Metabolic Syndrome Phenotype Research Articles

QTc Interval is Associated with Atrial Fibrillation in Individuals with Metabolic Syndrome Phenotype.

PurposeManifestations of metabolic syndrome (MetS) carry risks for atrial fibrillation (AF). The study determined whether any electrocardiographic parameter can reflect increased AF risk in individuals with MetS.Patients and MethodsFrom our University Hospital database, we examined the presence of AF and its correlation with MetS manifestations, renal function, lipid profiles, and electrocardiographic parameters (P wave duration, PR interval, QRS width, and QTc intervals). Between January 2008 and December 2015, data from 4479 adults (women 41.6% vs men 58.4%) were identified.ResultsThe overall prevalence of AF was 12.4%, without sex differences (women, 12.8% vs men, 12.1%). Patients with AF were older (age 73.9 ± 11.8 vs non-AF 67 ± 13.5 years), with lower lipid levels (TG, total cholesterol, and LDL-cholesterol, all p < 0.0001), and at lower eGFR level (64.1 ± 30.9 vs non-AF 68.8 ± 41.4 mL/min/1.73m2, p < 0.0001). Besides, sex differences were present in all electrocardiographic parameters (all p < 0.05). Hypertension had the highest odds ratio (1.33; p = 0.026) for AF. Comparing AF to non-AF, the QTc of quartiles was significantly different (p < 0.0089). The shortest and longest QTc quartiles had an increased incidence of AF.ConclusionAF risk in patients with MetS phenotypes can be reflected by QTc quartiles.

Hypertension and Diabetes Mellitus: Coprediction and Time Trajectories

Type 2 diabetes mellitus and hypertension overlap in the population. In many subjects, development of diabetes mellitusis characterized by a relatively rapid increase in plasma glucose values. Whether a similar phenomenon occurs duringthe development of hypertension is not known. We analyzed the pattern of blood pressure (BP) changes during thedevelopment of hypertension in patients with or without diabetes mellitus using data from the MCDS and in the FOSduring a 7-year follow-up. Diabetes mellitus at baseline was a significant predictor of incident hypertension (in FOS,odds ratio, 3.14; 95% confidence interval, 2.17–4.54) independently of sex, age, body mass index, and familial diabetesmellitus. Conversely, hypertension at baseline was an independent predictor of incident diabetes mellitus. In comparisonwith the nonconverters group, hypertension and diabetes mellitus converters shared a metabolic syndrome phenotype(hyperinsulinemia, higher body mass index, waist girth, BP, heart rate and pulse pressure, and dyslipidemia). Overall,results were similar in the 2 ethnic groups. We conclude that (1) development of hypertension and diabetes mellitustrack each other over time, (2) transition from normotension to hypertension is characterized by a sharp increase in BPvalues, and (3) insulin resistance is one common feature of both prediabetes and prehypertension and an antecedent ofprogression to 2 respective disease states.

FADS Polymorphisms Affect the Clinical and Biochemical Phenotypes of Metabolic Syndrome.

Long-chain polyunsaturated fatty acids (LC-PUFAs) play important roles in human health, from controlling inflammation to lipid and glucose homeostasis. In our previous study, which employed a cluster analysis of a plasma fatty acid (FA) pattern, we identified two clusters of metabolic syndrome (MetS) independent of clinical and biochemical parameters within the whole study group (controls together with metabolic syndrome (MetS) patients). FA desaturase (FADS) genes are the key regulators of LC-PUFA metabolism. The aim of this study was to analyze associations between FADS polymorphisms and clusters of MetS. The study group consisted of 188 controls and 166 patients with MetS. The first cluster contained 71 controls (CON1) and 109 MetS patients (MetS1). The second cluster consisted of 117 controls (CON2) and 57 MetS patients (MetS2). In comparison with MetS2, cluster MetS1 displayed a more adverse risk profile. Cluster CON1 had, in comparison with CON2, higher body weight and increased triacylglycerol levels (p < 0.05). We found that the FADS rs174537 (p < 0.001), rs174570 (p < 0.01), and rs174602 (p < 0.05) polymorphisms along with two inferred haplotypes had statistically significant genotype associations with the splitting of MetS into MetS1 and MetS2. Conversely, we observed no significant differences in the distribution of FADS polymorphisms between MetS and CON subjects, or between CON1 and CON2. These associations between FADS polymorphisms and two clusters of MetS (differing in waist circumference, HOMA-IR, lipolysis, and oxidative stress) implicate the important influence of genetic factors on the phenotypic manifestation of MetS.

Excess fructose enhances oleatic cytotoxicity via reactive oxygen species production and causes necroptosis in hepatocytes

Non-alcoholic fatty liver disease (NAFLD), the hepatic phenotype of metabolic syndrome, has been identified as a major health concern as the number of cirrhosis and deaths associated with NAFLD is expected to increase. Although fructose intake has been considered to be a progressive factor in the pathophysiology of NAFLD, it remains unclear how fructose contributes to hepatocellular damage during lipotoxicity. In the present study, we aimed to analyze the hepatotoxicity of fructose in steatosis. Fructose effects on lipotoxicity were evaluated in HepG2 cells, primary mouse hepatocytes, and in mice fed a high-fat diet with or without sucrose (HFDS/HFD). Oleate induced caspase 3-independent cell death in HepG2 cells and primary mouse hepatocytes cultured in fructose-supplemented medium, and induced cleavage of caspase-1 in primary mouse hepatocytes. In addition, the number of cells stained positive for reactive oxygen species (ROS) was significantly increased, and N-acetyl cysteine was found to inhibit ROS production and cell death. Cell death was confirmed to be through necrotic cell death, and phosphorylation of mixed lineage kinase domain-like (MLKL) protein was observed. Taken together, hepatocyte cytotoxicity was due to excess fructose with oleate-induced ROS-mediated necroptosis. HFDS mice showed progressive hepatic fibrosis and inflammation and a higher NAS score than HFD mice or mice fed a control diet. The expression of hemoxygenase-1, phosphorylation of MLKL, cleavage of caspase1, and apoptosis were significantly increased in the livers of mice fed a HFDS. Overall, excess fructose intake induces necroptosis through the production of ROS and enhances the toxicity of oleatic cytotoxicity.

Nuts and Metabolic Syndrome: Reducing the Burden of Metabolic Syndrome in Menopause.

Menopause imposes a dramatic fall in estrogens, which is followed by an increase in the proportion of fat. The rising androgen/estrogen ratio along the menopause transition favors the accumulation of central fat, which contributes to insulin resistance and a series of concatenated effects, leading to a higher incidence of metabolic syndrome. The modulatory effect of diet on the metabolic syndrome phenotype has been shown for the Mediterranean diet, and nuts are key determinants of these health benefits. This review of the impact of nuts on the risk factors of the metabolic syndrome cluster examined studies—prioritizing meta-analyses and systemic reviews—to summarize the potential benefits of nut ingestion on the risk of metabolic syndrome associated with menopause. Nuts have a general composition profile that includes macronutrients, with a high proportion of unsaturated fat, bioactive compounds, and fiber. The mechanisms set in motion by nuts have shown different levels of efficacy against the disturbances associated with metabolic syndrome, but a beneficial impact on lipids and carbohydrate metabolism, and a potential, but minimal reduction in blood pressure and fat accumulation have been found.

Association between Serum Zinc and Hs-Crp Concentrations in Different Metabolic Syndrome Phenotypes

Background: Metabolic syndrome (MetS) is associated with an increased risk of cardiovascular disease and all-cause mortality. Zinc (Zn) is an essential trace element for the synthesis, storage, and release of insulin. In this study, we have evaluated whether serum Zn levels are associated with hsCRP level according to MetS phenotypes. Method: A total of 9493 individuals (3768 men and 5635 women) were recruited as part of the Mashhad Stroke and Heart Association Disorder (MASHAD) study. We measured the concentration of serum Zn by flame atomic absorption (Varian AA240FS) and we divided the subjects into quartile of serum Zn. We used SPSS version 18 statistical analyses for all. Graph Pad Prism 6 for figures was used. Results: In this study, there were significant differences between quartiles of Zn according to sex. The results showed that the level of serum hs-CRP were higher in subjects with metabolic syndrome who also had a serum Zn &gt;95 µg/dl. In subjects with serum Zn &lt;70 µg/dl, an increase in serum hs-CRP was associated with an increased risk of MetS by 2.2%, 1.022(CI: 1.01-1.034). Moreover, among subjects in the first, second and third quartiles of serum Zn, some phenotypes of metabolic syndrome were associated with a risk of increasing hs-CRP level (p &lt; 0.05). Conclusion: Serum hs-CRP concentrations were related to MetS phenotypes. This relationship was modified by serum Zn level. According to the number of MetS components serum, Zn levels decreased as the number of MetS component increased, and low serum zinc levels (Q1) showed an overall greater prevalence of MetS.

POS-300 BODY MASS INDEX AND METABOLIC SYNDROME PHENOTYPES AND THEIR ASSOCIATION WITH KIDNEY DISORDERS: EVIDENCE FROM A CROSS-SECTIONAL STUDY

Although accumulating evidences suggested that body mass index (BMI) are positively associated with development of chronic kidney disease (CKD), this association might be modified by metabolic syndrome. Therefore, the present study aimed to evaluate the association of combined BMI and metabolic syndrome phenotypes with CKD.

Association of childhood metabolic syndrome and metabolic phenotypes with the carotid intima-media thickness (CIMT) in early adulthood: Tehran lipid and glucose study

BackgroundThe clinical significance of metabolic syndrome (MetS) during adolescence and its association with adulthood adverse outcomes is a controversial issue. This study aimed to investigate the association of MetS and metabolic phenotypes with a high carotid intima-media thickness (CIMT) in early adulthood. MethodsMetS was defined as proposed by Cook, de Ferranti, the National Cholesterol Education Program (NCEP), and the pediatric International Diabetes Federation (IDF). Metabolic phenotypes were defined based on the binary clustering of cardiovascular risk factors. The participants were adolescent's individual selected from a large cohort study and followed for 18.2 years. Multivariate-adjusted odds ratios (ORs) were calculated for a high CIMT incidence (≥95th percentile). ResultsIn this study, 862 adolescents (52.3% males), with the mean age of 13.4 ± 2.2 years, were included. The presence of MetS, based on the definitions proposed by Cook (OR = 1.90, 95% CI: 1.01–3.57, P = 0.046) and de Ferranti (OR = 1.74; 95% CI: 1.04–2.90, P = 0.033), was associated with the increased risk of a high CIMT in early adulthood. Metabolic phenotypes, including high waist circumference (WC)/hypertension (HTN), high WC/low high-density lipoprotein-cholesterol (HDL-C), and high triglyceride (TG)/high WC, showed higher risks of a high CIMT. However, these positive associations become insignificant after adjusting for the adulthood BMI, except for the high WC/low HDL-C phenotype (OR = 2.04, 95% CI: 1.02–4.11, P = 0.044). ConclusionThe high WC/low HDL-C phenotype had a better predictive value and could be used as a simpler alternative for MetS to identify adolescents with a higher risk of high CIMT during early adulthood.

Verification of the Impact of Blood Glucose Level on Liver Carcinogenesis and the Efficacy of a Dietary Intervention in a Spontaneous Metabolic Syndrome Model.

Metabolic syndrome (MS) is a risk factor for type 2 diabetes mellitus, vascular inflammation, atherosclerosis, and renal, liver, and heart diseases. Non-alcoholic steatohepatitis (NASH) is a progressive representative liver disease and may lead to the irreversible calamities of cirrhosis and hepatocellular carcinoma. Metabolic disorders such as hyperglycemia have been broadly reported to be related to hepatocarcinogenesis in NASH; however, direct evidence of a link between hyperglycemia and carcinogenesis is still lacking. Tsumura Suzuki Obese Diabetic (TSOD) mice spontaneously develop metabolic syndrome, including obesity, insulin resistance, and NASH-like liver phenotype, and eventually develop hepatocellular carcinomas. TSOD mice provide a spontaneous human MS-like model, even with significant individual variations. In this study, we monitored mice in terms of their changes in blood glucose levels, body weights, and pancreatic and liver lesions over time. As a result, liver carcinogenesis was delayed in non-hyperglycemic TSOD mice compared to hyperglycemic mice. Moreover, at the termination point of 40 weeks, liver tumors appeared in 18 of 24 (75%) hyperglycemic TSOD mice; in contrast, they only appeared in 5 of 24 (20.8%) non-hyperglycemic mice. Next, we investigated three kinds of oligosaccharide that could lower blood glucose levels in hyperglycemic TSOD mice. We monitored the levels of blood and urinary glucose and assessed pancreatic lesions among the experimental groups. As expected, significantly lower levels of blood and urinary glucose and smaller deletions of Langerhans cells were found in TSOD mice fed with milk-derived oligosaccharides (galactooligosaccharides and lactosucrose). At the age of 24 weeks, mild steatohepatitis was found in the liver but there was no evidence of liver carcinogenesis. Steatosis in the liver was alleviated in the milk-derived oligosaccharide-administered group. Taken together, suppressing the increase in blood glucose level from a young age prevented susceptible individuals from diabetes and the onset of NAFLD/NASH, as well as carcinogenesis. Milk-derived oligosaccharides showed a lowering effect on blood glucose levels, which may be expected to prevent liver carcinogenesis.

The hypertriglyceridemic-waist phenotype as a valuable and integrative mirror of metabolic syndrome traits

Rates of non-communicable diseases (NCDs), such as obesity, diabetes, cardiovascular events and cancer, continue to rise worldwide, which require objective instruments for preventive and management actions. Diverse anthropometric and biochemical markers have been used to qualitatively evaluate degrees of disease, metabolic traits and evolution of nutritional status. The aim of this study was to integrate and assess the interactions between an anthropometric measurement, such as waist circumference (WC), and biochemical data, such as the triglyceride glucose index (TyG), in order to individually characterize metabolic syndrome (MetS) features considering the hypertriglyceridemic waist phenotype as a marker. An ancillary cross-sectional study was conducted using anthropometric measurements, such as weight, height, waist and hip circumferences, as well as fasting biochemical data of 314 participants. Different indices based on WC (WC, WC*TG and WC*TyG) were estimated to compute MetS components and accompanying comorbidities. ROC curves were fitted to define the strength of the analyses and the validity of the relationships. Associations were confirmed between anthropometric, biochemical and combined indices with some chronic disease manifestations, including hyperglycemia, hypertension and dyslipidemia. Both WC*TG and WC*TyG indices showed similar performance in diagnosing MetS (area under the ROC curve = 0.81). Interestingly, when participants were categorized according to a reference value of the WC*TyG index (842.7 cm*mg/dl), our results evidenced that subjects classified over this limit presented statistically higher prevalence of MetS and accompanying individual components with clinical relevance for interventions. These results revealed that WC*TyG mirrors the hypertriglyceridemic phenotype, which suggests may serve as a good indicator to define the metabolic syndrome phenotype and a suitable, sensitive, and simple proxy to complement others. A reference point was proposed with a good clinical performance and maximized sensitivity and specificity values.

Prevalence and biomarkers in metabolic syndrome

The prevalence of metabolic syndrome (MS) has a worldwide tendency to increase and depends on many components, which explains the complexity of diagnostics and approaches to the prevention and treatment of this pathology. Age, lifestyle, socioeconomic status, insulin resistance (IR), dyslipidemia, obesity and genetic predisposition are factors influencing the risk of developing and progression of MS. Features of the distribution and dysfunction of adipose tissue are important factors in the development of IR, with obesity, as well as the risk of the formation of cardiometabolic diseases and MS. ­Understanding of mechanisms is linked to advances in metabolic phenotyping. Metabolic phenotyping of obese persons is important for the development of important diseases in relation to the study of the pathophysiology of metabolic disorders, the possible concomitant disease and the search for innovative strategies for the prevention and treatment of MS. The understanding of MS mechanisms is associated with advances in metabolic phenotyping. Therefore, the relevance of further study of the pathophysiological mechanisms underlying various metabolic phenotypes of MS is one of the promising areas of modern scientific research. This review summarizes the current literature data on the prevalence of MS depending on gender, age, population, area of residence, education, level of physical activity, and many other parameters. Metabolic risks of MS development are detailed. Biological markers of MS are considered. The necessity of metabolic phenotyping of MS has been shown, which may have potential therapeutic value.

Decaffeinated light-roasted green coffee and green tea extract combination improved metabolic parameters and modulated inflammatory genes in metabolic syndrome rats

Background: Individually, green tea and green coffee have been extensively studied for mitigation of metabolic syndrome (MS) in both rats and humans; however, their combined effect requires further investigation. Thus, we compared the metabolic effect of combining green tea and decaffeinated light roasted green coffee on MS in rats. Methods: An MS animal model was constructed by feeding Sprague-Dawley rats with a high-fat-high-sucrose (HFHS) diet for eight weeks and a low dose of streptozotocin (STZ) injection at week 2. Rats fed with HFHS diets and injected with STZ successfully developed MS phenotypes, indicated by higher body weight, systolic blood pressure, plasma triglyceride level, plasma fasting blood glucose level, and lower plasma HDL-C level, compared to those fed with a normal chow diet. Subsequently, MS rats were continuously fed with HFHS and divided into four groups: MS rats, MS with 300 mg/bw.t green tea extract (GT), MS with 200 mg/bw.t green coffee extract (GC), and MS with combined green tea and green coffee extract (CM) for nine weeks. Results: Combining green tea and green coffee have synergistic effects on reducing plasma fasting blood glucose and triglyceride level. Inflammatory markers both in plasma and liver tissue robustly decreased in CM group rats. However, the reduction of systolic blood pressure was observed only in GT and CM groups. Moreover, all treatment resulted in an increase in plasma HDL-C level in MS rats. Conclusions: Our data highlighted that, in MS animal models, combined green tea and decaffeinated light roasted green coffee augment their several individual beneficial effects of improved metabolic parameters and modulated inflammatory genes.

Central Feminization of Male Mice Reduces Metabolic Syndrome

Metabolic syndrome encompasses a spectrum of conditions that increases the risk for adverse cardiovascular and metabolic diseases. Sexual dimorphism is clearly established, with men more predisposed to metabolic syndrome complications than women. It is widely accepted that the female sex hormone estrogen plays a protective role in premenopausal women through peripheral as well as central nervous system (CNS) mechanisms. However, most work to date has been based on the loss of estrogen in females (e.g. menopause). Interestingly, transgender individuals receiving feminizing gender affirming therapy (i.e. estrogen) appear to be relatively protected from metabolic syndrome conditions. Furthermore: 1) CNS estrogen is critically involved in metabolic regulation; and 2) CNS estrogen receptors in several nuclei are present at the same density in males and females. Based on this, we hypothesized that central estrogen supplementation in males would rescue metabolic syndrome phenotypes. To investigate this, six week old male C57Bl/6J mice were fed a normal chow or high fat diet (HFD) for 10 wks and were then instrumented with intracerebroventricular cannulas (ICV; n=4-6). Following surgical recovery, β-Estradiol (E2;30 mg/kg/day) or saline control was administered ICV once daily over 6 days. One week of central E2 supplementation resulted in a slight, albeit significant, decrease in body weight (42± 3 vs 37±2 g, saline vs. E2, p<0.05), that was not accompanied by changes in food/water intake or energy expenditure. Upon sacrifice it was evident that estrogen supplementation significantly altered adiposity. In particular, estrogen supplementation resulted in decreases in visceral white adipose depots including abdominal (1±0.1 vs. 0.5±0.1 g, saline vs. E2, p<0.05) and epididymal fat, whereas subcutaneous inguinal and brown fat (0.18±0.02 vs. 0.15±0.02 g, saline vs. E2, p>0.05) were unchanged. Building on this, we also evaluated hepatic lipid accumulation, (i.e. non-alcoholic fatty liver disease), a liver disorder that is common in ~70% of metabolic syndrome individuals. Oil Red O staining of the liver demonstrated that, relative to control animals, one-week supplementation with E2 resulted in a clear reduction in hepatic steatosis (23.8±4.3 vs. 15.0±1.5 percent area, Saline vs E2, p=0.05). Together, these findings indicate that short-term central estrogen supplementation in males is an effective means to reduce metabolic syndrome risk factors including visceral adiposity and hepatic steatosis. Moreover, these data may help explain why premenopausal females and transgender females are relatively protected from metabolic syndrome.

Methanolic Extract of Lysimachia Candida Lindl. Prevents High-Fat High-Fructose-Induced Fatty Liver in Rats: Understanding the Molecular Mechanism Through Untargeted Metabolomics Study.

Fatty liver is one of the most common metabolic syndrome affecting the global population. Presently, limited treatment modalities with symptomatic approach are available for alleviating fatty liver. Traditional and herbal treatment modalities have shown evidence to improve the disease pathology. In the present research work, evaluation of a selected medicinal plant Lysimachia candida Lindl. was carried out to investigate its beneficial effects on fatty liver disease in rats. Male Sprague Dawley (SD) rats were fed with high-fat high-fructose diet to induce fatty liver phenotypes. After induction for 15 weeks, methanolic extract of Lysimachia candida Lindl. (250 mg/kg b. w. p. o.) was administrated to the rats daily for the next 17 weeks. Blood samples were collected at different time points to analyze fasting blood glucose levels and relevant biochemical parameters important for the assessment of metabolic disease phenotypes. Liquid chromatography-mass spectrometry (LC-MS) based metabolomics was done to study the dynamics of metabolic changes in the serum during disease progression and how the medicinally important plant extract treatment reversed the metabolic diseases. Multivariate data analysis approaches have been employed to understand the metabolome changes and disease pathology. This study has identified the interplay of some metabolic pathways that alter the disease progression and their reversal after administration of the plant extract. Different group of metabolites mainly bile acids, fatty acids, carnitines, and their derivatives were found to be altered in the diseased rats. However, all the metabolites identified between control and disease groups are mainly related to lipid metabolism. The results depict that the treatment with the above-mentioned plant extract improves the regulation of aberrant lipid metabolism, and reverses the metabolic syndrome phenotype. Therefore, the present study reveals the potential mechanism of the herbal extract to prevent metabolic syndrome in rats.

Identify the Characteristics of Metabolic Syndrome and Non-obese Phenotype: Data Visualization and a Machine Learning Approach.

Introduction: A third of the world's population is classified as having Metabolic Syndrome (MetS). Traditional diagnostic criteria for MetS are based on three or more of five components. However, the outcomes of patients with different combinations of specific metabolic components are undefined. It is challenging to be discovered and introduce treatment in advance for intervention, since the related research is still insufficient.Methods: This retrospective cohort study attempted to establish a method of visualizing metabolic components by using unsupervised machine learning and treemap technology to discover the relations between predicting factors and different metabolic components. Several supervised machine-learning models were used to explore significant predictors of MetS and to construct a powerful prediction model for preventive medicine.Results: The random forest had the best performance with accuracy and c-statistic of 0.947 and 0.921, respectively, and found that body mass index, glycated hemoglobin, and controlled attenuation parameter (CAP) score were the optimal primary predictors of MetS. In treemap, high triglyceride level plus high fasting blood glucose or large waist circumference group had higher CAP scores (>260) than other groups. Moreover, 32.2% of patients with high CAP scores during 3 years of follow-up had metabolic diseases are observed. This reveals that the CAP score may be used for detecting MetS, especially for the non-obese MetS phenotype.Conclusions: Machine learning and data visualization can illustrate the complicated relationships between metabolic components and potential risk factors for MetS.

Presence or Absence of Skeletal Muscle Dysfunction in Chronic Obstructive Pulmonary Disease is Associated With Distinct Phenotypes

IntroductionReduced skeletal muscle function and cognitive performance are common extrapulmonary features in Chronic Obstructive Pulmonary Disease (COPD) but their connection remains unclear. Whether presence or absence of skeletal muscle dysfunction in COPD patients is linked to a specific phenotype consisting of reduced cognitive performance, comorbidities and nutritional and metabolic disturbances needs further investigation. MethodsThirty-seven patients with COPD (grade II–IV) were divided into two phenotypic cohorts based on the presence (COPD dysfunctional, n=25) or absence (COPD functional, n=12) of muscle dysfunction. These cohorts were compared to 28 healthy, age matched controls. Muscle strength (dynamometry), cognitive performance (Trail Making Test and STROOP Test), body composition (Dual-energy X-Ray Absorptiometry), habitual physical activity, comorbidities and mood status (questionnaires) were measured. Pulse administration of stable amino acid tracers was performed to measure whole body production rates. ResultsPresence of muscle dysfunction in COPD was independent of muscle mass or severity of airflow obstruction but associated with impaired STROOP Test performance (p=0.04), reduced resting O2 saturation (p=0.003) and physical inactivity (p=0.01), and specific amino acid metabolic disturbances (enhanced leucine (p=0.02) and arginine (p=0.06) production). In contrast, COPD patients with normal muscle function presented with anxiety, increased fat mass, plasma glucose concentration, and metabolic syndrome related comorbidities (hypertension and dyslipidemia). ConclusionCOPD patients with muscle dysfunction show characteristics of a cognitive – metabolic impairment phenotype, influenced by the presence of hypoxia, whereas those with normal muscle function present a phenotype of metabolic syndrome and mood disturbances.

Evaluation of arterial stiffness in patients affected by hand osteoarthritis: a cross-sectional study

Purpose: An higher cardiovascular (CV) risk and increased mortality were found in several osteoarthritis studies, in particular for hand osteoarthritis (HOA) patients. Greater carotid-femoral pulse wave velocity (PWV), which reflect arterial stiffness, is an independent risk factor for the occurrence of CV events in the general population. An early detection of CV risk in HOA patients may allow preventive care management. Our study aimed to measure arterial stiffness in HOA patients by assessing carotid-femoral PWV in comparison to healthy patients. Methods: A prospective cross-sectional study was conducted including 82 patients between 45 to 65 years old in two age/sex matched groups, with or without HOA. Patients with current or previous CV disease or inflammatory rheumatism were excluded. A multivariate linear regression adjusted for age and Systematic COronary Risk Estimation (SCORE) score was performed. Results: Independently of age and gender, the HOA group was significantly overweight (24.5 kg/m2 versus 22.6 kg/m2; p=0.042), with an higher abdominal perimeter (85.33cm versus 77.88cm; p = 0.006). Furthermore, HOA patients were more sedentary (6/37 versus 1/45; p = 0.097), with an higher SCORE score (1.35 versus 0.85; p = 0.047). 20/37 patients had ≥1erosive joint involvement. The carotid-femoral PWV did not show statistical difference between the two groups (7.70 m/s in the HOA group versus 7.20 m/s in the control group; p = 0.084). The results were similar after adjustment for age and the SCORE score. Conclusions: Our study did not demonstrate any significant increase in arterial stiffness or worsening of other cardiovascular parameters in patients with HOA compared to control patients. Nevertheless, HOA patients had more often a metabolic syndrome phenotype suggesting the interest to perform a careful and regular screening for CV risk factors.

Two Weekly Sessions of High-Intensity Interval Training Improve Metabolic Syndrome and Hypertriglyceridemic Waist Phenotype in Older Adults: A Randomized Controlled Trial.

Background: Exercise training provides physiological benefits for maintaining good health. A common exercise strategy is high-intensity interval training (HIIT). HIIT may alleviate metabolic syndrome (MetS) and hypertriglyceridemic waist (HTGW) phenotype, but remains largely unstudied in ageing participants. The aim of this research was to investigate the impact of 2 weekly HIIT sessions on MetS markers and HTGW-related factors in older adults. Methods: In this randomized controlled trial, 140 older men and women were randomized into two groups, the experimental group (EG), and the control group (CG). The EG performed 2 weekly sessions of HIIT during 12 weeks. HIIT sessions consisted of 40 min treadmill running/walking: a 10 min warm-up at 50%-60% of maximum heart rate (HRmax), followed by 10 sets of 1 min bouts at 85%-90% of HRmax interspersed with 1 min walking at self-selected pace (totaling 20 min), and 10 min cool-down walking at self-selected pace. The CG did not perform any type of intense exercise during the intervention period. Results: Participants in the EG of both sexes decreased MetS, HTGW, blood pressure, cholesterol, and glycemia (P < 0.05). After training, the number of hypertensive men decreased by 100% and women by 70%. There was a 75% reduction in women with diabetes, a 100% reduction in MetS indicators and over 80% reduction in HTGW in participants of both sexes. Conclusion: Two weekly sessions of HIIT proved to be feasible and effective to induce clinically relevant improvements in MetS and HTGW indicators.

Risk of metabolic syndrome and metabolic phenotypes in relation to biomarker-calibrated estimates of energy and protein intakes: an investigation from the Women’s Health Initiative

Metabolic syndrome (MetS) is associated with increased mortality independent of BMI, resulting in discordant metabolic phenotypes, such as metabolically healthy obese and metabolically unhealthy normal-weight individuals. Studies investigating dietary intake in MetS have reported mixed results, due in part to the limitations of self-reported measures. To investigate the role of biomarker-calibrated estimates of energy and protein in MetS and metabolic phenotypes. Postmenopausal participants from the Women's Health Initiative (WHI) study who were free of MetS at baseline, had available data from FFQs at baseline, and had components of MetS at Year 3 (n=3963) were included. Dietary energy and protein intakes were estimated using biomarker calibration methods. MetS was defined as 3 or more of the following: elevated serum triglycerides (≥150 mg/dL), low HDL cholesterol (<50 mg/dL), hypertension [systolic blood pressure (BP) ≥130 or diastolic BP≥85 mmHg], elevated serum glucose (>100 mg/dL), and abdominal adiposity (waist circumference>89 cm). Models were adjusted for age, WHI study component, race/ethnicity, education, income, smoking, recreational physical activity, disease history, and parity. For every 10% increment in total calibrated energy intake, women were at a 1.37-fold elevated risk of MetS (95% CI, 1.15-1.63); a 10% increment in calibrated total protein intake was associated with a 1.21-fold elevated risk of MetS (95% CI, 1.00-1.47). Specifically, animal protein intake was associated with MetS (OR, 1.08; 95% CI, 1.02-1.14), whereas vegetable protein intake was not (OR, 0.99; 95% CI, 0.95-1.03). No differences were seen when examining metabolic phenotypes. We found that higher calibrated total energy, total protein, and total animal protein intakes were strongly associated with MetS. If replicated in clinical trials, these results will have implications for the promotion of energy and animal protein restrictions for the reduction of MetS risks.

Reciprocal association of serum Mac-2 binding protein and HDL-cholesterol concentrations

BackgroundMac-2 binding protein (Mac-2BP) is used as a serum biomarker of nonalcoholic steatohepatitis, considered to be a liver phenotype of metabolic syndrome (MetS). In this study, we investigated the serum Mac-2BP concentrations-correlated MetS-related clinical parameters in vivo, and the underlying mechanism in vitro. Materials & methodsWe enrolled 54 healthy Japanese men who underwent health examination at Osaka University Health Care Center in this study. Physical and serum biochemical parameters were obtained from all the subjects. In the cultured HepG2 cells, the effects of interferon (IFN)-γ on the expression of Mac-2BP, apolipoprotein (apo) A-I, and ATP binding cassette transporter A1 (ABCA1) were studied. ResultsSerum Mac-2BP concentrations correlated negatively with HDL-C, and positively with body mass index and systolic blood pressure in univariate analysis. These results suggested the association between Mac-2BP and MetS, although none of these 3 parameters had significant correlation with serum Mac-2BP concentrations in multivariate analysis. In HepG2 cells, IFN-γ stimulation resulted in the increased Mac-2BP and the decreased ABCA1 and apo A-I mRNA concentrations, while Mac-2BP had no effects on ABCA1 and apo A-I concentrations. ConclusionsThe serum Mac-2BP concentrations are negatively correlated with HDL-C concentrations in healthy subjects, as a result of chronic inflammation.