scholarly journals Chronic Inflammation in Obesity and the Metabolic Syndrome

2010 ◽  
Vol 2010 ◽  
pp. 1-10 ◽  
Author(s):  
Rosário Monteiro ◽  
Isabel Azevedo

The increasing incidence of obesity and the metabolic syndrome is disturbing. The activation of inflammatory pathways, used normally as host defence, reminds the seriousness of this condition. There is probably more than one cause for activation of inflammation. Apparently, metabolic overload evokes stress reactions, such as oxidative, inflammatory, organelle and cell hypertrophy, generating vicious cycles. Adipocyte hypertrophy, through physical reasons, facilitates cell rupture, what will evoke an inflammatory reaction. Inability of adipose tissue development to engulf incoming fat leads to deposition in other organs, mainly in the liver, with consequences on insulin resistance. The oxidative stress which accompanies feeding, particularly when there is excessive ingestion of fat and/or other macronutrients without concomitant ingestion of antioxidant-rich foods/beverages, may contribute to inflammation attributed to obesity. Moreover, data on the interaction of microbiota with food and obesity brought new hypothesis for the obesity/fat diet relationship with inflammation. Beyond these, other phenomena, for instance psychological and/or circadian rhythm disturbances, may likewise contribute to oxidative/inflammatory status. The difficulty in the management of obesity/metabolic syndrome is linked to their multifactorial nature where environmental, genetic and psychosocial factors interact through complex networks.

2020 ◽  
Author(s):  
Carine Teles Sangaleti ◽  
Keyla Yukari Katayama ◽  
Kátia De Angelis ◽  
Tércio Lemos de Moraes ◽  
Amanda Aparecida Araújo ◽  
...  

AbstractBackgroundThe metabolic syndrome (MetS) is an obesity-driven disorder with pandemic proportions and limited treatment options. Oxidative stress, low-grade inflammation and altered autonomic regulation, are important components of MetS pathophysiology. We recently reported that galantamine, an acetylcholinesterase inhibitor and an FDA-approved drug (for Alzheimer’s disease) alleviates the inflammatory state in MetS subjects. Here we examined the effects of galantamine on oxidative stress in parallel with inflammatory and cardio-metabolic parameters in subjects with MetS.MethodsThe effects of galantamine treatment, 8 mg daily for 4 weeks, followed by 16 mg daily for 8 weeks or placebo were studied in randomly assigned subjects with MetS (n=22 per group) of both genders. Oxidative stress, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase activities, lipid and protein peroxidation, and nitrite levels were analyzed before and at the end of the treatment. In addition, plasma cytokine and adipokine levels, insulin resistance (HOMA-IR) and other relevant cardio-metabolic indices were analyzed. Autonomic regulation was also examined by heart rate variability (HRV) before treatment, and at every 4 weeks of treatment.ResultsGalantamine treatment significantly increased antioxidant enzyme activities, including SOD (+1.65 USOD/mg protein, [95% CI 0.39 to 2.92], P=0.004) and CAT (+0.93 nmol/mg, [95% CI 0.34 to 1.51], P=0.011), decreased lipid peroxidation (thiobarbituric acid reactive substances, -5.45 pmol/mg, [95% CI -10.97 to 0.067], P=0.053) and systemic nitrite levels (-0.05 nit/mg protein, [95% CI -0.21 to 0.10], P=0.038) compared with placebo. In addition, galantamine significantly alleviated the inflammatory state and insulin resistance, and decreased the low frequency/high frequency ratio of HRV, following 8 and 12 weeks of drug treatment.ConclusionLow-dose galantamine alleviates oxidative stress, alongside beneficial anti-inflammatory, and metabolic effects, and modulates autonomic regulation in subjects with MetS. These findings are of considerable interest for further studies with galantamine to ameliorate MetS pathophysiology.


2013 ◽  
Vol 91 (1) ◽  
pp. 22-30 ◽  
Author(s):  
Sean Bryan ◽  
Boran Baregzay ◽  
Drew Spicer ◽  
Pawan K. Singal ◽  
Neelam Khaper

Metabolic syndrome (MetS) comprises interrelated disease states including obesity, insulin resistance and type 2 diabetes (T2DM), dyslipidemia, and hypertension. Essential to normal physiological function, and yet massively damaging in excess, oxidative stress and inflammation are pivotal common threads among the pathologies of MetS. Increasing evidence indicates that redox and inflammatory dysregulation parallels the syndrome's physiological, biochemical, and anthropometric features, leading many to consider the pro-oxidative, pro-inflammatory milieu an unofficial criterion in itself. Left unchecked, cross-promotion of oxidative stress and inflammation creates a feed-forward cycle that can initiate and advance disease progression. Such redox-inflammatory integration is evident in the pathogenesis of obesity, insulin resistance and T2DM, atherogenic dyslipidemia, and hypertension, and is thus hypothesized to be the “common soil” from which they develop. The present review highlights the synergistic contributions of redox-inflammatory processes to each of the components of the MetS.


2021 ◽  
Author(s):  
Gláucia Maria Senhorinha ◽  
Arlys Emanuel Mendes da Silva Santos ◽  
Douglas Daniel Dophine

Background: Metabolic syndrome (MS) leads to the deposits formation of insoluble protein aggregates, neuroinflammation, oxidative stress, neuronal insulin resistance, progressive insulin resistance, desensitization and β-amyloid amyloidosis in the brain, besides direct ischemic effects which are closely associated with Alzheimer’s disease (AD).1 Objectives: The present study seeks to understand the role of the metabolic syndrome in the pathophysiology of Alzheimer’s disease and to describe preventive and therapeutic interventions. Methods: PUBMED and Web of Science were the databases used, the following descriptors were used to search the articles: “Alzheimer Disease” OR “Alzheimer Dementia” AND “Metabolic Syndrome”. Results: The studies in general have shown that MS is related to AD through brain insulin resistance, triggered by oxidative stress and neuroinflammation. It is related to the progressive atrophy of brain regions involved in the progression of AD. Insulin resistance in the brain is related to the progressive atrophy of the brain regions from initial progression of AD. These regions are cingulate cortices, medial temporal lobe, prefrontal gyri and other regions.³ Thus, there is an inhibition of the mechanisms of beta-amyloid removal, leading to its accumulation, which generates neuroinflammation, that in turn potentiates insulin resistance in the central nervous system, contributing to the genesis and progression of cognitive damage.2,3 Conclusions: Insulin resistance plays a major role in the initiation and perpetuation of cognitive impairment in AD. Furthermore, the components of the MS associated with AD, when treated with preventive and therapeutic measures, break this association by promoting rebalancing of the metabolism.


2007 ◽  
Vol 293 (2) ◽  
pp. E500-E506 ◽  
Author(s):  
R. Scott Rector ◽  
Shana O. Warner ◽  
Ying Liu ◽  
Pamela S. Hinton ◽  
Grace Y. Sun ◽  
...  

Obesity and insulin resistance (IR) increase the risk for coronary heart disease; however, much of this risk is not attributable to traditional risk factors. We sought to determine whether weight loss associated with supervised aerobic exercise beneficially alters biomarkers of oxidative stress and whether these alterations are associated with improvements in measures of insulin resistance. Twenty-five sedentary and overweight to obese [body mass index (BMI) = 33.0 ± 0.8 kg/m2] individuals, with characteristics of the metabolic syndrome, participated in a 4- to 7-mo weight loss program that consisted of energy restriction (reduced by ∼500 kcal/day) and supervised aerobic exercise (5 days/wk, 45 min/day at 60% V̇o2 max; ∼375 kcal/day). IR and insulin sensitivity were assessed by the calculation of the homeostasis model assessment (HOMA) and quantitative insulin sensitivity check index (QUICKI), respectively. Oxidative stress was assessed by oxidized LDL (oxLDL), myeloperoxidase (MPO), and low- and high- density lipoprotein (LDL and HDL) lipid hydroperoxide concentrations in serum. Indexes for antioxidative status included apolipoprotein A1 (apoA1) concentrations and paraoxonase-1 (PON1) activity and protein concentrations. Exercise- and diet-induced weight loss (∼10%) significantly ( P < 0.05) increased insulin sensitivity and reduced IR, oxLDL, and LDL lipid hydroperoxides but did not alter HDL lipid hydroperoxides or MPO concentrations. Lifestyle modification impacted systemic antioxidative status by increasing apoA1 concentrations and reducing serum PON1 protein and activity. Changes in oxidative stress were not associated with alterations in HOMA or QUICKI. Diet- and exercise-induced weight loss (∼10%) improves measures of insulin sensitivity and beneficially alters biomarkers of oxidative status.


2013 ◽  
Vol 36 (1) ◽  
pp. 1 ◽  
Author(s):  
Eugenia Hopps ◽  
Gregorio Caimi

Purpose: Oxidative stress plays a pivotal role in the pathogenesis of the metabolic syndrome and in the progression of its complications. Carbonylated proteins are a stable marker of severe oxidative stress because damage to the protein structure is irreversible and may cause an inhibition of their enzymatic activity or an increased susceptibility to proteolysis. There are few data regarding protein oxidation in metabolic syndrome, although elevated levels of carbonyl groups are often detected in subjects with obesity, diabetes mellitus, hypertension or dyslipidemia, well-known components of the metaboic syndrome. In particular, obesity, insulin resistance and diabetes mellitus are frequently associated with increased protein carbonylation. A relationship between insulin resistance, protein oxidative stress and inflammation has also been suggested as well as protein oxidation products are correlated with overexpression of resistin, TNF-α and IL-6. Conclusion: Therapeutic interventions based on lifestyle modifications and pharmacological agents in order to correct all the main risk factors influence oxidative stress and protein carbonylation.


2011 ◽  
Vol 30 (2) ◽  
pp. 115-120 ◽  
Author(s):  
Nina Veigas ◽  
Mala Dharmalingam ◽  
Sara Marcus

Oxidative Stress in Obesity and Metabolic Syndrome in Asian IndiansOxidative stress is associated with the individual components of metabolic syndrome and has been implicated in the development of complications of these metabolic disorders. In this study oxidative stress levels have been compared in obese Indians (a high-risk population for diabetes and cardiovascular disorders) with and without metabolic syndrome. 30 adult normotensive, normoglycemic obese subjects and 35 adults with metabolic syndrome of either sex with BMI >23 kg/m2were compared with 30 adult, healthy volunteers with BMI <23 kg/m2. Anthropometric parameters, blood pressure, biochemical parameters, hydroperoxides levels and total antioxidant capacity were estimated. The obese groups with and without metabolic syndrome had significantly increased anthropometric parameters like waist circumference and index of central obesity and aqueous phase hydroperoxides when compared with normal controls. The metabolic syndrome group also had significantly increased blood sugar levels, lipid profile and hydroperoxide levels when compared to obese or control groups. There was no alteration in the total antioxidant capacity in any of the groups. The Triglyceride/HDL-Cholesterol ratio (>3), a surrogate marker of insulin resistance, indicates insulin resistance in the metabolic syndrome group. The anthropometric profile, insulin resistance and oxidative stress seen in obesity are further elaborated in metabolic syndrome. Thus, the early identification of high-risk individuals based on anthropometric parameters, lipid profile, insulin resistance and indices of oxidative stress may help to prevent the development of complications of metabolic syndrome.


2020 ◽  
Vol 5 (5) ◽  
pp. 324-331
Author(s):  
O. O. Hurenko ◽  
◽  
S. B. Drozdovska

Metabolic syndrome is a cluster of cardiometabolic risk factors. They include obesity, dyslipidemia, hypertension, and insulin resistance. Central obesity and resistance to insulin, in particular, are recognized as causative factors, which form the development of metabolic syndrome. Metabolic syndrome is a progressive and genetically determined condition. The result of its progression is that carbohydrate, lipid and purine metabolism break down. The intestinal microbiome has a significant role in the pathogenesis of metabolic syndrome. One of the methods of influencing the micribiotic composition is the physical activity. The human intestinal microbiome is a complex ecosystem consisting not only of microorganisms, but also including bacteria, archaea, fungi and viruses. Biodiversity and the overall composition of the microbiota play a crucial role in maintaining normal homeostasis in the human body. With the recent advent of the possibility of studying the intestinal microbiome, the impact on its taxonomic composition and metabolism through exercise is the subject of scientific interest. Recent studies showed that the intestinal microbiota was directly involved in the formation of the metabolic syndrome. The function of the microbiome is just as important as the function of the "metabolic organs" that affect energy homeostasis and control body weight. In addition, changes in the intestinal microbiotic composition lead to increased intestinal permeability, endotoxemia, which plays a role in the development of chronic inflammation in the host, contributing to the development of metabolic syndrome and related chronic metabolic diseases. Intestinal microbiota in its own right is injected into the development of systemic inflammation in obesity, such a rank, inappropriate insertions in development or regression of insulin resistance, and hyperglycemia in metabolic syndrome. Physical activity can affect not only the composition of the microbial composition, but also the metabolic activity of the intestinal microbiome. The health-improving effect of physical exercises is connected with their ability to change the composition of an intestinal microbiota. Studies involving professional athletes and a specially selected control group indicated that athletes had a lower pro-inflammatory status and a high degree of bacterial diversity. Due to this, there is a positive dynamics of improving carbohydrate metabolism and the impact on the course of pathological processes associated with the metabolic syndrome, through the introduction of regular physical activity. Conclusion. The literature review presents data on the metabolic syndrome, its pathogenesis and components of the spectrum of development of metabolic disorders. We also analyzed material on influence of gut microbiota on development of metabolic disturbances and inreraction of structure of a microbiotic composition with physical exercises


Antioxidants ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 79
Author(s):  
Grzegorz K. Jakubiak ◽  
Kamila Osadnik ◽  
Mateusz Lejawa ◽  
Tadeusz Osadnik ◽  
Marcin Goławski ◽  
...  

Metabolic syndrome (MS) is not a homogeneous entity, but this term refers to the coexistence of factors that increase the risk for the development of type 2 diabetes and cardiovascular disease. There are different versions of the criteria for the diagnosis of MS, which makes the population of patients diagnosed with MS heterogeneous. Research to date shows that MS is associated with oxidative stress (OS), but it is unclear which MS component is most strongly associated with OS. The purpose of the study was to investigate the relationship between the parameters of OS and the presence of individual elements of MS in young adults, as well as to identify the components of MS by means of principal components analysis (PCA) and to investigate how the parameters of OS correlate with the presence of individual components. The study included 724 young adults with or without a family history of coronary heart disease (population of the MAGNETIC study). Blood samples were taken from the participants of the study to determine peripheral blood counts, biochemical parameters, and selected parameters of OS. In addition, blood pressure and anthropometric parameters were measured. In subjects with MS, significantly lower activity of superoxide dismutase (SOD), copper- and zinc-containing SOD (CuZnSOD), and manganese-containing SOD (MnSOD) were found, along with significantly higher total antioxidant capacity (TAC) and significantly lower concentration of thiol groups per gram of protein (PSH). We identified three components of MS by means of PCA: “Obesity and insulin resistance”, “Dyslipidemia”, and “Blood pressure”, and showed the component “Obesity and insulin resistance” to have the strongest relationship with OS. In conclusion, we documented significant differences in some parameters of OS between young adults with and without MS. We showed that “Obesity and insulin resistance” is the most important component of MS in terms of relationship with OS.


Author(s):  
Oksana N. Belousova ◽  
Marina V. Chupakha

Metabolic syndrome currently remains one of the most pressing problems in medicine, since it makes its decisive contribution to the development of cardiovascular diseases and cerebral complications. Another important problem of modern medicine is arterial hypertension, which is one of the constituent criteria of metabolic syndrome, whose mechanism of development is due to a disruption in the work of the renin-angiotensin-aldosterone system, the sympathoadrenal system, an increased content of pro-inflammatory cytokines, as well as an imbalance in the adipokine system. Adipose tissue now acts not just as a structure that provides our body with energy only, but now it acts as an organ of the endocrine system, producing a large number of metabolically active substances. Patients with metabolic syndrome have been found to have elevated levels of proinflammatory cytokines were increased: monocytic chemotactic protein-1 (MCP-1), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). These cytokines are thought to be synthesised by adipose tissue macrophages and are involved in the pathogenesis of the metabolic syndrome. Oxidative stress can induce insulin resistance in adipocytes. The pathogenesis of oxidative stress in adipocytes in MS is still a mystery. This knowledge would be very useful in developing new approaches to MS therapy. Given the significant effect of chemokines in MS on the development of systemic inflammation, insulin resistance, and arterial hypertension, scientists have an important task not only to describe the actions of individual chemokines in hypertension, but also to characterize how the effect on one chemokine modulates the expression and/or function of other chemokines and their related receptors.


2021 ◽  
Vol 12 ◽  
Author(s):  
Carine Teles Sangaleti ◽  
Keyla Yukari Katayama ◽  
Kátia De Angelis ◽  
Tércio Lemos de Moraes ◽  
Amanda Aparecida Araújo ◽  
...  

Background: The metabolic syndrome (MetS) is an obesity-associated disorder of pandemic proportions and limited treatment options. Oxidative stress, low-grade inflammation and altered neural autonomic regulation, are important components and drivers of pathogenesis. Galantamine, an acetylcholinesterase inhibitor and a cholinergic drug that is clinically-approved (for Alzheimer's disease) has been implicated in neural cholinergic regulation of inflammation in several conditions characterized with immune and metabolic derangements. Here we examined the effects of galantamine on oxidative stress in parallel with inflammatory and cardio-metabolic parameters in subjects with MetS.Trial Design and Methods: The effects of galantamine treatment, 8 mg daily for 4 weeks or placebo, followed by 16 mg daily for 8 weeks or placebo were studied in randomly assigned subjects with MetS (n = 22 per group) of both genders. Oxidative stress, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase activities, lipid and protein peroxidation, and nitrite levels were analyzed before and at the end of the treatment. In addition, plasma cytokine and adipokine levels, insulin resistance (HOMA-IR) and other relevant cardio-metabolic indices were analyzed. Autonomic regulation was also examined by heart rate variability (HRV) before treatment, and at every 4 weeks of treatment.Results: Galantamine treatment significantly increased antioxidant enzyme activities, including SOD [+1.65 USOD/mg protein, [95% CI 0.39–2.92], P = 0.004] and CAT [+0.93 nmol/mg, [95% CI 0.34–1.51], P = 0.01], decreased lipid peroxidation [thiobarbituric acid reactive substances [log scale 0.72 pmol/mg, [95% CI 0.46–1.07], P = 0.05], and systemic nitrite levels [log scale 0.83 μmol/mg protein, [95% CI 0.57–1.20], P = 0.04] compared with placebo. In addition, galantamine significantly alleviated the inflammatory state and insulin resistance, and decreased the low frequency/high frequency ratio of HRV, following 8 and 12 weeks of drug treatment.Conclusion: Low-dose galantamine alleviates oxidative stress, alongside beneficial anti-inflammatory, and metabolic effects, and modulates neural autonomic regulation in subjects with MetS. These findings are of considerable interest for further studies with the cholinergic drug galantamine to ameliorate MetS.


Sign in / Sign up

Export Citation Format

Share Document