Search Results

You are looking at 1 - 10 of 187 items for :

  • low-grade inflammation x
  • All content x
Clear All
Free access

Milos Mraz and Martin Haluzik

in AT and their role in the development of low-grade inflammation and insulin resistance (IR). Metabolism, immunity, and inflammation Inflammation is a series of cellular and humoral reactions aimed at defending the body from various insults including

Free access

Rachel Botchlett, Shih-Lung Woo, Mengyang Liu, Ya Pei, Xin Guo, Honggui Li, and Chaodong Wu

-associated inflammation is a low-grade, chronic state ( Neels & Olefsky 2006 ). Furthermore, inflammation in obesity is a systemic progression that involves the activation of several inflammatory pathways, and the subsequent generation of proinflammatory cytokines, which

Free access

M K Piya, P G McTernan, and S Kumar

Evolution and inflammation Chronic low-grade inflammation is thought to be key in the pathogenesis of insulin resistance, type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD) that is associated with obesity-mediated diabetes

Free access

Camilla Alexanderson, Elias Eriksson, Elisabet Stener-Victorin, Malin Lönn, and Agneta Holmäng

postnatal oestrogen exposure may regulate insulin sensitivity by inducing chronic, low-grade systemic and skeletal muscle inflammation in adulthood. The dose of 0.35 mg oestradiol benzoate used in this study is based on our previous study ( Alexanderson et

Free access

Gemma Llauradó, Victòria Ceperuelo-Mallafré, Carme Vilardell, Rafael Simó, Pilar Gil, Albert Cano, Joan Vendrell, and José-Miguel González-Clemente

. 2005 ). In this context, we have recently shown that low-grade inflammation is independently associated with an increase in AS in type 1 diabetes ( Llaurado et al . 2012 ). However, other mechanisms, such as the formation of advanced glycation end

Free access

Craig S Nunemaker, H Grace Chung, Gretchen M Verrilli, Kathryn L Corbin, Aditi Upadhye, and Poonam R Sharma

Introduction Chronic low-grade inflammation is increasingly considered as a contributing factor to many metabolic diseases including type 2 diabetes (T2D). Obesity leads to excess fatty acids and lipids in the body, which have toxic and damaging

Free access

Ljupka Gligorovska, Biljana Bursać, Sanja Kovačević, Nataša Veličković, Gordana Matić, and Ana Djordjevic

-abdominal adiposity and dysfunction of the adipose tissue, resulting in the infiltration of immune cells and development of chronic low-grade inflammation ( Monteiro & Azevedo 2010 ). Macrophage migration inhibitory factor (MIF) is a pleiotropic ubiquitously

Free access

Pegah JafariNasabian, Julia E Inglis, Wendimere Reilly, Owen J Kelly, and Jasminka Z Ilich

. 2015 ). Furthermore, it is also important to note that low-grade chronic inflammation (LGCI) increases with age and persists in older individuals, even when other illnesses are not present ( Ilich et al. 2014a ). As recently reviewed, both dietary

Free access

Clara Lefranc, Malou Friederich-Persson, Roberto Palacios-Ramirez, and Aurelie Nguyen Dinh Cat

by WAT, leading to systemic and tissue specific low-grade inflammation and insulin resistance ( Malnick & Knobler 2006 , Choe et al. 2016 ). In obese patients, adipose tissue mainly releases pro-inflammatory cytokines, among which are tumor

Restricted access

Marion Régnier, Matthias Van Hul, Claude Knauf, and Patrice D Cani

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.