Abstract #790101: The Anti-Inflammatory Effects of Insulin and Hydrocortisone Combination in Obese Subjects

2020 ◽  
Vol 26 ◽  
pp. 90
Author(s):  
Rujuta Katkar
2018 ◽  
Vol 51 (3) ◽  
pp. 1051-1068 ◽  
Author(s):  
Jèssica Latorre ◽  
José M. Moreno-Navarrete ◽  
Mónica Sabater ◽  
Maria Buxo ◽  
José I. Rodriguez-Hermosa ◽  
...  

Background/Aims: Obesity is characterized by the immune activation that eventually dampens insulin sensitivity and changes metabolism. This study explores the impact of different inflammatory/ anti-inflammatory paradigms on the expression of toll-like receptors (TLR) found in adipocyte cultures, adipose tissue, and blood. Methods: We evaluated by real time PCR the impact of acute surgery stress in vivo (adipose tissue) and macrophages (MCM) in vitro (adipocytes). Weight loss was chosen as an anti-inflammatory model, so TLR were analyzed in fat samples collected before and after bariatric surgery-induced weight loss. Associations with inflammatory and metabolic parameters were analyzed in non-obese and obese subjects, in parallel with gene expression measures taken in blood and isolated adipocytes/ stromal-vascular cells (SVC). Treatments with an agonist of TLR3 were conducted in human adipocyte cultures under normal conditions and upon conditions that simulated the chronic low-grade inflammatory state of obesity. Results: Surgery stress raised TLR1 and TLR8 in subcutaneous (SAT), and TLR2 in SAT and visceral (VAT) adipose tissue, while decreasing VAT TLR3 and TLR4. MCM led to increased TLR2 and diminished TLR3, TLR4, and TLR5 expressions in human adipocytes. The anti-inflammatory impact of weight loss was concomitant with decreased TLR1, TLR3, and TLR8 in SAT. Cross-sectional associations confirmed increased V/ SAT TLR1 and TLR8, and decreased TLR3 in obese patients, as compared with non-obese subjects. As expected, TLR were predominant in SVC and adipocyte precursor cells, even though expression of all of them but TLR8 (very low levels) was also found in ex vivo isolated and in vitro differentiated adipocytes. Among SVC, CD14+ macrophages showed increased TLR1, TLR2, and TLR7, but decreased TLR3 mRNA. The opposite patterns shown for TLR2 and TLR3 in V/ SAT, SVC, and inflamed adipocytes were observed in blood as well, being TLR3 more likely linked to lymphocyte instead of neutrophil counts. On the other hand, decreased TLR3 in adipocytes challenged with MCM dampened lipogenesis and the inflammatory response to Poly(I:C). Conclusion: Functional variations in the expression of TLR found in blood and hypertrophied fat depots, namely decreased TLR3 in lymphocytes and inflamed adipocytes, are linked to metabolic inflammation.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1265-1265
Author(s):  
Mohamed Madkour ◽  
Rasha Hassan ◽  
Najla Sherif ◽  
Samir Awadallah ◽  
Ahmed Serafi ◽  
...  

Abstract Objectives A mounting evidence confirms the effect of caloric restriction and intermittent fasting in ameliorating body oxidative stress and inflammation. A growing body of evidence supports that chronic inflammation and increased level of oxidative stress augment the way for the development of metabolic diseases, such as diabetes and cancers. Objectives: This research was conducted to examine the effect of Ramadan diurnal intermittent fasting (RDIF) on the gene expression of cellular metabolism (SIRT1 and SIRT3) and antioxidant genes (TFAM, SOD2, and Nrf2). Methods One-hundred fourteen (75 males and 39 females) overweight and obese subjects and twelve healthy body weight controls were followed-up before and after Ramadan. Dietary, anthropometric and biochemical assessments were performed before and at the end of Ramadan fasting month. Results Results showed that the relative gene expressions in obese subjects in comparison to counterpart expressions of controls showed a significant (P < 0.001) increase in the anti-inflammatory cytokine (IL-10), along with significant (P < 0.001) reductions in the proinflammatory cytokines (IL-6 and TNF-alpha). Expression of TFAM, SOD2, and Nrf2 significantly increased at the end of Ramadan (90.5%, 54.1%, and 411.5%, respectively). However, the metabolism-controlling gene (SIRT3) showed a highly significant (P < 0.001) downregulation accompanied by a trend for reduction in the SIRT1 gene at the end of Ramadan month, with % decrements of 61.8% and 10.4%, respectively. Conclusions Results suggest that RIF ameliorates the genetic expression of antioxidant and anti-inflammatory and metabolic regulatory genes. Thus, RIF presumably may entail a protective impact against oxidative stress and its adverse metabolic-related derangements in non-diabetic obese patients. Funding Sources University of Sharjah, UAE.


2016 ◽  
Vol 2 ◽  
pp. 25-30 ◽  
Author(s):  
Gilson Pires Dorneles ◽  
Ivy Reichert Vital da Silva ◽  
Arthiese Korb ◽  
Karine Bertoldi ◽  
Ionara Rodrigues Siqueira ◽  
...  

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 274-LB
Author(s):  
PARESH DANDONA ◽  
HUSAM GHANIM ◽  
MANAV BATRA ◽  
KELLY GREEN ◽  
SANAA ABUAYSHEH ◽  
...  

2011 ◽  
Vol 9 (3) ◽  
pp. 189-195 ◽  
Author(s):  
Gael Bories ◽  
Robert Caiazzo ◽  
Bruno Derudas ◽  
Corinne Copin ◽  
Violeta Raverdy ◽  
...  

Visceral obesity is a chronic, low-grade inflammatory disease that predisposes people to the metabolic syndrome, type 2 diabetes and its cardiovascular complications. Adipose tissue is not a passive storehouse for fat, but an endocrine organ synthesizing and releasing a variety of bioactive molecules, some of which are produced by infiltrated immune-inflammatory cells including macrophages. Two different subpopulations of macrophages have been identified in adipose tissue: pro-inflammatory ‘classical’ M1 and anti-inflammatory ‘alternative’ M2 macrophages, and their ratio is suggested to influence the metabolic complications of obesity. These macrophages derive primarily from peripheral blood mononuclear cells (PBMCs). We hypothesised that obesity and the metabolic syndrome modulate PBMC functions. Therefore, alteration of the monocyte response, and more specifically their ability to differentiate toward alternative anti-inflammatory macrophages, was assessed in PBMCs isolated from lean and obese subjects with or without alterations in glucose homeostasis. Our results indicate that PBMCs from obese subjects have an altered expression of M2 markers and that their monocytes are less susceptible to differentiate toward an alternative phenotype. Thus PBMCs in obesity are programmed, which may contribute to the inflammatory dysregulation and increased susceptibility to inflammatory diseases in these patients.


2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Karen Fjeldborg ◽  
Steen B. Pedersen ◽  
Holger J. Møller ◽  
Tore Christiansen ◽  
Marianne Bennetzen ◽  
...  

Objective. Adipose tissue (AT) macrophages are increased in obesity and associated with low grade inflammation. We aimed to characterize the phenotype of AT macrophages in humans in relation to obesity and insulin resistance.Design. Gene-expression levels of general macrophage markers (CD68 and CD14), proinflammatory markers/M1 (TNF-α, MCP-1, and IL-6), and anti-inflammatory markers/M2 (CD163, CD206, and IL-10) were determined by RT-PCR in subcutaneous AT samples from lean and obese subjects. Insulin resistance was determined by HOMA-IR.Results. All the macrophage markers were elevated in the AT from obese compared to lean subjects (P<0.001). To determine the phenotype of the macrophages the level of CD14 was used to adjust the total number of macrophages. The relative expression of CD163 and IL-10 was elevated, and TNF-αand IL-6 were reduced in AT from obese subjects (allP<0.05). In a multivariate regression analysis CD163 was the only macrophage marker significantly associated with HOMA-IR (β: 0.57;P<0.05). Conclusion. Obesity is associated with elevated numbers of macrophages in the AT. Unexpectedly, the macrophages change phenotype by obesity, with a preponderance of M2 and a decrement of M1 markers in AT from obese subjects. Moreover, CD163 was the only macrophage marker associated with HOMA-IR after multiple adjustments.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Amra Jujić ◽  
J. Korduner ◽  
H. Holm ◽  
G. Engström ◽  
E. Bachus ◽  
...  

AbstractObesity associates with reduced life expectancy, type 2 diabetes, hypertension and cardiovascular disease, and is characterized by chronic inflammation. Phosphorylcholine (PC) is an epitope on oxidized low-density lipoprotein, dead cells and some microorganisms. Antibodies against PC (anti-PC) have anti-inflammatory properties. Here, we explored the role of anti-PC in hospitalized versus non-hospitalized obese. One-hundred-and-twenty-eight obese (BMI ≥ 30 kg/m2) individuals (59.8 (± 5.5) years, 53.9% women) from the Malmö Diet and Cancer Cardiovascular Cohort were examined and IgM, IgG1 and IgG2 anti-PC were analyzed by ELISA. Individuals with at least one recorded history of hospitalization prior to study baseline were considered hospitalized obese (HO). Associations between IgM, IgG1 and IgG2 anti-PC and HO (n = 32)/non-hospitalized obese (NHO) (n = 96), but also with metabolic syndrome and diabetes were analysed using logistic regressions. Both IgM and IgG1 anti-PC were inversely associated with HO, also after controlling for age and sex. When further adjusted for waist circumference, systolic blood pressure, glucose levels and smoking status, only IgG1 anti-PC remained significantly associated with HO. In multivariate models, each 1 standard deviation of increment in anti-PC IgG1 levels was inversely associated with prevalence of HO (odds ratio 0.57; CI 95% 0.33–0.98; p = 0.044). IgG2 anti-PC did not show any associations with HO. Low levels of IgM and IgG1 anti-PC are associated with higher risk of being a HO individual independent of sex and age, IgG1 anti-PC also independently of diabetes and metabolic syndrome. The anti-inflammatory properties of these antibodies may be related to inflammation in obesity and its complications.


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