MetS Disorders Research Articles

Jaboticaba peel improves postprandial glucose and inflammation: A randomized controlled trial in adults with metabolic syndrome

The modulation of glucose metabolism through dietary sources has been recognized as 1 of the most sustainable approaches for preventing of cardiometabolic diseases. Although fibers and phenolic compounds derived from jaboticaba (Plinia jaboticaba) peel have demonstrated improvements in metabolic pathways in preclinical models, their beneficial effects in clinical trials remain to be fully determined. This study aimed to assess the impact of jaboticaba peel (JP) powder supplementation on glucose metabolism compared with a placebo in individuals with metabolic syndrome (MetS). A single-blind, parallel, randomized, placebo-controlled trial involving 49 individuals with MetS was conducted. Participants were assigned to receive either a JP supplement (15 g/day) or a matched placebo. Anthropometry measurements, body composition, blood pressure, metabolic and inflammatory parameters, and a mixed-meal tolerance test were assessed at weeks 0 and 5. Daily intake of JP improved the area under the curve of glucose (P = .025) and the interleukin-6 (IL-6) (P = .045). No significant time × treatment effects were observed for blood pressure, body weight, body composition, lipid metabolism, glucagon-like peptide-1, inflammatory cytokines (tumor necrosis factor-α, IL-1β), C-reactive protein, and insulin sensitivity and resistance indexes. JP supplementation may be a promising approach for managing MetS disorders, potentially by reducing the area under the curve for glucose and the proinflammatory cytokine IL-6. This research is registered at the Brazilian Registry of Clinical Trials (RBR-8wwq9t).

Prevalence and characteristics of metabolic syndrome and its components among adults living with and without HIV in Nigeria: a single-center study

BackgroundPersons living with HIV (PLHIV) now live longer due to effective combination antiretroviral therapy. However, emerging evidence indicates that they may be at increased risk for some cardiometabolic disorders. We compared the prevalence of metabolic syndrome (MetS) and its component disorders between persons living with and without HIV in Nigeria.MethodsThis was a cross-sectional analysis of baseline data from a prospective cohort study of non-communicable diseases among PLHIV along with age- and sex-matched persons without HIV (PWoH) at the University of Abuja Teaching Hospital Nigeria. We collected sociodemographic and clinical data, including anthropometric measures and results of relevant laboratory tests. MetS was defined using a modification of the third report of the National Cholesterol Education Program Adult Treatment Panel (NCEP ATP III) criteria.ResultsOf the 440 PLHIV and 232 PWoH, women constituted 50.5% and 51.3% respectively. The median age of the PLHIV was 45 years while that of the PWoH was 40 years. The prevalence of MetS was 30.7% (95% CI: 26.4%, 35.2%) and 22.8% (95% CI: 17.6%, 28.8%) among the PLHIV and PWoH respectively (P = 0.026). Independent associations were found for older age (P < 0.001), female sex (P < 0.001), family history of diabetes (P < 0.001), family history of hypertension (P = 0.013) and alcohol use (P = 0.015). The prevalence of component disorders for PLHIV versus PWoH were as follows: high blood pressure (22.3% vs 20.3%), prediabetes (33.8% vs 21.1%), diabetes (20.5% vs 8.2%), high triglycerides (24.5% vs 17.2%), low HDL-Cholesterol (51.1% vs 41.4%), and abdominal obesity (38.4% vs 37.1%). Adjusting for age and sex, prediabetes, diabetes, and low HDL-Cholesterol were significantly associated with HIV status. Duration on antiretroviral therapy, protease inhibitor-based regimen, CD4 count, and viral load were associated with some of the disorders mostly in unadjusted analyses.ConclusionWe found a high burden of MetS and its component disorders, with significantly higher prevalence of dysglycemia and dyslipidemia among PLHIV as compared to PWoH. Integration of strategies for the prevention and management of MetS disorders is needed in HIV treatment settings.

Correlation of White Blood Cell, Neutrophils, and Hemoglobin with Metabolic Syndrome and Its Components.

Metabolic syndrome (MetS) is a global health problem. White blood cell (WBC), neutrophils and neutrophil-to-lymphocyte ratio (NLR) are valid indicators involved in acute and chronic inflammation. The aims of our study were to analyze the correlation and severity of these indicators with MetS and its components, and explore the diagnostic value of their combined tests for MetS. A total of 7726 subjects were recruited, and laboratory biomarkers were collected. The differences of indicators between MetS group and non-MetS group were analyzed. The linear trend between each indicator and the increasing number of metabolic disorders was analyzed using trend variance test. The correlation between each indicator and MetS with its components was analyzed by logistic regression. The levels of WBC, neutrophil, and hemoglobin grew significantly in the MetS group compared to non-MetS group, and gradually increased with the increased number of MetS disorders. Logistic regression analysis indicated significant correlations between WBC, neutrophils, and hemoglobin with MetS and its components. ROC curve analysis showed WBC, neutrophils, and hemoglobin served as good predictors for MetS, especially in adults aged under 40. Our study indicated that WBC, neutrophils, and hemoglobin are efficient indicators for predicting MetS and evaluate its severity.

Chronically Hypertensive Transgenic Mice Expressing Human AT1R Haplotype‐I Exhibit Increased Susceptibility To Francisella Tularensis

Angiotensin receptor type 1 (AT1R), a G-protein coupled receptor mediates the effect of angiotensin-II and contributes to the pathophysiological consequences of metabolic disorders leading to vascular remodeling, hypertension, and end-organ damage. Genetic variations that increase human AT1R (hAT1R) expression can cause above pathological outcomes due to renin-angiotensin system overactivity. Previously we have shown that transgenic (TG) mice containing haplotype-I (Hap-I, hypertensive genotype) of human AT1R gene are more prone to develop the metabolic syndrome (MetS) related disorders as compared to the TG mice containing haplotype-II (Hap-II, normotensive genotype). We have also shown that as compared to Hap-II, the aged Hap-I TG mice overexpress the hAT1R gene resulting in an increase in blood pressure, inflammatory molecules, and renal dysfunction. Aging together with an increased risk of hypertension, can affect multiple organ systems in a complex manner, including susceptibility to various infections. The current study, therefore, was designed to examine the potential effect of aging and associated MetS disorders in our hAT1R containing TG mice model, in response to the infection by Francisella tularensis live vaccine strain (LVS) inhalation. Our results show that Hap-I TG mice have a significantly high mortality rate two weeks post-infection as compared to the Hap-II animals. Histochemical analysis of lung tissues from adult and aged animals show a comparatively elevated pathology in mice containing Hap-I of hAT1R. The lung tissue and plasma from Hap-I TG mice also show a relatively higher bacterial load five days post-infection. Preliminary RT-PCR experiments show increased inflammatory markers like IL-6, TGF-β, TNF-α, CRP and redox markers like NOX1, NOX4 in lung tissues of Hap-I TG mice. These studies suggest that haplotype dependent over-expression of hAT1R gene, leads to an enhanced mortality and lung pathology to F. tularensis LVS infection, which gets aggravated in aged animals. Clinically, our results may help in exploring the role of AT1R induced hypertension in pulmonary infections.

The Novel Angiotensin-(1-7) Analog, A-1317, Improves Insulin Resistance by Restoring Pancreatic β-Cell Functionality in Rats With Metabolic Syndrome.

In previous studies we have shown that oral Ang-(1–7) has a beneficial therapeutic effect on cardiometabolic disturbances present in metabolic syndrome (MetS). Based on the fact that Ang-(1–7) acts through release of nitric oxide (NO), a new peptide, A-1317 was engineered adding the amino acid L-Arginine, the NO precursor, to the N-terminal portion of the Ang-(1–7). Therefore, in a single molecule the substrate and the activator of NO are combined. In the present study, we evaluated the effect of A-1317 oral treatment on liver-glucose metabolism in MetS induced by high fat (HF) diet in rats. Rats were subjected to control (AIN-93M, CT) or HF diets for 15 weeks to induce MetS and treated with A-1317, Ang-(1–7) included into hydroxypropyl-β-cyclodextrin (HPβCD) or empty HPβCD (E), in the last 7 weeks. At the end of 15 weeks, hemodynamic, biometric, and biochemical parameters, redox process, and qRT-PCR gene expression of NO synthase and RAS components were evaluated in the liver. HF/E rats increased body mass gain, adiposity index, despite the reduction in food intake, increased plasma leptin, total cholesterol, triglycerides, ALT, fasting blood glucose, OGTT and insulin, HOMA-IR and MAP and HR. Furthermore, the MetS rats presented increased in liver angiotensinogen, AT1R, ACE mRNA gene expression and concentration of MDA and carbonylated protein. Both Ang-(1–7) and A-1317 oral treatment in MetS rats reverted most of these alterations. However, A-1317 was more efficient in reducing body mass gain, ALT, AST, total cholesterol, insulin, fasting blood glucose, ameliorating β cell capacity by increasing HOMA-β and QUICKI, whereas Ang-(1–7) reduced HOMA-β and QUICKI. In addition, Ang-(1–7) increased Mas and AKT liver mRNA gene expression, while A-1317 increased both Mas and MRGD and AMPK liver mRNA gene expression, suggesting a distinct pathway of action of Ang-(1–7) and A-1317 in MetS rats. Taken together, our data showed that treatment with A-1317 was able to ameliorate MetS disorders and suggested that this effect was mainly via MRGD via activation of AMPK and increasing β cell function.

The role of oxidation of low-density lipids in pathogenesis of osteoarthritis: A narrative review.

Osteoarthritis (OA) is a chronic joint disorder that causes degeneration of cartilage, synovial inflammation, and formation of osteophytes. Aging, obesity, and sex are considered the main risk factors of OA. Recent studies have suggested that metabolic syndrome (MetS) disorders, such as hypertension, hyperlipidemia, diabetes mellitus, and obesity, may be involved in the pathogenesis and progression of OA. MetS disorders are common diseases that also result in atherosclerosis. Researchers believe that OA and atherosclerosis have underlying similar molecular mechanisms because the prevalence of both diseases increases with age. Oxidation of low-density lipoprotein (ox-LDL) is believed to play a role in the pathogenesis of atherosclerosis. Recent reports have shown that ox-LDL and low-density lipoprotein receptor 1 (LOX-1) are involved in the pathogenesis of OA. The purpose of this narrative review is to summarize the current understanding of the role of the LOX-1/ox-LDL system in the pathogenesis of OA and to reveal common underlying molecular pathways that are shared by MetS in OA and the LOX-1/ox-LDL system.

Psychophysiological Status and Life Quality in Individuals with Metabolic Syndrome Living in Central Kazakhstan

BACKGROUND: Morbidity rate of circulatory system diseases (CSD) in Kazakhstan continues to grow and the metabolic syndrome (MetS) contributes significantly to cardiovascular risk development. It was known that MetS altered autonomic nervous system (ANS) by decreasing parasympathetic activity and global heart rate variability (HRV), at the same time, the decrease in sympathetic modulation is unclear. Studies investigated associations between anxiety and MetS disorders are rather controversial. Research findings of the MetS influence on health-related quality of life (HRQoL) were also contradictory. The above-mentioned justifies the necessity of research to clarify and deepen the MetS etiology and pathogenesis, as well as to improve its diagnostics efficiency and treatment.&#x0D; AIM: The research goals were to study psychophysiological status and HRQoL in individuals with MetS living in Central Kazakhstan.&#x0D; MATERIALS AND METHODS: Three hundred MetS patients were examined in Karaganda city clinical hospital. Statistical methods and spectral analysis of HRV, simple visual-motor reaction (SVMR), the Spielberger State-Trait Anxiety Inventory, and the Lüscher color test were used. SF-36 questionnaire was used for HRQoL assessment.&#x0D; RESULTS: General decrease in the activity of both sympathetic and parasympathetic branches of ANS was observed in MetS patients. More than half of the examined MetS patients have had a high level of trait anxiety. Most MetS patients have had a low level of the central nervous system (CNS) functional activity. MetS patients are active both in physical and social spheres. Bodily pain syndrome greatly influences MetS patients’ life quality. The patients evaluate their health level as being low.&#x0D; CONCLUSION: Individuals with MetS living in Central Kazakhstan had decreased activity of ANS, prevalence of inhibition processes in CNS, high level of trait anxiety, and bodily pain syndrome affecting life quality.

WWOX somatic ablation in skeletal muscles alters glucose metabolism

ObjectiveWWOX, a well-established tumor suppressor, is frequently lost in cancer and plays important roles in DNA damage response and cellular metabolism. MethodsWe re-analyzed several genome-wide association studies (GWAS) using the Type 2 Diabetes Knowledge Portal website to uncover WWOX's association with metabolic syndrome (MetS). Using several engineered mouse models, we studied the effect of somatic WWOX loss on glucose homeostasis. ResultsSeveral WWOX variants were found to be strongly associated with MetS disorders. In mouse models, somatic ablation of Wwox in skeletal muscle (WwoxΔSKM) results in weight gain, glucose intolerance, and insulin resistance. Furthermore, WwoxΔSKM mice display reduced amounts of slow-twitch fibers, decreased mitochondrial quantity and activity, and lower glucose oxidation levels. Mechanistically, we found that WWOX physically interacts with the cellular energy sensor AMP-activated protein kinase (AMPK) and that its loss is associated with impaired activation of AMPK, and with significant accumulation of the hypoxia inducible factor 1 alpha (HIF1α) in SKM. ConclusionsOur studies uncover an unforeseen role of the tumor suppressor WWOX in whole-body glucose homeostasis and highlight the intimate relationship between cancer progression and metabolic disorders, particularly obesity and type-2 diabetes. Subject areasGenetics, Metabolic Syndrome, Diabetes.

Effect of personalized moderate exercise training on Wistar rats fed with a fructose enriched water

BackgroundMetabolic Syndrom has become a public health problem. It mainly results from the increased consumption of fat and sugar. In this context, the benefits of personalized moderate exercise training were investigated on a metabolic syndrome male wistar rat model food with fructose drinking water (20–25% w/v). Different markers including body weight, metabolic measurements, blood biochemistry related to metabolic syndrome complications have been evaluated.MethodsMale Wistar rats were randomly allocated to 4 groups: control (sedentary (C, n = 8) and exercise trained (Ex, n = 8)), fructose fed (sedentary (FF, n = 8) and exercise trained fructose fed rats (ExFF, n = 10)). ExFF and Ex rats were trained at moderate intensity during the last 6 weeks of the 12 weeks-long protocol of fructose enriched water. Metabolic control was determined by measuring body weight, fasting blood glucose, HOMA 2-IR, HIRI, MISI, leptin, adiponectin, triglyceridemia and hepatic dysfunction.ResultsAfter 12 weeks of fructose enriched diet, rats displayed on elevated fasting glycaemia and insulin resistance. A reduced food intake, as well as increased body weight, total calorie intake and heart weight were also observed in FF group. Concerning biochemical markers, theoretical creatinine clearance, TG levels and ASAT/ALAT ratio were also affected, without hepatic steatosis. Six weeks of 300 min/week of moderate exercise training have significantly improved overweight, fasting glycaemia, HOMA 2-IR, MISI without modify HIRI. Exercise also decreased the plasma levels of leptin, adiponectin and the ratio leptin/adiponectin. Regarding liver function and dyslipidemia, the results were less clear as the effects of exercise and fructose-enriched water interact together, and, sometimes counteract each other.ConclusionOur results indicated that positive health effects were achieved through a personalized moderate training of 300 min per week (1 h/day and 5 days/week) for 6 weeks. Therefore, regular practice of aerobic physical exercise is an essential triggering factor to attenuate MetS disorders induced by excessive fructose consumption.

Developmental Programming of the Metabolic Syndrome: Can We Reprogram with Resveratrol?

Metabolic syndrome (MetS) is a mounting epidemic worldwide. MetS can start in early life, in a microenvironment that is now known as the developmental origins of health and disease (DOHaD). The concept of DOHaD also offers opportunities for reprogramming strategies that aim to reverse programming processes in early life. Resveratrol, a polyphenolic compound has a wide spectrum of beneficial effects on human health. In this review, we first summarize the epidemiological and experimental evidence supporting the developmental programming of MetS. This review also presents an overview of the evidence linking different molecular targets of resveratrol to developmental programming of MetS-related disorders. This will be followed by studies documenting resveratrol as a reprogramming agent to protect against MetS-related disorders. Further clinical studies are required in order to bridge the gap between animal models and clinical trials in order to establish the effective dose and therapeutic duration for resveratrol as a reprogramming therapy on MetS disorders from developmental origins.

Different associations of apoE gene polymorphism with metabolic syndrome in the Vojvodina Province (Serbia).

The metabolic syndrome (MetS) is a polygenic multifactorial metabolic disorder with strong socioeconomic influence. MetS has became a worldwide epidemic, that directly increases the risk of cardiovascular diseases and type 2 diabetes mellitus. The human apoE gene, coding Apolipoprotein E, has three common polymorphisms in human population: e2, e3 and e4, which are proved to be associated with impaired lipid metabolism. The contribution of apoE polymorphism to MetS disorders has not been investigated previously in Vojvodina Province, region with the highest number of obese people in Serbia. The aim of this study was to evaluate apoE gene polymorphism in relation to MetS disorders. The healthy control group of 30 individuals and 63 MetS patients were examined for apoE variants in relation to biochemical and anthropometric parameters. The genotypes were determined by PCR-RFLP. Regarding all parameters, significantly higher values were detected in MetS group compared to control. The MetS group of patients had significantly higher frequency of e4 allele. In addition, positive relation was revealed between e4 allele presence and all measured parameters. It was found that the e4 allele was related with a significantly increased OR of MetS disorders according to the International Diabetes Federation definition. These results suggested that e4 allele may act as a one of determinants for development of metabolic syndrome.

Is vitamin D status relevant to metabolic syndrome?

Review of the evidence on hypovitaminosis D as a risk factor for metabolic syndrome and its sequelae, T2DM and CVD, suggests long-term vitamin D repletion could reduce these risks. There is mechanistic evidence for protective effects for MetS and the balance of evidence, (cross-sectional and prospective), supports this postulate. Much of the data so far available from randomized controlled trials is weakened by inadequate power, low vitamin D dosages, starting supplementation too late in life or after MetS disorders have developed or, most importantly, by non-inclusion of many recognizable confounders. On balance, therefore, maintenance of US 2010 recommended intakes for bone protection has the potential to prove protective for MetS. Supplementation has been shown to increase survival in patients with cardiac disorders; whether higher doses would provide useful protection for apparently healthy people in the general population awaits the outcomes of ongoing randomized-controlled trials that, it is hoped, will prove or disprove causality for hypovitaminosis D in MetS and its long-term ill-effects.