Features Of Metabolic Syndrome Research Articles

Au-NP-based colorimetric assay for sugar detection and quantification

Sugars have been associated with health problems such as metabolic syndrome, obesity, elevated triglycerides, and other features of metabolic disorders. Here, we report on the design and characterization of a highly sensitive gold nanoparticle (AuNP)-based assay for measuring sugars levels in fluids. AuNPs are functionalized with 4-mercaptobenzoic acid (4MBA) to modulate surface plasmonic resonance (SPR) frequency and fluorescent energy absorption by AuNPs, based on a fixed concentration of fluorescein introduced along with a fluid sample containing a determined quantity of sugar. We find the driving mechanism to be kinetic competition between fluorescein and saccharide which occupies the active carboxylic sites of the functional groups on the nanoparticle surface. This drives a colorimetric response in the 4MBA-AuNP solution, from orange to green, discernible to the naked eye. The aggregation of functionalized AuNPs as a result of increasing sugar concentration was confirmed via UV–vis spectroscopy and identified by a spectral peak of 620–675 nm. The limit of detection (LOD) was (55.8 ± 1.1) µM, with a highly repeatable calibration curve in the range of 0.09 – 2.45 mM. The assay's cost-effectiveness, speed, and simplicity open the door to multiple applications associated with detecting and quantifying sugars, including food science. The sensory platform was successfully tested in mixed sugar solutions to study the sensitivity capacity and applied to strawberry and kiwi freeze-dried samples. The results are validated by HPLC with refractive index detection.

Concordance/discordance between serum apolipoprotein B, low density lipoprotein cholesterol and non-high density lipoprotein cholesterol in NATPOL 2011 participants – An epidemiological perspective

BackgroundThe study compared the distribution of serum LDL-C, non-HDL-C, and apolipoprotein B (apoB) among participants of the NATPOL 2011 survey and analysed concordance/discordance of results in the context of the risk for atherosclerotic cardiovascular disease (ASCVD). MethodsSerum levels of apoB, LDL-C, non-HDL-C and small dense LDL-C were measured/calculated in 2067–2098 survey participants. The results were compared between women and men, age groups and in relation to body mass index (BMI), fasting glucose and TG levels, and the presence of CVD. Percentile distribution of lipid levels and concordance/discordance analysis were based on medians and ESC/EAS 2019 target thresholds for ASCVD risk and on comparison of measured apoB levels and levels calculated from linear regression equations with serum LDL- C and non-HDL-C as independent variables. ResultsSerum apoB, LDL-C and non-HDL-C were similarly related to sex, age, BMI, visceral obesity, cardiovascular disease, and fasting glucose and triglyceride levels. Serum apoB, LDL-C and non-HDL-C very high- and moderate- target thresholds were exceeded in 83%, 99% and 96.9% and in 41%, 75% and 63.7% of subjects, respectively. The incidence of the discordances between the results depended on the dividing values used and ranged from 0.2% to 45.2% of the respondents. Subjects with high apoB / low LDL-C/non-HDL-C discordance had features of metabolic syndrome. ConclusionsDiagnostic discordances between apoB and LDL-C/non-HDL-C indicate limitations of serum LDL-C/non-HDL-C in ASCVD risk management. Due to the high apoB/low LDL-C/non-HDL-C discordance, obese/metabolic syndrome patients may benefit from replacing LDL-C/non-HDL-C by apoB in ASCVD risk assessment and lipid-lowering therapy.

P07-067-23 The Effect of Source of Protein Fed During Pregnancy on Development of Characteristics of Metabolic Syndrome in Offspring of Obese Wistar Rats

P07-067-23 The Effect of Source of Protein Fed During Pregnancy on Development of Characteristics of Metabolic Syndrome in Offspring of Obese Wistar Rats

Atrial Fibrillation Development Risk Associated with Metabolic Syndrome

Even in the absence of antecedent myocardial infarction or congestive heart failure, atrial fibrillation (AF) is the most frequent arrhythmia seen in daily practice. There are several important predisposing factors for the initiation of AF, including growing older, being a man, being female, having high blood pressure, and having cardiac and noncardiac illnesses. Metabolic syndrome (MS) contributes to the progression of AF through its impact on the atrial substrate. MS involves metabolic risk factors that increase the likelihood of atherosclerotic cardiovascular disease and type 2 diabetes. Insulin resistance plays a significant role in MS pathophysiology, leading to glucose and lipid metabolism dysregulation, increased inflammation, and neurohormonal activation. These processes contribute to the development of hypertension, a major risk factor for AF. Atrial remodeling, including electrical and structural changes, is a common substrate for AF, and MS components further contribute to this remodeling. Hypertension, a key feature of MS, is associated with structural, contractile, and electrical remodeling in the atria, increasing the risk of AF. The renin-angiotensin-aldosterone system, implicated in hypertension regulation, also influences the pathophysiology of AF through fibrosis, ion channel alterations, oxidative stress, and inflammation. Understanding the intricate interplay between MS and AF can provide insights into therapeutic strategies for managing these conditions and reducing cardiovascular risks.

Liver Fibrosis in Non-Alcoholic Fatty Liver Disease and Progression to Hepatocellular Carcinoma in Patients with Inflammatory Bowel Disease: A Systematic Review

The aim of the systematic review is to assess the prevalence and risk factors of liver fibrosis in patients with Inflammatory Bowel Disease (IBD) and Non-Alcoholic Fatty Liver Disease (NAFLD) and to discuss the role of liver fibrosis in the progression to hepatocellular carcinoma (HCC). We performed a structured search in PubMed, Web of Science, Embase, and Scopus up to 3 March 2023 to identify observational studies reporting liver fibrosis in patients with NAFLD and IBD. Quality of studies was assessed using the Newcastle-Ottawa Scale (NOS) score. A total of 23 studies met our inclusion criteria, including 629,781 patients. A total of 10 cross-sectional, 3 case-control, and 10 cohort studies were included. Fourteen studies had a NOS score ≥ 7 points. NAFLD was diagnosed in 2162/6332 (34.1%) IBD participants. However, NAFLD diagnosis was established in 924/2962 (31.2%) healthy individuals without IBD. Advanced liver fibrosis was found in 116 (11.6%) of 992 IBD patients with NAFLD. Most studies found an association between NAFLD and classic cardiovascular risk factors such as older age, male sex, higher BMI, diabetes, hypertension and dyslipidemia. In addition, metabolic syndrome features were also associated with an increased risk of significant and advanced liver fibrosis. Although no strong association between NAFLD and IBD therapy was reported, some studies associated NAFLD with IBD diagnosis, Crohn’s Disease, a complicated course of IBD, disease activity, and IBD duration. Advanced liver fibrosis was also associated with Crohn’s disease in several studies. In conclusion, NAFLD and advanced liver fibrosis are prevalent and clinically relevant extraintestinal manifestations, so its diagnosis and potential progression to HCC should be carefully considered in daily clinical practice.

Antipsychotic-Induced Metabolic Syndrome: A Review.

Schizophrenia, a serious psychiatric disorder, is among the top 10 global causes of disability and affects nearly 1% of the world population. Antipsychotics constitute the best treatment for patients with schizophrenia, however, this treatment class carries a high risk of metabolic syndrome, including lipid abnormalities. Indeed, the risk of metabolic syndrome would be increased in the population with schizophrenia compared to the general population. The objective is to summarize the prevalence, the mechanisms, and the potential treatments of antipsychotic-induced metabolic syndrome. This is a narrative review of the literature. We searched the electronic database Medline, accessed through PubMed, to find studies that investigated the prevalence and treatments of metabolic syndrome in the adult population using antipsychotics. The prevalence of metabolic syndrome in patients treated with antipsychotics ranges from 37% to 63%. Antipsychotic iatrogenic effects include weight gain/increased waist circumference, dyslipidemia, insulin resistance/type 2 diabetes, and hypertension. Clozapine and olanzapine are reported to precipitate the onset of metabolic syndrome features. In patients with metabolic syndrome, an antipsychotic with less metabolic side effects such as lurasidone, lumateperone, ziprasidone, and aripiprazole should be prioritized. Unlike medications, aerobic exercise and dietetic counseling were found to be efficient as the nonpharmacologic treatment of antipsychotic-induced metabolic syndrome. Few pharmacological treatments were proven effective against weight gain in this patient population. The risk of metabolic syndrome induced by antipsychotics should be early recognized and closely monitored. Primary and secondary prevention of metabolic syndrome or onset of its feature might help reduce the risk of death for patients using antipsychotics.

1678-P: B6-Alms1-del Mice, a Metabolic Syndrome Animal Model, Shows Semaglutide Benefits on Obesity, Hyperglycemia, and NAFL

Metabolic syndrome is a cluster of conditions that occur together, increasing the risk of heart disease, stroke and type 2 diabetes. These conditions include obesity, hyperglycemia, hypertension, hyperlipidemia. Leptin and leptin receptor mutant mice, ob/ob and db/db, are two classic metabolic syndrome animal model. However, the transient hyperglycemia of ob/ob and severe hyperglycemia induced premature death of db/db limit the application of these two models. To fill the gap, GemPharmatech developed a metabolic disorder model based on the mutation of Alms1 gene in mice (B6-Alms1-del mice). B6-Alms1-del mice gradually developed obesity from 8 weeks old with chow diet, accompanied by hyperglycemia, glucose and insulin intolerance, dyslipidemia and impaired liver function. Moreover, B6-Alms1-del mice developed severe non alcoholic fatty liver spontaneously as early as 21 weeks old and no premature death was observed around 5~8 months of ages. As B6-Alms1-del mice copied major features of metabolic syndrome, we further tested whether B6-Alms1-del mice could response to the positive drug semaglutide, an agonist of GLP-1R. 16 weeks old B6-Alms1-del mice were treated with vehicle and semaglutide for 5 weeks, respectively. Our results indicate that semaglutide lead to benefit on metabolic syndrome, including body weight control, improvement in hyperglycemia, hyperlipidemia, liver injury and hepatic steatosis. In conclusion, we have established a metabolic syndrome animal model that develop clinically relevant metabolic phenotypes and overcome the limitation of ob/ob and db/db. Furthermore, B6-Alms1-del mice responds to the approval anti-obesity drug semaglutide, which provide a useful model to assess the efficacy of novel metabolic syndrome therapies. Disclosure Z.Chen: None. M.Gao: None. X.Zhao: None. Z.Li: None. J.Zhao: None. C.Ju: None. X.Gao: None.

Obesity, obesities and gastrointestinal cancers

Obesity has been recognized to be increasing globally and is designated a disease with adverse consequences requiring early detection and appropriate care. In addition to being related to metabolic syndrome disorders such as type 2 diabetes, hypertension, stroke, and premature coronary artery disease. Obesity is also etiologically linked to several cancers. The non-gastrointestinal cancers are breast, uterus, kidneys, ovaries, thyroid, meningioma, and thyroid. Gastrointestinal (GI) cancers are adenocarcinoma of the esophagus, liver, pancreas, gallbladder, and colorectal. The brighter side of the problem is that being overweight and obese and cigarette smoking are mostly preventable causes of cancers.Epidemiology and clinical studies have revealed that obesity is heterogeneous in clinical manifestations. In clinical practice, BMI is calculated by dividing a person's weight in kilograms by the square of the person's height in square meters (kg/m2). A BMI above 30 kg/m2 (defining obesity in many guidelines) is considered obesity. However, obesity is heterogeneous. There are subdivisions for obesity, and not all obesities are equally pathogenic.Adipose tissue, in particular, visceral adipose tissue (VAT), is endocrine and abdominal obesity (a surrogate for VAT) is evaluated by waist-hip measurements or just waist measures. Visceral Obesity, through several hormonal mechanisms, induces a low-grade chronic inflammatory state, insulin resistance, components of metabolic syndrome, and cancers. Metabolically obese, normal-weight (MONW) individuals in several Asian countries may have BMI below normal levels to diagnose obesity but suffer from many obesity-related complications. Conversely, some people have high BMI but are generally healthy with no features of metabolic syndrome. Many clinicians advise weight loss by dieting and exercise to metabolically healthy obese with large body habitus than to individuals with metabolic obesity but normal BMI.The GI cancers (esophagus, pancreas, gallbladder, liver, and colorectal) are individually discussed, emphasizing the incidence, possible pathogenesis, and preventive measures.From 2005 to 2014, most cancers associated with overweight and Obesity increased in the United States, while cancers related to other factors decreased. The standard recommendation is to offer or refer adults with a body mass index (BMI) of 30 or more to intensive, multicomponent behavioral interventions. However, the clinicians have to go beyond. They should critically evaluate BMI with due consideration for ethnicity, body habitus, and other factors that influence the type of obesity and obesity-related risks. In 2001, the Surgeon General's ``Call to Action to Prevent and Decrease Overweight and Obesity'' identified obesity as a critical public health priority for the United States. At government levels reducing obesity requires policy changes that improve the food and physical activity for all. However, implementing some policies with the most significant potential benefit to public health is politically tricky. The primary care physician, as well as subspecialists, should identify overweight and Obesity based on all the variable factors in the diagnosis. The medical community should address the prevention of overweight and Obesity as an essential part of medical care as much as vaccination in preventing infectious diseases at all levels- from childhood, to adolescence, and adults.

MIND dietary pattern adherence is inversely associated with visceral adiposity and features of metabolic syndrome

The effects of following the Mediterranean-Dietary Approaches to Stop Hypertension (DASH) Intervention for Neurodegenerative Delay (MIND) diet on metabolic health remains understudied. This cross-sectional analysis of 163 adults investigated associations between adherence to the MIND, Mediterranean, DASH, and Healthy Eating Index (HEI-2015) diets and metabolic syndrome (MetS) features and visceral adiposity. We hypothesized that the MIND diet would show the most beneficial associations with MetS risk factors. Diet adherence was assessed using the Dietary History Questionnaire II. Visceral adipose was assessed using dual-energy X-ray absorptiometry. Waist circumference and systolic and diastolic blood pressures were obtained. Fasting blood triglycerides, high-density lipoprotein cholesterol, and glucose concentrations were determined. Stepwise regression analyses were applied. Waist circumference was inversely associated with DASH (β = –0.21, P < .01), HEI-2015 (β = –0.18, P = .01), and MIND (β = –0.19, P < .01). Triglycerides were inversely associated with DASH (β = –0.19, P = .01), HEI-2015 (β = –0.18, P = .02), and MIND (β = –0.23, P < .01). High-density lipoprotein cholesterol was positively associated with Mediterranean (β = 0.18, P = .02) and MIND (β = 0.21, P < .01). Systolic blood pressure was inversely associated with Mediterranean (β = –0.18, P = .02), DASH (β = –0.30, P < .01), HEI-2015 (β = –0.24, P < .01), and MIND (β = –0.25, P < .01). Diastolic blood pressure was inversely associated with Mediterranean (β = –0.26, P < .01), DASH (β = –0.34, P < .01), HEI-2015 (β = –0.24, P < .01), and MIND (β = –0.31, P < .01). Fasting glucose was inversely associated with MIND (β = –0.19, P = .02). Visceral adiposity was inversely associated with Mediterranean (β = –0.19, P < .01), DASH (β = –0.22, P < .01), HEI-2015 (β = –0.22, P < .01), and MIND (β = –0.28, P < .01). Although each diet exhibited potential benefits for metabolic outcomes, only greater MIND diet adherence was associated with lower visceral adiposity and each MetS feature in adults.

Lipoprotein(a), metabolic profile and new-onset type 2 diabetes in patients with familial combined hyperlipidemia: A 9 year follow-up study

Lipoprotein(a) [Lp(a)] appears to have an inverse association with the risk of type 2 diabetes mellitus in the general population. This study aimed to investigate the prognostic role of Lp(a) regarding the development of type-2 diabetes in the special population of subjects with familial combined hyperlipidemia (FCH). This cohort study included 474 patients (mean age 49.7±11.3 years, 64% males) with FCH, without diabetes at baseline who were followed for a mean period of 8.2±6.8 years. At baseline evaluation venous blood samples were obtained for the determination of lipid profile and Lp(a) levels. The endpoint of interest was the development of diabetes. Patients with increased Lp(a) levels ≥30mg/dl compared to those with low Lp(a) levels <30mg/dl had lower levels of triglycerides (238±113 vs 268±129 mg/dl, p=0.01), greater levels of high-density lipoprotein (HDL) cholesterol (44±10 vs 41±10 mg/dl, p=0.01) and hypertension in a greater percentage (42% vs 32%, p=0.03). The incidence of new-onset diabetes during the follow-up period was 10.1% (n=48). Multiple Cox regression analysis revealed that increased Lp(a) is an independent predictor of lower diabetes incidence (HR 0.39, 95% CI 0.17-0.90, p=0.02) after adjustment for confounders. Among subjects with FCH those with higher Lp(a) levels have lower risk for the development of type 2 diabetes. Moreover, the presence of increased Lp(a) seems to differentiate the expression of metabolic syndrome characteristics in patients with FCH, as increased Lp(a) is related to lower levels of triglycerides, greater prevalence of hypertension and higher levels of HDL cholesterol.

THE EFFECTIVENESS OF ETHANOL EXTRACT OF JAMBLANG LEAVES (Syzygium cumini L.) IN INCREASING HDL LEVELS IN WISTAR RATS MODELS OF METABOLIC SYNDROME

One of the characteristics of metabolic syndrome (MetS) is the low high-density lipoprotein (HDL) levels. Jamblang leaves (Syzygium cumini L.) contain various phytochemicals, which have antihyperglycemic, antihyperlipidemic, and antioxidant properties. This study aims to demonstrate the effectiveness of ethanol extract of jamblang leaves in increasing HDL levels in the Wistar rats model of MetS. A pretest-posttest with a control group design was conducted using 30 male Wistar rats, divided into five groups randomly, with six rats for each group. Here, KN means normal control group, K- negative control group, and P1, P2, and P3: treatment groups that were administered the 100 mg/kg/day, 150 mg/kg/day, and 200 mg/kg/day of ethanol extract of jamblang leaves for 28 days, respectively. The rat MetS model was developed by administering the high-fat fructose diet and streptozotocin-nicotinamide. The data were analyzed using paired t-test and one-way ANOVA (α=0.05). This study found that extract administration in P2 and P3 increased HDL levels significantly, but not with the P1 group. However, HDL levels in P1 were significantly higher compared to the K- group. Moreover, increasing the dose was significantly followed by higher HDL levels, although the highest dose did not reach the HDL level as in the KN group.

Blocking soluble TNF decreases diet‐induced hyperglycemia and modulates immune alterations in 5xFAD animal model of Alzheimer’s disease

AbstractBackgroundRegulatory interactions between the gut and the brain are essential for energy homeostasis across systems. Current evidence indicates high‐fat, high‐carbohydrate diets (HFHC) impact Alzheimer’s disease (AD) pathophysiology, however, the mechanisms underlying this association are poorly understood. We hypothesize that (1) Tumor Necrosis Factor (TNF) mediates metabolic inflammation in an obesogenic environment with impacts across the gut‐brain axis and (2) that HFHC interacts with an AD‐relevant genetic background to promote metabolic and immune dysregulation that accelerates pathological and behavioral dysfunction in an animal model of AD.MethodTo investigate the effects of chronic systemic inflammation on AD‐associated pathology, 2‐month old female 5xFAD mice were fed HFHC or a control diets (CD) for 8 weeks. One month following dietary intervention, the brain‐permeant soluble TNF inhibitor XPro1595 or a brain‐impermeant pan (sol and membrane‐bound) TNF inhibitor Etanercept (Enbrel, Amgen‐Wyeth) or vehicle (saline) were dosed twice weekly for 4 weeks. Behavioral test were performed to assess cognitive parameters. Plasma, brain and gut were collected for evaluation of insulin impairment, metabolic and immune parameters. Cortical tissues were subjected to RNAseq analysis to determine gene pathways modified by interactions between diet, genotype, and TNF inhibition.ResultHFHC promoted metabolic syndrome features associated with increases in adiposity, body weight, and plasma glucose, cholesterol, leptin, and insulin. TNF inhibition did not rescue diet‐induced insulin increases, however XPro specifically reduced plasma glucose, while Enbrel increased HOMA‐IR in HFHC‐fed mice. HFHC diet increased circulating IL‐6, CXCL1, CXCL2 and CCL2 and TNF neutralization with either drug decreased IL‐6 in HFHC‐fed groups. In the colon, HFHC diet decreased CCL3 and TNF blockade increased colonic IL‐15 in HFHC‐fed mice. Ongoing behavioral assessment, cortical transcriptional analysis, and hippocampal protein profiles of insulin signaling and inflammatory markers will determine additional effects of TNF and HFHC in the 5XFAD animal model of AD.ConclusionCollectively, these results suggest that TNF modulates systemic metabolic and inflammatory pathways induced by HFHC consumption and associated with neurodegeneration and neuroinflammation. Blocking soluble TNF decreases hyperglycemia triggered during diet‐induce obesity. Future studies focusing on the impact of TNF on energy homeostasis and inflammation will provide targets for new therapeutics against neurological disease.

Supplementation with a New Standardized Extract of Green and Black Tea Exerts Antiadipogenic Effects and Prevents Insulin Resistance in Mice with Metabolic Syndrome.

Insulin resistance is one of the main characteristics of metabolic syndrome (MetS) and the main cause of the development of type II diabetes. The high prevalence of this syndrome in recent decades has made it necessary to search for preventive and therapeutic agents, ideally of natural origin, with fewer side effects than conventional pharmacological treatments. Tea is widely known for its medicinal properties, including beneficial effects on weight management and insulin resistance. The aim of this study was to analyze whether a standardized extract of green and black tea (ADM® Complex Tea Extract (CTE)) prevents the development of insulin resistance in mice with MetS. For this purpose, C57BL6/J mice were fed for 20 weeks with a standard diet (Chow), a diet with 56% kcal from fat and sugar (HFHS) or an HFHS diet supplemented with 1.6% CTE. CTE supplementation reduced body weight gain, adiposity and circulating leptin levels. Likewise, CTE also exerted lipolytic and antiadipogenic effects in 3T3-L1 adipocyte cultures and in the C. elegans model. Regarding insulin resistance, CTE supplementation significantly increased plasma adiponectin concentrations and reduced the circulating levels of insulin and the HOMA-IR. Incubation of liver, gastrocnemius muscle and retroperitoneal adipose tissue explants with insulin increased the pAkt/Akt ratio in mice fed with Chow and HFHS + CTE but not in those fed only with HFHS. The greater activation of the PI3K/Akt pathway in response to insulin in mice supplemented with CTE was associated with a decrease in the expression of the proinflammatory markers Mcp-1, IL-6, IL-1β or Tnf-α and with an overexpression of the antioxidant enzymes Sod-1, Gpx-3, Ho-1 and Gsr in these tissues. Moreover, in skeletal muscle, mice treated with CTE showed increased mRNA levels of the aryl hydrocarbon receptor (Ahr), Arnt and Nrf2, suggesting that the CTE's insulin-sensitizing effects could be the result of the activation of this pathway. In conclusion, supplementation with the standardized extract of green and black tea CTE reduces body weight gain, exerts lipolytic and antiadipogenic effects and reduces insulin resistance in mice with MetS through its anti-inflammatory and antioxidant effects.

Eryngium billardieri extract affects cardiac gene expression of master regulators of cardiomyaopathy in rats with high fatdiet-induced insulin resistance

For years, numerous studies have focused on identifying approaches to increase insulin sensitivity by modifying the signaling factors. In the present study, we examined the effects of Eryngium billardieri extract, as an anti-diabetic herbal medication, on the heart mRNA level of Akt serine/threonine kinase (Akt), mechanistic target of rapamycin kinase (mTOR), peroxisome proliferator-activated receptor gamma (PPARγ), and Forkhead box o1 (Foxo1) in rats with high-fat diet (HFD)-induced insulin resistance (IR). We also assessed the anti-diabetic effects of E.billardieri extract in rats with insulin resistance. Twenty-seven male Wistar rats were divided into two groups. Nine rats were fed a normal diet (control group), and 18 rats were fed an HFD for 13 weeks (HFD group). To confirm the induction of insulin resistance, the oral glucose tolerance test (OGTT) was performed and homeostatic model assessment for insulin resistance (HOMA-IR) was calculated. Then rats with IR were randomly divided into the following groups: the HFD group, which continued an HFD, and the group treated with E.billardieri extract, which received the extract at a concentration of 50mg/kg for 30 days. On the 30th day, the animals were sacrificed and serum samples were collected for biochemistry analyses. Furthermore, the expression of Akt, mTOR, PPARγ, and Foxo1 was measured in heart tissue using the real-time polymerase chain reaction (PCR) method. Real-time PCR analyses revealed that an HFD can significantly decrease the expression level of Akt, mTOR, and PPARγ in the heart tissue. However, an HFD significantly increased the expression level of Foxo1 in the HFD group compared to the control group (P<0.05). In addition, our data showed that the administration of E. billardieri extract significantly enhanced the mRNA levels of Akt, PPARγ, and mTOR in the heart tissue compared to the HFD group (P<0.05), while it significantly decreased the Foxo1 mRNA levels (P<0.01). Given that Akt, mTOR, PPARγ, and Foxo1 are critical factors in insulin resistance, the present study suggests that E.billardieri could probably be used as an alternative treatment for IR as a major feature of metabolic syndrome.

The fat body cortical actin network regulates Drosophila inter-organ nutrient trafficking, signaling, and adipose cell size.

Defective nutrient storage and adipocyte enlargement (hypertrophy) are emerging features of metabolic syndrome and type 2 diabetes. Within adipose tissues, how the cytoskeletal network contributes to adipose cell size, nutrient uptake, fat storage, and signaling remain poorly understood. Utilizing the Drosophila larval fat body (FB) as a model adipose tissue, we show that a specific actin isoform-Act5C-forms the cortical actin network necessary to expand adipocyte cell size for biomass storage in development. Additionally, we uncover a non-canonical role for the cortical actin cytoskeleton in inter-organ lipid trafficking. We find Act5C localizes to the FB cell surface and cell-cell boundaries, where it intimately contacts peripheral LDs (pLDs), forming a cortical actin network for cell architectural support. FB-specific loss of Act5C perturbs FB triglyceride (TG) storage and LD morphology, resulting in developmentally delayed larvae that fail to develop into flies. Utilizing temporal RNAi-depletion approaches, we reveal that Act5C is indispensable post-embryogenesis during larval feeding as FB cells expand and store fat. Act5C-deficient FBs fail to grow, leading to lipodystrophic larvae unable to accrue sufficient biomass for complete metamorphosis. In line with this, Act5C-deficient larvae display blunted insulin signaling and reduced feeding. Mechanistically, we also show this diminished signaling correlates with decreased lipophorin (Lpp) lipoprotein-mediated lipid trafficking, and find Act5C is required for Lpp secretion from the FB for lipid transport. Collectively, we propose that the Act5C-dependent cortical actin network of Drosophila adipose tissue is required for adipose tissue size-expansion and organismal energy homeostasis in development, and plays an essential role in inter-organ nutrient transport and signaling.

Metabolic and vascular effect of a new standardized bergamot phytocomplex: a three-arm, placebocontrolled, double-blind clinical trial.

In addition to healthy lifestyle and balanced diet, nutraceutical supplementation may be useful to maintain overall metabolic wellness. The aim of the present study was to assess the metabolic and vascular effects of a new, highly standardized bergamot phytocomplex supplement in healthy volunteers with the features of metabolic syndrome. We carried out a double-blind, randomized, placebo-controlled, three-arm, parallel-group clinical trial in 90 adult subjects (30 per group) treated for 12 weeks with two different dosages of a highly standardized bergamot phytocomplex (Endoberg by AKHYNEX and Kalita by Giellepi) or placebo. Lipid plasma levels, glycemia, plasma hs-CRP, HOMA-IR, body fat, endothelial reactivity and fatty liver index were assessed at baseline, after 6 weeks and at the end of treatment in all subjects. At the end of treatment, both tested bergamot extract doses were able to significantly improve atherogenic dyslipidemia and insulin sensitivity (p < 0.05) compared to placebo. In the high-dose treated group, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), non high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG) improved versus placebo (p < 0.05) just after 6 weeks of treatment. After 12 weeks of treatment, TC decreased by 13.2 ±2.1%, LDL-C by 17.7 ±3.2%, non-HDL-C by 17.5 ±3.1%, TG by 16.6 ±3.3%, TG/HDL-C by 22.5 ±4.4%, homeostasis insulin resistance index (HOMA-IR) by 12.2 ±2.1%, γ-glutamyl transferase (GGT) by 22.2 ±4.6%, and high-sensitivity C-reactive protein (hs-CRP) by 17.9 ±3.4% versus baseline (p < 0.05) and vs. placebo (p < 0.05). Percentage body fat and endothelial reactivity improved versus baseline, but not versus placebo, in the high-dose treatment only (p < 0.05). The tested bergamot phytocomplex was able to significantly improve glucose and lipid metabolism, as well as inflammation, and might represent a novel multi-target approach to control metabolic syndrome.

Prevalence and Demographic characteristics of Metabolic Syndrome in Iraqi Patients with Acute Coronary Syndrome

Background: The demographic characteristics of Iraqi patients with the metabolic syndrome (MS) and presenting with acute coronary syndrome (ACS) has been scarcely studied before. Aim of the study To study the socio-demographic characteristics of a group of Iraqi patients with MS presenting with ACS. Patients and Methods: A convenience sample of 150 cases presenting with ACS and admitted to the coronary care unit (CCU) of Al-Yarmouk Teaching Hospital in Baghdad from mid-January through July 2011 were included in the current cross-sectional study. The data needed for the study was collected through a direct interview to fill a questionnaire by all cases carried out by a consultant physician.

A Scoping Review of the Relationship between Intermittent Fasting and the Human Gut Microbiota: Current Knowledge and Future Directions

Intermittent fasting (IF) has been promoted as an alternative to dietary caloric restriction for the treatment of obesity. IF restricts the amount of food consumed and improves the metabolic balance by synchronizing it with the circadian rhythm. Dietary changes have a rapid effect on the gut microbiota, modulating the interaction between meal timing and host circadian rhythms. Our paper aims to review the relationships between IF and human gut microbiota. In this study, the primary area of focus was the effect of IF on the diversity and composition of gut microbiota and its relationship with weight loss and metabolomic alterations, which are particularly significant for metabolic syndrome characteristics. We discussed each of these findings according to the type of IF involved, i.e., time-restricted feeding, Ramadan fasting, alternate-day fasting, and the 5:2 diet. Favorable metabolic effects regarding the reciprocity between IF and gut microbiota changes have also been highlighted. In conclusion, IF may enhance metabolic health by modifying the gut microbiota. However additional research is required to draw definitive conclusions about this outcome because of the limited number and diverse designs of existing studies.

Somatotype and morphological characteristics of metabolic syndrome in patients with schizophrenia and persons without mental disorders

Objective: identify differences or comparability of constitutional-morphological characteristics and indicators of the fatty constitution between patients with schizophrenia and people with MetS and without mental disorders.Materials and methods. We examined 63 patients with schizophrenia and MetS (25 women, 38 men), aged 30 [33;52], and 50 mentally healthy individuals with MetS (28 women, 22 men) aged 57 [49; 60]. The main criterion for inclusion in the study was the presence of a verified MetS according to the criteria of the International Diabetes Federation. Anthropometric examination was performed according to the method of V.V. Bunak (1941) with the underlying calculation of integral indices. The determination of the fat component included: measuring waist circumference; non-invasive bioimpedancemetry – body weight, BMI, total and visceral fat content; determination of the total fat fold (electronic caliper). In the blood serum, the concentration of glucose, total cholesterol, HDL, TG was determined using standard commercial kits, the calculation of LDL and the Atherogenic Index.Results. Differences in the prevalence of the constitutional-morphological type and the type of somatic sexual differentiation were not established in the groups. The level of visceral fat and BMI were higher in mentally healthy individuals with MetS than in schizophrenic patients with MetS (p = 0.005 and p = 0.0001, respectively). Patients with schizophrenia and MetS had low serum glucose levels compared with individuals without mental disorders (p = 0.0001). An increase in the level of TG and the Atherogenic Index was found in patients with schizophrenia with MetS (p = 0.026 and p = 0.03, respectively), and the level of HDL was reduced (p = 0.022).Conclusion. The constitutional and morphological basis of MetS in patients with schizophrenia and persons without mental disorders is the same, however, changes in the fat constitution were determined for mentally healthy individuals. Changes in the lipid profile and glucose concentration may be associated with the presence of MetS-specific risk factors for patients with schizophrenia.

Emerging healthy lifestyle factors and all-cause mortality among people with metabolic syndrome and metabolic syndrome-like characteristics in NHANES

BackgroundThe impact of integrated lifestyles on health has attracted a lot of attention. It remains unclear whether adherence to low-risk healthy lifestyle factors is protective in individuals with metabolic syndrome and metabolic syndrome-like characteristics. We aimed to explore whether and to what extent overall lifestyle scores mitigate the risk of all-cause mortality in individuals with metabolic syndrome and metabolic syndrome-like characteristics.MethodsIn total, 6934 participants from the 2007 to 2014 National Health and Nutrition Examination Survey (NHANES) were included. The weighted healthy lifestyle score was constructed based on smoking, alcohol consumption, physical activity, diet, sleep duration, and sedentary behavior information. Generalized linear regression models and restricted cubic splines were used to analyze the association between healthy lifestyle scores and all-cause mortality. ​ResultsCompared to participants with relatively low healthy lifestyle scores, the risk ratio (RR) in the middle healthy lifestyle score group was 0.51 (RR = 0.51, 95% CI 0.30–0.88), and the high score group was 0.26 (RR = 0.26, 95% CI 0.15–0.48) in the population with metabolic syndrome. The difference in gender persists. In females, the RRs of the middle and high score groups were 0.47 (RR = 0.47, 95% CI 0.23–0.96) and 0.21 (RR = 0.21, 95% CI 0.09–0.46), respectively. In males, by contrast, the protective effect of a healthy lifestyle was more pronounced in the high score group (RR = 0.33, 95% CI 0.13–0.83) and in females, the protective effects were found to be more likely. The protective effect of a healthy lifestyle on mortality was more pronounced in those aged < 65 years. Higher lifestyle scores were associated with more prominent protective effects, regardless of the presence of one metabolic syndrome factor or a combination of several factors in 15 groups. What's more, the protective effect of an emerging healthy lifestyle was more pronounced than that of a conventional lifestyle.ConclusionsAdherence to an emerging healthy lifestyle can reduce the risk of all-cause mortality in people with metabolic syndrome and metabolic syndrome-like characteristics; the higher the score, the more obvious the protective effect. Our study highlights lifestyle modification as a highly effective nonpharmacological approach that deserves further generalization.