scholarly journals Serum Levels of Interleukin-13 Increase in Subjects with Insulin Resistance but Do Not Correlate with Markers of Low-Grade Systemic Inflammation

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Camilo P. Martínez-Reyes ◽  
Angélica Y. Gómez-Arauz ◽  
Israel Torres-Castro ◽  
Aarón N. Manjarrez-Reyna ◽  
León F. Palomera ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Systemic Inflammation ◽  
Serum Levels ◽  
Blood Levels ◽  
Low Grade ◽  
Anthropometric Parameters ◽  
Necrosis Factor Alpha ◽  
Insulin Resistant ◽  
Factor Alpha ◽  
Relationship Of

Experimental evidence in mice suggests a role for interleukin- (IL-) 13 in insulin resistance and low-grade systemic inflammation. However, IL-13 serum levels have not been assessed in subjects with insulin resistance, and associations of IL-13 with parameters of low-grade systemic inflammation are still unknown. Our main goal was to examine the systemic levels of IL-13 in patients with insulin resistance, while also studying the relationship of IL-13 with anthropometric, metabolic, and low-grade systemic inflammatory markers. Ninety-two participants were included in the study and divided into insulin-resistant patients and noninsulin-resistant controls. Blood levels of IL-13, glucose, insulin, triglycerides, cholesterol, tumor necrosis factor-alpha (TNF-α), IL-10, proinflammatory (Mon-CD11c+CD206−), and anti-inflammatory (Mon-CD11c−CD206+) monocytes, as well as anthropometric parameters, were measured in all volunteers. Insulin-resistant patients showed 2.5-fold higher serum levels of IL-13 than controls (P<0.0001) and significantly increased values of TNF-α and Mon-CD11c+CD206−, with concomitant reductions in IL-10 and Mon-CD11c−CD206+. Increased IL-13 was extraordinarily well associated with hyperglycemia (r=0.7362) and hypertriglyceridemia (r=0.7632) but unexpectedly exhibited no significant correlations with TNF-α (r=0.2907), IL-10 (r=−0.3882), Mon-CD11c+CD206− (r=0.2745) or Mon-CD11c−CD206+ (r=−0.3237). This study demonstrates that IL-13 serum levels are elevated in patients with insulin resistance without showing correlation with parameters of low-grade systemic inflammation.

scholarly journals Resistin - a mediator of obesity-associated insulin resistance or an innocent bystander?

2002 ◽  
pp. 571-574 ◽  
Author(s):  
O Ukkola
Keyword(s):  
Insulin Resistance ◽  
Peptide Hormone ◽  
Current Evidence ◽  
Necrosis Factor Alpha ◽  
Insulin Resistant ◽  
Protein Levels ◽  
Resistance To Insulin ◽  
Factor Alpha ◽  
Near Future

The objective of this review is to summarize the current evidence of a novel adipocytokine, resistin. Resistin is a novel peptide hormone that belongs to a family of tIssue-specific resistin-like molecules originally named for its resistance to insulin. Although a seminal proposal by Steppan et al. suggested resistin to be a hormone that links obesity to diabetes, several studies have subsequently been published supporting the concept that insulin resistance and obesity are actually associated with a decreased resistin expression. Resistin expression is regulated by a variety of agents and hormones, including thiazolidinediones, insulin, tumor necrosis factor alpha and growth hormone. Studies about their role in the regulation of resistin expression are, however, inconsistent in many cases. Experiments in humans have shown no differences in resistin expression between normal, insulin-resistant or type 2 diabetic samples. However, some recent genetic studies have demonstrated an association between resistin and insulin resistance and obesity. In addition, regional variation in the expression of resistin mRNA and protein levels in humans is an interesting finding with the highest levels found in the abdominal depot. In conclusion, resistin is a fascinating new hormone for which a definite role in metabolism will be revealed in the near future.

scholarly journals Scutellaria baicalensis Alleviates Insulin Resistance in Diet-Induced Obese Mice by Modulating Inflammation

2019 ◽  
Vol 20 (3) ◽  
pp. 727 ◽  
Author(s):  
Hyun-Young Na ◽  
Byung-Cheol Lee
Keyword(s):  
Insulin Resistance ◽  
Inflammatory Responses ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Postprandial Glucose ◽  
Scutellaria Baicalensis ◽  
Necrosis Factor Alpha ◽  
Insulin Resistant ◽  
The Metabolic Syndrome ◽  
Epididymal Fat

Insulin resistance is strongly associated with the metabolic syndrome, and chronic inflammation is known to be a major mechanism of insulin resistance and is a therapeutic target. This study was designed to evaluate the effect of Scutellaria baicalensis (SB) in high-fat diet (HFD)-induced insulin-resistant mice and to investigate its mechanism based on inflammatory responses. Mice were fed a HFD to induce insulin resistance and then administered SB for nine weeks. Body weight, glucose, lipid, insulin, epididymal fat pad and liver weights, and histologic characteristics were evaluated to determine the effect on insulin resistance. In order to evaluate the effects on the inflammatory process, we analyzed the proportions of macrophages in liver and epididymal fat and measured inflammatory gene expression. Fasting and postprandial glucose, fasting insulin, HOMA-IR, triglycerides, and low density lipoprotein cholesterol levels were significantly decreased by SB administration. The epididymal fat and liver showed significant weight decreases and histological improvements. Total adipose tissue macrophages (ATMs) decreased (27.71 ± 3.47% vs. 45.26 ± 7.26%, p < 0.05), M2 ATMs increased (47.02 ± 6.63% vs. 24.28 ± 8.00%, p < 0.05), and CD11b+ Kupffer cells decreased. The expression levels of tumor necrosis factor alpha and F4/80 in the liver were significantly decreased (12.03 ± 1.47% vs. 25.88 ± 4.57%, p < 0.05) compared to HFD group. These results suggest that SB improved insulin resistance through inhibition of macrophage-mediated inflammation.

scholarly journals Increased Serum Levels of Tumor Necrosis Factor-Alpha, Resistin, and Visfatin in the Children with Autism Spectrum Disorders: A Case-Control Study

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Mohammad Ali Ghaffari ◽  
Elham Mousavinejad ◽  
Forough Riahi ◽  
Masoumeh Mousavinejad ◽  
Mohammad Reza Afsharmanesh
Keyword(s):  
Autism Spectrum Disorders ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Serum Levels ◽  
Autism Spectrum ◽  
Necrosis Factor Alpha ◽  
Children With Asd ◽  
Factor Alpha ◽  
Spectrum Disorders ◽  
Necrosis Factor

Background. Autism spectrum disorders (ASDs) are complex disorders where the pathogenesis is not fully understood. Several proinflammatory and immunoinflammatory disturbances have been observed in the etiology of ASD. There is, however, limited knowledge on variations of adipokines in ASD. The present study aimed to analyze the serum levels of resistin, visfatin, and tumor necrosis factor-alpha (TNF-α) in children with ASD in relation to body weight, gender, and ASD severity level. Method. In total, 30 children with ASD (mean age: 7.72±2.65 y; range; 4–12 y) and 30 healthy children (mean age: 8.4±2.66 y; range: 4–12 y), including males and females, were matched for age, gender, and body mass index (BMI). Serum samples were collected, and visfatin, resistin, and TNF-α serum levels were measured using an enzyme-linked immunosorbent assay (ELISA) kit. Result. Serum visfatin, resistin, and TNF-α levels in children with ASD were significantly higher than that in the healthy patients (p<0.05). Two significant correlations were found: a correlation between resistin and visfatin with TNF-α in children with ASD (R = 0.8 and R = 0.62, resp.) and a correlation between resistin and visfatin in children with ASD (R = 0.66). Conclusion. Higher TNF-α, resistin, and visfatin levels were found in children with ASD in comparison with controls, suggesting that elevated levels of serum proinflammatory agents may be implicated in the pathophysiology of ASD.

scholarly journals My D88-Dependent Interplay Between Myeloid and Endothelial Cells in the Initiation and Progression of Obesity-Associated Inflammatory Diseases

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. SCI-44-SCI-44
Author(s):  
Xiaoxia Li
Keyword(s):  
Insulin Resistance ◽  
Endothelial Cells ◽  
Adipose Tissue ◽  
Systemic Inflammation ◽  
Conflicts Of Interest ◽  
Ex Vivo ◽  
Inflammatory Diseases ◽  
Critical Role ◽  
Low Grade

Abstract Low-grade systemic inflammation is often associated with metabolic syndrome, which plays a critical role in the development of the obesity-associated inflammatory diseases, including insulin resistance and atherosclerosis. Here, we investigate how Toll-like receptor-MyD88 signaling in myeloid and endothelial cells coordinately participates in the initiation and progression of high fat diet-induced systemic inflammation and metabolic inflammatory diseases. MyD88 deficiency in myeloid cells inhibits macrophage recruitment to adipose tissue and their switch to an M1-like phenotype. This is accompanied by substantially reduced diet-induced systemic inflammation, insulin resistance, and atherosclerosis. MyD88 deficiency in endothelial cells results in a moderate reduction in diet-induced adipose macrophage infiltration and M1 polarization, selective insulin sensitivity in adipose tissue, and amelioration of spontaneous atherosclerosis. Both in vivo and ex vivo studies suggest that MyD88-dependent GM-CSF production from the endothelial cells might play a critical role in the initiation of obesity-associated inflammation and development of atherosclerosis by priming the monocytes in the adipose and arterial tissues to differentiate into M1-like inflammatory macrophages. Collectively, these results implicate a critical MyD88-dependent interplay between myeloid and endothelial cells in the initiation and progression of obesity-associated inflammatory diseases. Disclosures No relevant conflicts of interest to declare.

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