Physical Activity and Inflammation Phenotype Conversion

ABSTRACT Inflammation is a protective response to infection or injury; however, persistent microtraumas at the tissue level may result in chronic low-grade inflammation that plays both direct and indirect roles in the development of many diseases and aging. The purpose of this review is to describe the underlying physiology of low-grade inflammation and highlight potential inflammation lowering effects of physical activity (PA). Unique contributions of this review are to introduce the concept of inflammation phenotype flexibility in contrast to the low-grade inflammation state and describe how PA influences inflammation phenotype by altering muscle, gut, adipose, and postprandial metabolism. Pro-inflammatory M1 macrophages and cytokines—such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6—contribute to low-grade inflammation. Among the mechanisms that commonly contribute to low-grade inflammation are dysfunctional adipose tissue, a leaky gut, gut microbiota that promotes inflammation, and large postprandial glycemic and lipidemic responses. Physical activity may lower inflammation by decreasing M1 macrophages in visceral adipose tissue, decreasing adipose tissue volume, production of anti-inflammatory myokines, promotion of butyrate-producing members of the gut microbiota, improved gut barrier function, and lowering of postprandial glycemic and lipidemic responses. While exercise has many anti-inflammatory mechanisms, phenotype conversion is complex, multifaceted, and difficult to achieve. Our understanding of how PA influences inflammation must include acute exercise-induced anti-inflammatory effects, contribution to the inflammation state from multiple sources in the body, and phenotypic shifts underpinning low-grade inflammation.

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Dietary Fiber's Effect on High Sensitivity C-reactive Protein Serum in Sedentary Workers

World Nutrition Journal ◽

10.25220/wnj.v05.i1.0006 ◽

2021 ◽

Vol 5 (1) ◽

pp. 40

Author(s):

Livia Kurniati Saputra ◽

Dian Novita Chandra ◽

Ninik Mudjihartini

Keyword(s):

Body Weight ◽

High Sensitivity ◽

The Body ◽

Low Grade ◽

C Reactive Protein ◽

Reactive Protein ◽

Dietary Fiber Intake ◽

Anti Inflammatory ◽

Low Grade Inflammation ◽

Inflammatory Effect

Low grade inflammation has been recognized of being involved in the pathogenesis of chronic disease pandemic. Individual lifestyle plays a major role in the development of low grade inflammation. Sedentary workers are at risk of low grade inflammation due to the nature of their work. Dietary habit also contributes to inflammatory status in the body. Dietary fiber intake indirectly affects the immune system. It has been hypothesized that fiber has anti-inflammatory effects, both body weight-related and body weight-unrelated This review will focus more on body weight-unrelated anti-inflammatory effect of fiber, especially through fiber’s fermentation metabolites, the short chain fatty acid (SCFA). Its anti-inflammatory effect can be seen by monitoring a biomarker of inflammation in the body, the high sensitivity C-reactive protein (hsCRP). This review’s objective is to cover the mechanisms and role of dietary fiber intake on serum hsCRP level as a marker of low grade inflammation on sedentary workers.

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Amelioration of metabolic syndrome by metformin associates with reduced indices of low-grade inflammation independently of the gut microbiota

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00245.2019 ◽

2019 ◽

Vol 317 (6) ◽

pp. E1121-E1130 ◽

Cited By ~ 8

Author(s):

Aneseh Adeshirlarijaney ◽

Jun Zou ◽

Hao Q. Tran ◽

Benoit Chassaing ◽

Andrew T. Gewirtz

Keyword(s):

Metabolic Syndrome ◽

Gut Microbiota ◽

Early Stage ◽

Mechanisms Of Action ◽

Low Grade ◽

Inflammatory Agent ◽

Frontline Treatment ◽

Anti Inflammatory ◽

Low Grade Inflammation

Metformin beneficially impacts several aspects of metabolic syndrome including dysglycemia, obesity, and liver dysfunction, thus making it a widely used frontline treatment for early-stage type 2 diabetes, which is associated with these disorders. Several mechanisms of action for metformin have been proposed, including that it acts as an anti-inflammatory agent, possibly as a result of its impact on intestinal microbiota. In accord with this possibility, we observed herein that, in mice with diet-induced metabolic syndrome, metformin impacts the gut microbiota by preventing its encroachment upon the host, a feature of metabolic syndrome in mice and humans. However, the ability of metformin to beneficially impact metabolic syndrome in mice was not markedly altered by reduction or elimination of gut microbiota, achieved by the use of antibiotics or germfree mice. Although reducing or eliminating microbiota by itself suppressed diet-induced dysglycemia, other features of metabolic syndrome including obesity, hepatic steatosis, and low-grade inflammation remained suppressed by metformin in the presence or absence of gut microbiota. These results support a role for anti-inflammatory activity of metformin, irrespective of gut microbiota, in driving some of the beneficial impacts of this drug on metabolic syndrome.

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Rice Bran Oil Attenuates Chronic Inflammation by Inducing M2 Macrophage Switching in High-Fat Diet-Fed Obese Mice

Foods ◽

10.3390/foods10020359 ◽

2021 ◽

Vol 10 (2) ◽

pp. 359

Author(s):

Hyejeong Park ◽

Seungmin Yu ◽

Wooki Kim

Keyword(s):

Adipose Tissue ◽

Rice Bran ◽

Rice Bran Oil ◽

Macrophage Polarization ◽

M2 Macrophage ◽

Low Grade ◽

Obese Mice ◽

Anti Inflammatory ◽

Low Grade Inflammation ◽

Inflammatory Effect

Macrophages are involved in all inflammatory processes from killing pathogens to repairing damaged tissue. In the obese state, macrophages infiltrate into enlarged adipose tissue and polarize into pro-inflammatory M1 macrophages, resulting in chronic low-grade inflammation due to the secretion of inflammatory mediators. Rice bran oil (RBO) is an edible oil containing tocopherols, tocotrienols, and γ-oryzanol. Previous research in normal diet-fed mice suggested that RBO mitigates inflammatory responses by modulating mitochondrial respiration of macrophages. Therefore, we investigated if RBO had an anti-inflammatory effect in diet-induced obese mice by assessing the expression of inflammatory markers in epididymal white adipose tissue (eWAT) and polarization of bone marrow-derived macrophages (BMDMs). Rice bran oil exerted a local anti-inflammatory effect in white adipose tissue by suppressing the production of inflammatory mediators and upregulating transcription of anti-inflammatory genes. Rice bran oil also promoted anti-inflammatory M2 macrophage polarization in BMDMs thereby affecting systemic inflammation. Overall, our in vivo and ex vivo results highlight the potential of RBO as a dietary mediator that can ameliorate obesity-induced chronic low-grade inflammation by mediating the expression of inflammation-related factors and macrophage polarization.

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Physical activity, exercise and low-grade systemic inflammation

Proceedings of The Nutrition Society ◽

10.1017/s0029665110001928 ◽

2010 ◽

Vol 69 (3) ◽

pp. 400-406 ◽

Cited By ~ 43

Author(s):

Julia Wärnberg ◽

Karen Cunningham ◽

Javier Romeo ◽

Ascension Marcos

Keyword(s):

Physical Activity ◽

Type Ii Diabetes ◽

The Body ◽

Low Grade ◽

Type Ii ◽

Active Lifestyle ◽

Physically Active ◽

Inflammatory State ◽

Physical Activity And Exercise ◽

Low Grade Inflammation

Prospective studies have shown that chronic low-grade inflammation may contribute to the pathogenesis of the most common chronic diseases and in particular CVD. Obesity has repeatedly been associated with moderately raised levels of inflammation, and this observation has led to the view that obesity is characterised by a state of chronic low-grade inflammation. There is now great interest in elucidating how physical activity and exercise modulate inflammation. This review summarises the current research addressing the influence of physical activity and exercise in mitigating the risks of obesity and diseases such as type-II diabetes and CVD, through its action on the low-grade inflammatory state. Most research on this topic hypothesised that the association between physical activity and inflammatory markers is independent of fatness, but very few studies have proven this. Given that physical activity and obesity are often inversely related, it is not clear as to whether the anti-inflammatory health benefits of a physically active lifestyle are due to exercise per se or result from favourable changes in the body composition.

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Metabolic endotoxemia: possible causes and consequences

Obesity and metabolism ◽

10.14341/omet12750 ◽

2021 ◽

Vol 18 (3) ◽

pp. 320-326

Author(s):

V. A. Beloglazov ◽

I. A. Yatskov ◽

E. D. Kumelsky ◽

V. V. Polovinkina

Keyword(s):

Adipose Tissue ◽

Defense Mechanisms ◽

Mutual Influence ◽

Immune Defense ◽

The Body ◽

Low Grade ◽

Endocrine Organ ◽

Depth Study ◽

Low Grade Inflammation ◽

The Relationship

This review article presents data from the literature, which provide an idea of the relationship between metabolic disorders occurring against the background of obesity and endotoxinemia, as well as the effect of these conditions on the maintenance of low-grade inflammation in the body. A description of the hormonal and immune restructuring of white adipose tissue, the main routes of entry and metabolism of endotoxin is given. Particular attention is paid to the mechanisms of the mutual influence of obesity and endotoxinemia. Described by Yakovlev M.Yu. in 1988 «endotoxin aggression» and Cani P.D. et al. in 2007, «metabolic endotoxinemia», in our opinion, is one of the most important triggers for the development and progression of a whole spectrum of acute and chronic diseases. Based on the data of recent years, adipose tissue is an active endocrine organ capable of influencing both metabolic processes and the state of innate and acquired immune defense mechanisms. It has now been proven that high-calorie diets lead not only to an increase in overweight, but also to an increase in the level of endotoxin circulating in the blood. An in-depth study of the ability of obesity and endotoxinemia to potentiate the mutual pro-inflammatory effect can help both in understanding the pathogenesis of the main cardiovascular, autoimmune, allergic and infectious (including viral) diseases, and in the development of methods for non-pharmacological and drug correction of these conditions.

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Getting the message across: mechanisms of physiological cross talk by adipose tissue

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00015.2009 ◽

2009 ◽

Vol 296 (6) ◽

pp. E1210-E1229 ◽

Cited By ~ 90

Author(s):

Do-Eun Lee ◽

Sylvia Kehlenbrink ◽

Hanna Lee ◽

Meredith Hawkins ◽

John S. Yudkin

Keyword(s):

Adipose Tissue ◽

Cross Talk ◽

Energy Homeostasis ◽

Cellular Level ◽

The Body ◽

Low Grade ◽

Storage Site ◽

Integrative Physiology ◽

Energy Excess ◽

Low Grade Inflammation

Obesity is associated with resistance of skeletal muscle to insulin-mediated glucose uptake, as well as resistance of different organs and tissues to other metabolic and vascular actions of insulin. In addition, the body is exquisitely sensitive to nutrient imbalance, with energy excess or a high-fat diet rapidly increasing insulin resistance, even before noticeable changes occur in fat mass. There is a growing acceptance of the fact that, as well as acting as a storage site for surplus energy, adipose tissue is an important source of signals relevant to, inter alia, energy homeostasis, fertility, and bone turnover. It has also been widely recognized that obesity is a state of low-grade inflammation, with adipose tissue generating substantial quantities of proinflammatory molecules. At a cellular level, the understanding of the signaling pathways responsible for such alterations has been intensively investigated. What is less clear, however, is how alterations of physiology, and of signaling, within one cell or one tissue are communicated to other parts of the body. The concepts of cell signals being disseminated systemically through a circulating “endocrine” signal have been complemented by the view that local signaling may similarly occur through autocrine or paracrine mechanisms. Yet, while much elegant work has focused on the alterations in signaling that are found in obesity or energy excess, there has been less attention paid to ways in which such signals may propagate to remote organs. This review of the integrative physiology of obesity critically appraises the data and outlines a series of hypotheses as to how interorgan cross talk takes place. The hypotheses presented include the “fatty acid hypothesis,”, the “portal hypothesis,”, the “endocrine hypothesis,”, the “inflammatory hypothesis,”, the “overflow hypothesis,”, a novel “vasocrine hypothesis,” and a “neural hypothesis,” and the strengths and weaknesses of each hypothesis are discussed.

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P2251Association between low-grade inflammation, metabolic factors, vascular biomarkers and gut microbiota in different age groups

European Heart Journal ◽

10.1093/eurheartj/ehz748.0729 ◽

2019 ◽

Vol 40 (Supplement_1) ◽

Author(s):

D Kashtanova ◽

O N Tkacheva ◽

Y U V Kotovskaya ◽

E N Dudinskaya ◽

N V Brailova ◽

...

Keyword(s):

Risk Factors ◽

Carotid Artery ◽

Gut Microbiota ◽

Laboratory Evaluation ◽

Metabolic Reconstruction ◽

Low Grade ◽

Metabolic Factors ◽

Wide Range ◽

Anti Inflammatory ◽

Low Grade Inflammation

Abstract Background Despite the growing interest to the theme, the gut microbiota (GM) composition and functional capacity in relation to cardiovascular diseases (CVD) have been poorly studied. It is not well studied in nonagenarians or centenarians who live much longer than others with postponed CVD. In this study, we assessed GM in association with different metabolic factors in healthy middle-aged adults and the elderly at the turn of a hundred years old. Purpose Our aim was to study GM in a healthy cohort (HC) with different metabolic risk factors and in an extremely elderly cohort (EC) of long livers from our city. Methods The study included HC of 104 untreated subjects aged from 25–76y (52±13) carefully selected through the exclusion of CVD and other chronic diseases by means of clinical (with different specialists consultations to exclude any factors of inflammation) and a wide range of laboratory evaluation, ECG, treadmill test, ECHOCG, carotid artery ultrasound and the second group of 20 long livers 97–100y (98±1). EC underwent a complex geriatric assessment, also a wide range of laboratory evaluation, ECG, ECHOCG, carotid artery ultrasound. GM composition was studied by the V3-V4 16S rRNA sequencing. Taxonomic units were identified with QIIME 1.9.1. Statistical analysis was done by using the Phyton v.3.2 programming language. Metabolic reconstruction was performed with PICRUSt algorithm. All GM analyzes performed with age, sex and FDR adjustments. Results One of the most pronounced differences in GM between groups was a significantly higher representation of antiinflammatory Bifidobacterium genus in long livers (p=0.026 (MaAsLin), LDA=4.304). Among risk factors, high body mass index (BMI) was associated with a high abundance of conditional pathogens of Prevotella genus in HC (p<0.002, GLM) and also in EC (p=0.013, MaAsLin). BMI was correlated with hs-CRP level in EC (p=0.04, rs = 0.634). Median hsCRP in EC was 2.4mg/l (Q3–Q1=5.58), 2.45mg/l (Q3–Q1=2.03) (no significant differences, U-test). Despite this, we found that microbiota of long livers had much higher potential to produce butyrate (anti-inflammatory agent, p=0.016 (MaAsLin), LDA=3.345, PICRUSt algorithm). Average intima-media thickness (IMT) in EC was 1.07±0.16mm, and 0.76±0.2mm in HC, the difference was not significant (p=0.37, t-test). We found the association between the IMT with Serratia (gram negative conditional pathogens) abundance (p=0.009) in HC but not in EC. Butyrate synthesis potential in EC vs HC Conclusions The EC were unexpectedly healthy. Considering the GM analysis, we may propose that EC microbiota protected long livers from the low-grade inflammation and thus protected them from the development of metabolic disorders by producing a high amount of butyrate, one of the most important anti-inflammatory agents in the human body. Conditional pathogens (the inflammation initiators) associated with BMI and IMT as well as butyrate producers may subsequently become a target for cardiovascular prevention. Acknowledgement/Funding Governmental support

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Gut microbiome, endocrine control of gut barrier function and metabolic diseases

Journal of Endocrinology ◽

10.1530/joe-20-0473 ◽

2020 ◽

Author(s):

Marion Régnier ◽

Matthias Van Hul ◽

Claude Knauf ◽

Patrice D Cani

Keyword(s):

Gut Microbiota ◽

Barrier Function ◽

Metabolic Diseases ◽

Overweight And Obesity ◽

Low Grade ◽

Gut Barrier ◽

Endocrine Control ◽

Gut Barrier Function ◽

Cardiometabolic Disorders ◽

Low Grade Inflammation

Overweight and obesity are associated with several cardiometabolic risk factors, including insulin resistance, type 2 diabetes, low-grade inflammation and liver diseases. The gut microbiota is a potential contributing factor regulating energy balance. However, although the scientific community acknowledges that the gut microbiota composition and its activity (e.g., production of metabolites and immune-related compounds) are different between healthy subjects and subjects with overweight/obesity, the causality remains insufficiently demonstrated. The development of low-grade inflammation and related metabolic disorders has been connected with metabolic endotoxaemia and increased gut permeability. However, the mechanisms acting on the regulation of the gut barrier and eventually cardiometabolic disorders are not fully elucidated. In this review, we debate several characteristics of the gut microbiota, gut barrier function and metabolic outcomes. We examine the role of specific dietary compounds or nutrients (e.g., prebiotics, probiotics, polyphenols, sweeteners, and a fructose-rich diet) as well as different metabolites produced by the microbiota in host metabolism, and we discuss how they control several endocrine functions and eventually have either beneficial or deleterious effects on host health.

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