Obesity-Induced Adipose Tissue Inflammation and Insulin Resistance

Hsieh, Po‐Shiuan

doi:10.5772/20561

Cited by 5 publications

(4 citation statements)

References 88 publications

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“…Adipocytes and adipose tissue-associated macrophages from obese individuals are an important source of inflammatory mediators such as tumour necrosis factor-a (TNF-a), interleukin (IL)-6, IL-1, and monocyte chemoattractant protein-1 (MCP)-1. 8 It has been proposed that adipokines such as leptin can induce T-helper cells to secrete pro-inflammatory cytokines including TNF-a, and interferon-g (IFN-g). 9,10 IL-1 suppresses adipocyte differentiation and the expression of lipoprotein lipase in adipose tissue.…”

Section: Introductionmentioning

confidence: 99%

“…11 Indeed, activation of inflammatory pathways in adipose tissue promotes the release of free fatty acids from triglyceride (TG) stores and results in macrophage infiltration into tissue. 8 In contrast, decreased concentrations of the anti-inflammatory cytokine, IL-10, have been shown to be associated with obesity and metabolic syndrome. IL-10 inhibits the synthesis of pro-inflammatory cytokines via suppression of NF-kB in macrophages.…”

Section: Introductionmentioning

confidence: 99%

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Cytokine profiles in overweight and obese subjects and normal weight individuals matched for age and gender

et al. 2016

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Background Obesity is associated with a state of systemic inflammation, mediated by adipose tissue-derived cytokines that may also have metabolic effects, including an effect on insulin resistance. The aim of this study was to compare the serum profile of pro- and anti-inflammatory cytokines in obese and non-obese subjects. Methods A total of 242 subjects who were either overweight or obese (body mass index [BMI] ≥ 25 kg/m) and non-obese subjects (body mass index <25 kg/m), were recruited in Mashhad in northeastern Iran. The concentrations of serum interleukin-1α, -1β, -2, -4, -6, -8 and -10 (IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-8 and IL-10), were measured in all subjects, together with serum vascular endothelial growth factor, interferon-γ, epidermal growth factor, monocyte chemoattractant protein-1 and tumour necrosis factor-α. Results The groups differed significantly with respect to measures of adiposity and fasted lipid profile. Serum pro-inflammatory cytokines interferon-γ and interleukin-1α, and anti-inflammatory cytokines, interleukin-10, and epidermal growth factor were significantly different between obese and non-obese individuals, as was serum high-sensitivity C-reactive protein. Multivariate regression showed that waist circumference was significantly and independently related to serum monocyte chemoattractant protein-1concentrations ( P = 0.001). Conclusion Despite significant differences in several cytokines between the groups, only monocyte chemoattractant protein-1appeared to be independently related to a measure of adiposity in this population sample from Iran.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Cytokine profiles in overweight and obese subjects and normal weight individuals matched for age and gender

et al. 2016

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“…Obesity pathophysiology comprises systemic chronic inflammation and altered immune function [10,11]. White adipose tissue has been characterized as a major source of inflammatory mediators, including secretion of cytokines, adipokines, free fatty acids, and regulation of acute-phase proteins [12], including tumor necrosis factor-α (TNF-α), interleukin (IL)−1, IL-10, IL-6, and chemoattractant proteins, all of which regulate adipogenesis and energy expenditure [13]. In juvenile obesity, inflammation is associated with early atherosclerotic vessel injury [14].…”

Section: Introductionmentioning

confidence: 99%

Sex dimorphism in inflammatory response to obesity in childhood

et al. 2021

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Background Childhood overweight and obesity are a global concern, with prevalence rising dramatically over the last decades. The condition is caused by an increase in energy intake and reduction of physical activity, leading to excessive fat accumulation, followed by systemic chronic inflammation and altered function of immune cell responses. This study aimed at providing new insights regarding sex-specificity on the inflammatory response to obesity in the young patient. Design Forty-three Brazilian obese adolescents (Female = 22 and Male=21, BMI (body mass index) Z-score average = 2.78 ± 0.51) and forty-nine eutrophic adolescents (Female = 24 and Male = 25, BMI Z-score average = −0.35 ± 0.88) were enrolled in the study. Anthropometrical analyses and blood cell counts were carried out. Using Luminex®xMAP™ technology, circulating serum cytokines, chemokines, and inflammatory biomarkers were analyzed. Two-way ANOVA test, Tukey’s test, and Spearman’s correlation coefficient were employed, with a significance threshold set at p < 0.05. Results We identified increased levels of serum amyloid A (SAA), platelets, and leukocytes solely in male obese patients. We found a noteworthy sex-dependent pattern in regard to inflammatory response: obese boys showed higher TNFβ, IL15, and IL2 and lower IL10 and IL13, while obese girls showed increased TNFα, CCL3, CCL4, and IP10 content in the circulation. BMI Z-score was significantly linearly correlated with neutrophils, leukocytes, platelets, SAA, TNFα, CCL3, CCL4, IP10, and IL13 levels within the entire cohort (non-sex-dependent). Conclusions Our data support a complex relationship between adiposity, blood cell count, and circulating inflammatory cytokine content. High SAA levels suggest that this factor may play a critical role in local and systemic inflammation. In the eutrophic group, females presented a lower status of inflammation, as compared to males. Both obese boys and girls showed an increased inflammatory response in relation to eutrophic counterparts. Taken together, results point out to clear sex dimorphism in the inflammatory profile of obese adolescents.

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“…7 In line with these findings, a number of convincing studies have recently shown that reducing carbohydrate intake significantly stabilises immune cell homeostasis and improves survival after systemic bacterial infection. [8][9][10] In these studies, the total amount of carbohydrates is reduced to approximately 10% of the overall calorie intake, whereas protein amounts are kept constant and fat amounts are increased. 11 12 The reduced availability of glucose results in increase of fatty acid oxidation with subsequent synthesis of ketone bodies to cover the body's energy demand and to generate sufficient amounts of adenosine triphosphate.…”

Section: Introductionmentioning

confidence: 99%

Impact of carbohydrate-reduced nutrition in septic patients on ICU: study protocol for a prospective randomised controlled trial

Rahmel

Hübner²,

Koos

et al. 2020

BMJ Open

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IntroductionSepsis is defined as detrimental immune response to an infection. This overwhelming reaction often abolishes a normal reconstitution of the immune cell homeostasis that in turn increases the risk for further complications. Recent studies revealed a favourable impact of ketone bodies on resolution of inflammation. Thus, a ketogenic diet may provide an easy-to-apply and cost-effective treatment option potentially alleviating sepsis-evoked harm. This study is designed to assess the feasibility, efficiency and safety of a ketogenic diet in septic patients.Methods and analysisThis monocentric study is a randomised, controlled and open-label trial, which is conducted on an intensive care unit of a German university hospital. As intervention enteral nutrition with reduced amount of carbohydrates (ketogenic) or standard enteral nutrition (control) is applied. The primary endpoint is the detection of ketone bodies in patients’ blood and urine samples. As secondary endpoints, the impact on important safety-relevant issues (eg, glucose metabolism, lactate serum concentration, incidence of metabolic acidosis, thyroid function and 30-day mortality) and the effect on the immune system are analysed.Ethics and disseminationThe study has received the following approvals: Ethics Committee of the Medical Faculty of Ruhr-University Bochum (No. 18-6557-BR). Results will be made available to critical care survivors, their caregivers, the funders, the critical care societies and other researchers by publication in a peer-reviewed journal.Trial registration numbersGerman Clinical Trial Register (DRKS00017710); Universal Trial Number (U1111-1237-2493).

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Obesity-Induced Adipose Tissue Inflammation and Insulin Resistance

Cited by 5 publications

References 88 publications

Cytokine profiles in overweight and obese subjects and normal weight individuals matched for age and gender

Cytokine profiles in overweight and obese subjects and normal weight individuals matched for age and gender

Sex dimorphism in inflammatory response to obesity in childhood

Impact of carbohydrate-reduced nutrition in septic patients on ICU: study protocol for a prospective randomised controlled trial

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