hadis Fathizadeh ◽

Alireza Milajerdi ◽

Željko Reiner ◽

Fariba Kolahdooz ◽

Maryam Chamani ◽

...

Keyword(s):

Serum Lipids ◽

Ldl Cholesterol ◽

Meta Analysis ◽

Hdl Cholesterol ◽

Health Conditions ◽

Carnitine Supplementation ◽

Randomized Controlled ◽

Cholesterol Levels ◽

Vldl Cholesterol ◽

Subgroup Analyses

Background: The findings of trials investigating the effects of L-carnitine administration on serum lipids are inconsistent. This meta-analysis of randomized controlled trials (RCTs) was performed to summarize the effects of L-carnitine intake on serum lipids in patients and healthy individuals. Methods: Two authors independently searched electronic databases including MEDLINE, EMBASE, Cochrane Library, Web of Science, PubMed and Google Scholar from 1990 until August 1, 2019, in order to find relevant RCTs. The quality of selected RCTs was evaluated using the Cochrane Collaboration risk of bias tool. Cochrane’s Q test and I-square (I2) statistic were used to determine the heterogeneity across included trials. Weight mean difference (SMD) and 95% CI between the two intervention groups were used to determine pooled effect sizes. Subgroup analyses were performed to evaluate the source of heterogeneity based on suspected variables such as, participant’s health conditions, age, dosage of L-carnitine, duration of study, sample size, and study location between primary RCTs. Results: Out of 3460 potential papers selected based on keywords search, 67 studies met the inclusion criteria and were eligible for the meta-analysis. The pooled results indicated that L-carnitine administration led to a significant decrease in triglycerides (WMD: -10.35; 95% CI: -16.43, -4.27), total cholesterol (WMD: -9.47; 95% CI: - 13.23, -5.70) and LDL-cholesterol (LDL-C) concentrations (WMD: -6.25; 95% CI: -9.30, -3.21), and a significant increase in HDL-cholesterol (HDL-C) levels (WMD: 1.39; 95% CI: 0.21, 2.57). L-carnitine supplementation did not influence VLDL-cholesterol concentrations. When we stratified studies for the predefined factors such as dosage, and age, no significant effects of the intervention on triglycerides, LDL-C, and HDL-C levels were found. Conclusion: This meta-analysis demonstrated that L-carnitine administration significantly reduced triglycerides, total cholesterol and LDL-cholesterol levels, and significantly increased HDL-cholesterol levels in the pooled analyses, but did not affect VLDL-cholesterol levels; however, these findings were not confirmed in our subgroup analyses by participant’s health conditions, age, dosage of L-carnitine, duration of study, sample size, and study location.

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