Genetics of The Metabolic Syndrome: A Future Research Opportunities

2020 ◽  
Vol 12 (02) ◽  
Keyword(s):  
Metabolic Syndrome ◽  
Future Research ◽  
Research Opportunities ◽  
The Metabolic Syndrome

Complement Components, C3 and C4, and the Metabolic Syndrome

2018 ◽  
Vol 15 (1) ◽  
pp. 44-48 ◽  
Author(s):  
Melanie Copenhaver ◽  
Chack-Yung Yu ◽  
Robert P. Hoffman
Keyword(s):  
Metabolic Syndrome ◽  
Significant Role ◽  
Complement System ◽  
Gene Copy ◽  
Future Research ◽  
Obese Adults ◽  
Complement Components ◽  
Cardiometabolic Diseases ◽  
The Metabolic Syndrome ◽  
The Complement System

Introduction: Increased systemic inflammation plays a significant role in the development of adult cardiometabolic diseases such as insulin resistance, dyslipidemia, atherosclerosis, and hypertension. The complement system is a part of the innate immune system and plays a key role in the regulation of inflammation. Of particular importance is the activation of complement components C3 and C4. C3 is produced primarily by the liver but is also produced in adipocytes, macrophages and endothelial cells, all of which are present in adipose tissues. Dietary fat and chylomicrons stimulate C3 production. Adipocytes in addition to producing C3 also have receptors for activated C3 and other complement components and thus also respond to as well as produce a target for complement. C3adesArg, also known as acylation stimulation factor, increases adipocyte triglyceride synthesis and release. These physiological effects play a significant role in the development of metabolic syndrome. Epidemiologically, obese adults and non-obese adults with cardiometabolic disease who are not obese have been shown to have increased complement levels. C4 levels also correlate with body mass index. Genetically, specific C3 polymorphisms have been shown to predict future cardiovascular events and. D decreased C4 long gene copy number is associated with increased longevity. Conclusion: Future research is clearly needed to clarify the role of complement in the development of cardiovascular disease and mechanisms for its action. The complement system may provide a new area for intervention in the prevention of cardiometabolic diseases.

Anti-Inflammatory Effects of Exercise on Metabolic Syndrome Patients: A Systematic Review and Meta-Analysis

2020 ◽  
pp. 109980042095806 ◽  
Author(s):  
Heidar Alizaei Yousefabadi ◽  
Arghavan Niyazi ◽  
Sahar Alaee ◽  
Mehrdad Fathi ◽  
Gholam Rasul Mohammad Rahimi
Keyword(s):  
Metabolic Syndrome ◽  
Exercise Training ◽  
Inflammatory Markers ◽  
Meta Analysis ◽  
Serum Levels ◽  
Future Research ◽  
The Metabolic Syndrome ◽  
Inflammatory Status ◽  
Tnf Α ◽  
Training Impact

Background: Increments in inflammatory indicators and low levels of physical activity are correlated to the expansion of the metabolic syndrome (MetS). Objective: The purpose of this study was to establish if exercise training ameliorates inflammatory status in MetS patients. Data sources: PubMed, CINAHL, and Medline, Google Scholar, and Scopus databases and reference lists of included studies were searched. Study selection: Twenty randomized controlled trials (RCTs) of exercise-training impact on inflammatory markers (tumor necrosis factor (TNF) α, C-reactive protein (CRP), interleukin (IL) 6, IL-8, IL-10, and IL-18) with concurrent control groups were included in this analysis. Results: Results demonstrated an overall significant decrease in serum levels of TNF-α (mean difference (MD): −1.21 pg/ml; 95% confidence interval (CI): −1.77, −0.66), CRP (MD: −0.52 mg/l; 95% CI: −0.79, −0.25), IL-8 (MD: −1.31 pg/ml; 95% CI: −2.57, −0.06), and a significant increase in IL-10 (MD: 0.48 pg/ml; 95% CI: 0.10, 0.86). But exercise training did not change the level of IL-6 (MD: −0.69 pg/ml; 95% CI: −1.53, 0.14) and IL-18 (MD: −53.01 pg/ml; 95% CI: −166.64, 60.62). Conclusion: Exercise training improves TNF-α, CRP, IL-8, and IL-10 levels in patients with MetS. For some variables, isolated aerobic exercise, and combined aerobic and resistance exercise appears to be optimal. Future research is needed to clarify the mechanisms underlying exercise training’s effect on this population’s inflammatory markers. More studies are required to confirm these findings.

Pre- and early postnatal nongenetic determinants of type 2 diabetes

2002 ◽  
Vol 4 (24) ◽  
pp. 1-14 ◽  
Author(s):  
Susan E. Ozanne ◽  
C. Nick Hales
Keyword(s):  
Gene Expression ◽  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Hormone Receptors ◽  
Early Growth ◽  
Growth Restriction ◽  
Future Research ◽  
Thrifty Phenotype ◽  
The Metabolic Syndrome

Epidemiological studies have revealed strong and internationally reproducible links between early growth restriction and subsequent risk of developing type 2 diabetes and the metabolic syndrome (glucose intolerance, hypertension and hypertriglyceridaemia). This effect can exist independently of genetic factors. There is also direct evidence that poor maternal nutrition and maternal smoking cause both a reduction in birthweight and subsequent loss of glucose tolerance. High rates of growth in childhood may add to these effects. The ‘thrifty phenotype’ hypothesis attempts to explain these associations in terms of an altered programming of growth and metabolism that aids survival both pre- and postnatally. Type 2 diabetes is envisaged as a consequence of a clash of this programming with adult obesity. Tests of this hypothesis in animal models have shown that both the metabolic syndrome and type 2 diabetes can result from early growth restriction in rats consequent upon rat dams being fed a reduced protein, isocaloric diet (in which the protein is replaced by an equal quantity of nonprotein energy). A variety of other models of early growth restriction in rats lead to a similar phenotype. Several structural and gene expression changes have been shown in many tissues, including pancreas, liver, kidney, muscle and adipose tissue. Changes in gene expression include those concerned with hormone receptors, signalling and glycolytic enzymes. Many important questions remain for future research.

scholarly journals The prevalence of pediatric metabolic syndrome—a critical look on the discrepancies between definitions and its clinical importance

2020 ◽  
Vol 45 (1) ◽  
pp. 12-24
Author(s):  
Carolin Reisinger ◽  
Benedicta N. Nkeh-Chungag ◽  
Per Morten Fredriksen ◽  
Nandu Goswami
Keyword(s):  
Risk Factors ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Abdominal Obesity ◽  
International Diabetes Federation ◽  
Clinical Importance ◽  
High Density Lipoproteins ◽  
Future Research ◽  
The Metabolic Syndrome ◽  
Definition Of

Abstract Introduction The Metabolic Syndrome (MetS) describes the clustering of cardio-metabolic risk factors—including abdominal obesity, insulin resistance, elevated blood pressure, high levels of triglycerides, and low levels of high-density lipoproteins—that increase the risk for developing cardiovascular diseases and type 2 diabetes mellitus. However, a generally accepted definition of MetS in pediatric patients is still lacking. Objectives The aim was to summarize current prevalence data of childhood MetS as well as to discuss the continuing disagreement between different pediatric definitions and the clinical importance of such diagnosis. Methodology A systematic literature search on the prevalence of pediatric MetS was conducted. Articles that were published during the past 5 years (2014–2019), using at least one of four predetermined classifications (International Diabetes Federation, Cook et al., Ford et al., and de Ferranti et al.), were included. Results The search resulted in 1167 articles, of which 31 publications met all inclusion criteria. Discussion The prevalence of MetS ranged between 0.3 and 26.4%, whereby the rising number of children and adolescents with MetS partly depended on the definition used. The IDF definition generally provided the lowest prevalences (0.3–9.5%), whereas the classification of de Ferranti et al. yielded the highest (4.0–26.4%). In order to develop a more valid definition, further research on long-term consequences of childhood risk factors such as abdominal obesity, insulin resistance, hypertension, and dyslipidemia is needed. There is also a temptation to suggest one valid, globally accepted definition of metabolic syndrome for pediatric populations but we believe that it is more appropriate to suggest definitions of MetS that are specific to males vs. females, as well as being specific to race/ethnicity or geographic region. Finally, while this notion of definitions of MetS specific to certain subgroups is important, it still needs to be tested in future research.

scholarly journals A Focused Review of the Metabolic Side-Effects of Clozapine

2021 ◽  
Vol 12 ◽  
Author(s):  
Jessica W. Y. Yuen ◽  
David D. Kim ◽  
Ric M. Procyshyn ◽  
William J. Panenka ◽  
William G. Honer ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Side Effects ◽  
Plasma Lipids ◽  
Treatment Options ◽  
Metabolic Effects ◽  
Future Research ◽  
Metabolic Dysregulation ◽  
The Metabolic Syndrome ◽  
Metabolic Side Effects ◽  
Biological Substrates

The second generation antipsychotic drug clozapine represents the most effective pharmacotherapy for treatment-resistant psychosis. It is also associated with low rates of extrapyramidal symptoms and hyperprolactinemia compared to other antipsychotic drugs. However, clozapine tends to be underutilized in clinical practice due to a number of disabling and serious side-effects. These are characterized by a constellation of metabolic side-effects which include dysregulation of glucose, insulin, plasma lipids and body fat. Many patients treated with clozapine go on to develop metabolic syndrome at a higher rate than the general population, which predisposes them for Type 2 diabetes mellitus and cardiovascular disease. Treatments for the metabolic side-effects of clozapine vary in their efficacy. There is also a lack of knowledge about the underlying physiology of how clozapine exerts its metabolic effects in humans. In the current review, we focus on key studies which describe how clozapine affects each of the main symptoms of the metabolic syndrome, and cover some of the treatment options. The clinical data are then discussed in the context of preclinical studies that have been conducted to identify the key biological substrates involved, in order to provide a better integrated overview. Suggestions are provided about key areas for future research to better understand how clozapine causes metabolic dysregulation.

Risk factors related to cardiovascular diseases and the metabolic syndrome in multiple sclerosis – a systematic review

2013 ◽  
Vol 19 (12) ◽  
pp. 1556-1564 ◽  
Author(s):  
Inez Wens ◽  
Ulrik Dalgas ◽  
Egon Stenager ◽  
Bert O Eijnde
Keyword(s):  
Risk Factors ◽  
Multiple Sclerosis ◽  
Systematic Review ◽  
Metabolic Syndrome ◽  
Type Ii Diabetes ◽  
Epidemiological Studies ◽  
Future Research ◽  
Cvd Risk ◽  
The Metabolic Syndrome ◽  
Increased Risk

Despite many epidemiological studies examining comorbidity in people with multiple sclerosis (pMS), there are conflicting opinions on whether pMS are at more or less risk of cardiovascular disease (CVD) and the metabolic syndrome compared with the general population. As pMS can now expect longer survival, this as an important question both at an individual and public health level. This study aimed to systematically review the literature linking MS to CVD risks and to the risk factors constituting the metabolic syndrome. This systematic review is based on a comprehensive literature search of six databases (Swemed+, Pubmed, Embase, Cochrane, PEDro and CINAHL). In total 34 studies were identified. Despite the high number of identified papers, only limited and inconsistent data exist on the risk factors of the metabolic syndrome and MS. Overall, the data suggest an increased CVD risk in pMS. From the existing studies it is not clear whether the increased risk of CVD is related to an increased risk of obesity or changes in body composition, hypertension, dyslipidemia or type II diabetes in pMS, indicating the need for future research in the field, if we are to advise pMS adequately in avoiding preventable comorbidity.

scholarly journals Advances in diet-induced rodent models of metabolically acquired peripheral neuropathy

2021 ◽  
Vol 14 (11) ◽  
Author(s):  
Stéphanie A. Eid ◽  
Eva L. Feldman
Keyword(s):  
Metabolic Syndrome ◽  
Neuropathic Pain ◽  
Peripheral Neuropathy ◽  
Dietary Fat ◽  
Future Research ◽  
Rodent Models ◽  
Diet Induced Obesity ◽  
The Metabolic Syndrome ◽  
Type 2 Diabetic

ABSTRACT Peripheral neuropathy (PN) is a severe complication that affects over 30% of prediabetic and 60% of type 2 diabetic (T2D) patients. The metabolic syndrome is increasingly recognized as a major driver of PN. However, basic and translational research is needed to understand the mechanisms that contribute to nerve damage. Rodent models of diet-induced obesity, prediabetes, T2D and PN closely resemble the human disease and have proven to be instrumental for the study of PN mechanisms. In this Perspective article, we focus on the development, neurological characterization and dietary fat considerations of diet-induced rodent models of PN. We highlight the importance of investigating sex differences and discuss some of the challenges in translation from bench to bedside, including recapitulating the progressive nature of human PN and modeling neuropathic pain. We emphasize that future research should overcome these challenges in the quest to better mimic human PN in animal models.

Sign in / Sign up

Export Citation Format

Share Document