scholarly journals The Effect of Natural Antioxidants in the Development of Metabolic Syndrome: Focus on Bergamot Polyphenolic Fraction

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1504 ◽  
Author(s):  
Cristina Carresi ◽  
Micaela Gliozzi ◽  
Vincenzo Musolino ◽  
Miriam Scicchitano ◽  
Federica Scarano ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Density Lipoprotein ◽  
Natural Antioxidants ◽  
Protective Role ◽  
Clinical Findings ◽  
Lipid Lowering ◽  
Atherosclerotic Cardiovascular Disease ◽  
Pathophysiological Mechanism ◽  
Beneficial Effects ◽  
Increased Risk

Metabolic syndrome (MetS) represents a set of clinical findings that include visceral adiposity, insulin-resistance, high triglycerides (TG), low high-density lipoprotein cholesterol (HDL-C) levels and hypertension, which is linked to an increased risk of developing type 2 diabetes mellitus (T2DM) and atherosclerotic cardiovascular disease (ASCVD). The pathogenesis of MetS involves both genetic and acquired factors triggering oxidative stress, cellular dysfunction and systemic inflammation process mainly responsible for the pathophysiological mechanism. In recent years, MetS has gained importance due to the exponential increase in obesity worldwide. However, at present, it remains underdiagnosed and undertreated. The present review will summarize the pathogenesis of MetS and the existing pharmacological therapies currently used and focus attention on the beneficial effects of natural compounds to reduce the risk and progression of MetS. In this regard, emerging evidence suggests a potential protective role of bergamot extracts, in particular bergamot flavonoids, in the management of different features of MetS, due to their pleiotropic anti-oxidative, anti-inflammatory and lipid-lowering effects.

scholarly journals Low Detection Rates of Genetic FH in Cohort of Patients With Severe Hypercholesterolemia in the United Arabic Emirates

2022 ◽  
Vol 12 ◽  
Author(s):  
Antoine Rimbert ◽  
Hinda Daggag ◽  
Peter Lansberg ◽  
Adam Buckley ◽  
Martijn Viel ◽  
...  
Keyword(s):  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Lipid Lowering ◽  
Published Data ◽  
Study Cohort ◽  
Atherosclerotic Cardiovascular Disease ◽  
Gulf Region ◽  
Detection Rates ◽  
Screening Programs ◽  
Increased Risk

Background: Programs to screen for Familial hypercholesterolemia (FH) are conducted worldwide. In Western societies, these programs have been shown to be cost-effective with hit/detection rates of 1 in 217–250. Thus far, there is no published data on genetic FH in the Gulf region. Using United Arab Emirates as a proxy for the Gulf region, we assessed the prevalence of genetically confirmed FH in the Emirati population sample.Materials and Methods: We recruited 229 patients with LDL-C >95th percentile and employed a customized next generation sequencing pipeline to screen canonical FH genes (LDLR, APOB, PCSK9, LDLRAP1).Results: Participants were characterized by mean total cholesterol and low-density lipoprotein cholesterol (LDL-c) of 6.3 ± 1.1 and 4.7 ± 1.1 mmol/L respectively. Ninety-six percent of the participants were using lipid-lowering medication with mean corrected LDL-c values of 10.0 ± 3.0 mmol/L 15 out of 229 participants were found to suffer from genetically confirmed FH. Carriers of causal genetic variants for FH had higher on-treatment LDL-c compared to those without causal variants (5.7 ± 1.5 vs 4.7 ± 1.0; p = 3.7E-04). The groups did not differ regarding high-density lipoprotein cholesterol, triglycerides, body mass index, blood pressure, glucose, and glycated haemoglobin.Conclusion: This study reveals a low 7% prevalence of genetic FH in Emiratis with marked hypercholesterolemia as determined by correcting LDL-c for the use of lipid-lowering treatment. The portfolio of mutations identified is, to a large extent, unique and includes gene duplications. Our findings warrant further studies into origins of hypercholesterolemia in these patients. This is further supported by the fact that these patients are also characterized by high prevalence of type 2 diabetes (42% in the current study cohort) which already puts them at an increased risk of atherosclerotic cardiovascular disease. These results may also be useful in public health initiatives for FH cascade screening programs in the UAE and maybe the Gulf region.

scholarly journals Association of breastfeeding and risk of metabolic syndrome and its components in postmenopausal parous women: Korea national health and nutrition examination survey (2010 ~ 2016)

2021 ◽  
Vol 79 (1) ◽  
Author(s):  
Jusuk Lee ◽  
Taehong Kim
Keyword(s):  
Metabolic Syndrome ◽  
Laboratory Data ◽  
Multivariate Logistic Regression Analysis ◽  
Density Lipoprotein ◽  
Cross Sectional Study ◽  
Korean Women ◽  
Cross Sectional ◽  
Increased Risk ◽  
Nationally Representative ◽  
Study Participants

Abstract Background Understanding the relationship between breastfeeding (BF) and metabolic syndrome (Mets) is important for maternal long-term health benefits and disease prevention. This study aimed to examine the association between BF and Mets and its components among postmenopausal parous Korean women. Methods This cross-sectional study on 10,356 Korean women used nationally representative data from the KNHANES from 2010 to 2016. Anthropometric, laboratory data and manual BP were measured. A multivariate logistic regression analysis was conducted to examine the association of BF with Mets and its components after adjusting for potential confounding variables. A p-value < 0.05 was to be considered statistically significant. Results Mets was present in 42% of the study participants. The BF group had low household income and education level. The prevalence of Mets in the BF group was higher than that in the non-BF group (42.69% vs. 34.76%, p <  0.001). BF was associated with increased risk of Mets (odds ratio [OR]: 1.4, 95% confidence interval [CI]: 1.18–1.65, p <  0.001). The BF group was at higher risks for diabetes (OR: 1.5, 95%CI: 1.14–1.98), hypertension (OR: 1.32, 95%CI: 1.03–1.68), hypertriglyceridemia (OR: 1.42, 95%CI: 1.02–1.99) and low high-density lipoprotein cholesterol (OR: 1.32, 95%CI: 1.06–1.65). Conclusion In this study, BF did not affect decreasing the prevalence of Mets and its components.

scholarly journals Cortisol, DHEAS, their ratio and the metabolic syndrome: evidence from the Vietnam Experience Study

2010 ◽  
Vol 162 (5) ◽  
pp. 919-923 ◽  
Author(s):  
Anna C Phillips ◽  
Douglas Carroll ◽  
Catharine R Gale ◽  
Janet M Lord ◽  
Wiebke Arlt ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Military Service ◽  
Fasting Blood Glucose ◽  
Density Lipoprotein ◽  
Cross Sectional ◽  
Us Army ◽  
Telephone Interviews ◽  
The Metabolic Syndrome ◽  
Increased Risk ◽  
Vietnam Era

ObjectivesThe aim of these analyses was to examine the association of cortisol, DHEAS and the cortisol:DHEAS ratio with the metabolic syndrome (MetS) and its components.DesignThe analyses were cross-sectional.MethodsParticipants were 4255 Vietnam era US army veterans. From military service files, telephone interviews and a medical examination, occupational, socio-demographic and health data were collected. MetS was ascertained from data on body mass index; fasting blood glucose or a diagnosis of diabetes; blood pressure or a diagnosis of hypertension; high-density lipoprotein cholesterol; and triglyceride levels. Contemporary morning fasted cortisol and DHEAS concentrations were determined. The outcomes were MetS and its components. Analysis was by logistic regression, first adjusting for age and then additionally for an array of candidate confounders.ResultsCortisol, although not in the fully adjusted analysis, and DHEAS were both related to MetS. Whereas high cortisol concentrations were associated with an increased risk of MetS, high DHEAS concentrations appeared protective. By far, the strongest associations with MetS were observed for the cortisol:DHEAS ratio; the higher the ratio, the greater the risk of having MetS. The ratio was also significantly related to four of the five MetS components.ConclusionsThe cortisol:DHEAS ratio is positively associated with MetS. Prospective analyses are needed to help untangle direction of causality, but this study suggests that the cortisol:DHEAS ratio is worthy of further study in this and other health contexts.

scholarly journals Reduction of renal triglyceride accumulation: effects on proximal tubule Na+/H+ exchange and urinary acidification

2009 ◽  
Vol 297 (5) ◽  
pp. F1419-F1426 ◽  
Author(s):  
I. Alexandru Bobulescu ◽  
Michele Dubree ◽  
Jianning Zhang ◽  
Paul McLeroy ◽  
Orson W. Moe
Keyword(s):  
Metabolic Syndrome ◽  
Proximal Tubule ◽  
Causative Role ◽  
Ammonium Excretion ◽  
Pathophysiological Mechanism ◽  
The Metabolic Syndrome ◽  
Triglyceride Accumulation ◽  
Urinary Acidification ◽  
Increased Risk ◽  
Zdf Rats

One main pathophysiological mechanism underlying the increased risk for uric acid nephrolithiasis in humans with the metabolic syndrome is the excretion of unduly acidic urine, in part because of reduced excretion of the main urinary buffer, ammonium. The Zucker diabetic fatty (ZDF) rat, an established rodent model of the metabolic syndrome, has similar urinary abnormalities, attributed in part to lower expression and activity of the principal mediator of proximal tubule ammonium excretion, brush-border membrane Na+/H+ exchanger 3 (NHE3). These defects are associated with renal tubular steatosis in ZDF rats, but the causal relationship between renal steatosis and defective urinary acidification has not been investigated in vivo. We hypothesized that reduction of renal steatosis would commensurately normalize urinary acidification parameters. We treated ZDF rats with thiazolidinediones to reduce nonadipose tissue steatosis. Four weeks of treatment reduced renal triglyceride accumulation and restored urinary acidification parameters in ZDF rats to levels comparable to their lean littermates; urinary acidification was not affected by treatment in lean rats. To further document the direct effects of fat, we showed that functional abnormalities induced by fat loading in a cell culture model of proximal tubule steatosis and lipotoxicity can be reversed by fat removal but not by thiazolidinediones alone. Together, these findings support the causative role of renal steatosis in the pathogenesis of urinary acidification defects, demonstrate reversibility upon lipid removal, and highlight a potential therapeutic strategy for renal abnormalities in the metabolic syndrome.

The Yin and Yang of High-density Lipoprotein and Atherosclerotic Cardiovascular Disease: Focusing on Functionality and Cholesterol Efflux to Reframe the HDL Hypothesis

2021 ◽  
Vol 28 ◽  
Author(s):  
Shiva Ganjali ◽  
Gerald F. Watts ◽  
Maciej Banach ◽  
Željko Reiner ◽  
Petr Nachtigal ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
High Density Lipoprotein ◽  
Cholesterol Efflux ◽  
Association Studies ◽  
Plasma Concentrations ◽  
Density Lipoprotein ◽  
High Density ◽  
Atherosclerotic Cardiovascular Disease ◽  
Genome Wide Association Studies ◽  
Increased Risk

Abstract: The inverse relationship between low plasma high-density lipoprotein cholesterol (HDL-C) concentrations and increased risk of Atherosclerotic Cardiovascular Disease (ASCVD) is well-known. However, plasma HDL-C concentrations are highly variable in subjects with ASCVD. In clinical outcome trials, pharmacotherapies that increase HDL-C concentrations are not associated with a reduction in ASCVD events. A causal relationship between HDL-C and ASCVD has also been questioned by Mendelian randomization studies and genome-wide association studies of genetic variants associated with plasma HDL-C concentrations. The U-shaped association between plasma HDL-C concentrations and mortality observed in several epidemiological studies implicates both low and very high plasma HDL-C concentrations in the etiology of ASCVD and non-ASCVD mortality. These data do not collectively support a causal association between HDL-C and ASCVD risk. Therefore, the hypothesis concerning the association between HDL and ASCVD has shifted from focus on plasma concentrations to the concept of functionality, in particular cellular cholesterol efflux and HDL holoparticle transport. In this review, we focus on these new concepts and provide a new framework for understanding and testing the role of HDL in ASCVD.

Cardiovascular event rates increase after each recurrence and associate with poor statin adherence

2020 ◽  
pp. 204748732090433 ◽  
Author(s):  
Mariann I Lassenius ◽  
Iiro Toppila ◽  
Susanne Bergius ◽  
Julia Perttilä ◽  
KE Juhani Airaksinen ◽  
...  
Keyword(s):  
Cardiovascular Event ◽  
Cardiovascular Events ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Lipid Lowering ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Increased Risk ◽  
Event Rates

Aims The study evaluated the quality of cardiovascular prevention in real-world clinical practice. The recurrence of up to five cardiovascular events was assessed, as data on recurrence beyond the first event and interindividual variations in event rates past the second event have been sparse. Low-density lipoprotein cholesterol concentrations and lipid-lowering therapy use were investigated. Methods This retrospective register-based study included adult patients with an incident cardiovascular event between 2004 and 2016 treated in the hospital district of southwest Finland. Patients were followed for consecutive cardiovascular events or cardiovascular death, low-density lipoprotein cholesterol and statin purchases. The timing of event recurrence was evaluated, and predictive factors were assessed. Results A wide interindividual variation in cardiovascular event recurrence was observed, each additional event caused an increased risk, the median time of recurrence decreased from 7 to one year for the second and fifth event. Event rates increased correspondingly from 12 to 43/100 patient-years and were most pronounced in the first years following the previous event. The low-density lipoprotein cholesterol goal (<1.8 mmol/l) was reached by 18% in the year after the event and statin underuse was associated with an increased risk of recurrence. Six months after the index event high intensity statins were used by only 22% of the cohort. Conclusion The study provides new perspectives on individual risk assessment showing that event rates are not stable for all patients but increase 1.2–1.9-fold per consecutive event. The underuse of statins and poor adherence support the identification of these patients for intensified multifactorial preventive measures.

scholarly journals Carvedilol Ameliorates Experimental Atherosclerosis by Regulating Cholesterol Efflux and Exosome Functions

2019 ◽  
Vol 20 (20) ◽  
pp. 5202 ◽  
Author(s):  
Chen ◽  
Tsui ◽  
Chuang ◽  
Chiang ◽  
Chen ◽  
...  
Keyword(s):  
Cholesterol Efflux ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Nuclear Factor Κb ◽  
Experimental Atherosclerosis ◽  
Atherosclerotic Cardiovascular Disease ◽  
Beneficial Effects ◽  
Abca1 Expression ◽  
Density Lipoprotein Receptor ◽  
And Function

Carvedilol (Cav), a nonselective β-blocker with α1 adrenoceptor blocking effect, has been used as a standard therapy for coronary artery disease. This study investigated the effects of Cav on exosome expression and function, ATP-binding cassette transporter A1 (ABCA1) expression, and cholesterol efflux that are relevant to the process of atherosclerosis. Human monocytic (THP-1) cell line and human hepatic (Huh-7) cells were treated with Cav, and cholesterol efflux was measured. Exosomes from cell culture medium or mice serum were isolated using glycan-coated recognition beads. Low-density lipoprotein receptor knockout (ldlr−/−) mice were fed with high-fat diet and treated with Cav. Cav accentuated cholesterol efflux and enhanced the expressions of ABCA1 protein and mRNA in both THP-1 and Huh-7 cells. In addition, Cav increased expression and function of exosomal ABCA1 in THP-1 macrophage exosomes. The mechanisms were associated with inhibition of nuclear factor-κB (NF-κB) and protein kinase B (Akt). In hypercholesterolemic ldlr−/− mice, Cav enhanced serum exosomal ABCA1 expression and suppressed atherosclerosis by inhibiting lipid deposition and macrophage accumulation. Cav halts atherosclerosis by enhancing cholesterol efflux and increasing ABCA1 expression in macrophages and in exosomes, possibly through NF-κB and Akt signaling, which provides mechanistic insights regarding the beneficial effects of Cav on atherosclerotic cardiovascular disease.

Low-Density Lipoprotein Subfractionation: What Is the Role of the Lab When Reporting Discrepant Results?

2020 ◽  
Vol 154 (Supplement_1) ◽  
pp. S8-S9
Author(s):  
Nicholas E Larkey ◽  
Leslie J Donato ◽  
Allan S Jaffe ◽  
Jeffrey W Meeusen
Keyword(s):  
Coronary Artery ◽  
High Risk ◽  
Clinical Decision Making ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Risk ◽  
Lipid Lowering ◽  
Low Density ◽  
Small Dense Ldl ◽  
Increased Risk

Abstract Plasma concentrations of low-density-lipoprotein cholesterol (LDL-C) are directly associated with risk for coronary artery disease (CAD). Multisociety guidelines define LDL-C&gt;160mg/dL as a risk factor for CAD and LDL-C&gt;190mg/dL as an indication for lipid lowering medication, regardless of other clinical factors. Subfractionation of LDL according to size (LDL-s) enables differentiation between two LDL phenotypes: large-buoyant LDL and small-dense LDL. The small-dense LDL phenotype reportedly conveys increased risk for CAD. Major societies do not recommend LDL subfractions be used for clinical decision making and most payers do not cover LDL subfraction testing. Despite these restrictions, LDL subfraction is routinely requested by clinicians. Nuclear magnetic resonance (NMR) spectroscopy measures LDL-C and LDL-s. Following inquiries regarding interpretation of conflicting LDL-C and LDL-s results, we investigated associations between LDL-C and LDL-s measured by NMR in order to determine how often they provide contradicting or additive information. Verification of NMR LDL-C accuracy was confirmed by ß-quantification in a subset of patient samples (n=250). The average bias was -4.5mg/dL and the correlation coefficient was 0.92. High-risk was defined as LDL-C&gt;160mg/dL or LDL-s&lt;20.5 nm (small-dense LDL); and low-risk was defined as LDL-C&lt;70mg/dL or LDL-s&gt;20.5nm (large-buoyant LDL). In 26,710 clinical NMR analyses, the median LDL-C was 94.0mg/dL (range:5-436mg/dL) with median LDL-s of 20.8 nm (range:19.4–23.0nm). LDL-s moderately correlated with LDL-C (Ï#129;=0.51;p&lt;0.01). Small-dense-LDL was identified in only 18% (407/2,191) of patients with elevated LDL-C (&gt;160mg/dL) and was more common (73.2% of 6,093) in patients with low LDL-C (&lt;70mg/dL;p&lt;0.001). Associations with CAD were investigated among patients without cholesterol-lowering medication treatment referred for angiography (n=356). CAD (defined as stenosis &gt;50% in one or more coronary artery) was diagnosed in 14% (1/7) of subjects with low LDL-C (&lt;70mg/dL) compared to 59% (47/80) of subjects with elevated LDL-C (p=0.01). When stratifying by LDL-s, CAD was diagnosed in 50% (57/115) of subjects with small-dense LDL compared to 43% (104/241) of subjects with large-buoyant LDL (p=0.2). Small-dense LDL was identified in only 33% (26/80) of cases with elevated LDL-C. Limiting to subjects with elevated LDL-C, CAD was diagnosed in 50% (13/26) of subjects with concordant (high-risk) small-dense LDL compared to 61% (33/54) of subjects with discordant (low-risk) large-buoyant LDL (LDL-s&gt;20.5nm) (p=0.3). Our data confirm that LDL-s subfraction measured by NMR is reported discordantly in most cases when LDL-C is unequivocally high or low. Furthermore, CAD diagnosis was significantly associated with LDL-C, but not with LDL-s. Our data also show that in discrepant samples, elevated LDL-C correlates better with disease state compared to LDL-s. Therefore, LDL-s should not be used to justify treatment decisions in patients with elevated LDL-C. Laboratories should consider carefully whether or not to report LDL-s when it is known that misleading and discordant values will be reported in a majority of cases.

Dyslipidemia: Reduction in Estimated Risk for Coronary Artery Disease After Use of Ezetimibe with a Statin

2007 ◽  
Vol 41 (9) ◽  
pp. 1345-1351 ◽  
Author(s):  
John S Sampalis ◽  
Stéphane Bissonnette ◽  
Rafik Habib ◽  
Stella Boukas
Keyword(s):  
Diabetes Mellitus ◽  
Coronary Artery Disease ◽  
Metabolic Syndrome ◽  
Coronary Artery ◽  
Density Lipoprotein ◽  
Lipid Lowering ◽  
Open Label ◽  
Statin Monotherapy ◽  
Artery Disease ◽  
The Impact

Background: The aim of lipid-lowering treatment is to reduce the risk for cardiovascular events. Patients not at target lipid levels while on hydroxymethylglutaryl coenzyme A reductase inhibitors (statin) monotherapy are at increased cardiovascular risk. Objective: To describe the impact of coadministration of ezetimibe with a statin on the estimated 10 year risk for coronary artery disease (E-RCAD) in patients with hypercholesterolemia and above-target low-density lipoprotein cholesterol (LDL-C) levels after statin monotherapy. Methods: Post hoc analysis was conducted of a prospective, open-label, single-cohort, multicenter Canadian study of 953 patients who were treated for 6 weeks with ezetimibe 10 mg/day coadministered with their current statin at an unaltered dose. For each patient, E-RCAD at baseline and at 6 weeks was calculated using the Framingham model. The primary outcome measure of the analysis was the change in E-RCAD. Results: A total of 825 patients with data at baseline and 6 weeks were included in the analysis. There were 423 (51.3%) patients with hypertension, 107 (13.0%) with diabetes mellitus but not metabolic syndrome, 160 (19.4%) with metabolic syndrome but not diabetes mellitus, and 235 (28.5%) with both diabetes mellitus and metabolic syndrome. After 6 weeks of ezetimibe coadministration with statin therapy, mean E-RCAD was reduced by 4.1% from 15.6% to 11.5%, which is equivalent to a 25.3% risk reduction (p < 0.001). Of the 225 (27.3%) patients with high E-RCAD (≥20.1%) at baseline, 144 (64.0%) converted to a lower E-RCAD category (p < 0.001). Patients with both diabetes mellitus and metabolic syndrome experienced the highest mean percent reduction in E-RCAD of –29.4% (p < 0.001). Conclusions: For patients with above-target LDL-C levels while on statin monotherapy, coadministration of ezetimibe with the statin is effective in significantly reducing the E-RCAD.

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