Tu-W22:6 Role of macrophage infiltration in inflammatory changes of obese subjects adipose tissue

2006 ◽  
Vol 7 (3) ◽  
pp. 165
Author(s):  
M. D'Adamo ◽  
C. Consoli ◽  
V. Guglielmi ◽  
P. Gentileschi ◽  
M. Federici ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Macrophage Infiltration ◽  
Obese Subjects ◽  
Inflammatory Changes

scholarly journals An Overview of Adipose Tissue ACE2 Modulation by Diet and Obesity. Potential Implications in COVID-19 Infection and Severity

2021 ◽  
Vol 22 (15) ◽  
pp. 7975
Author(s):  
Saioa Gómez-Zorita ◽  
Iñaki Milton-Laskibar ◽  
Laura García-Arellano ◽  
Marcela González ◽  
María P. Portillo
Keyword(s):  
Adipose Tissue ◽  
Protective Role ◽  
Inflammatory Factors ◽  
Current Evidence ◽  
Disease Outcomes ◽  
Lower Activation ◽  
Two Factors ◽  
Obese Subjects ◽  
Ace2 Gene

The present review is aimed at analysing the current evidence concerning the potential modulation of obesity and/or diet in adipose tissue ACE2. Additionally, the potential implications of these effects on COVID-19 are also addressed. The results published show that diet and obesity are two factors that effectively influence the expression of Ace2 gene in adipose tissue. However, the shifts in this gene do not always occur in the same direction, nor with the same intensity. Additionally, there is no consensus regarding the implications of increased adipose tissue ACE2 expression in health. Thus, while in some studies a protective role is attributed to ACE2 overexpression, other studies suggest otherwise. Similarly, there is much debate regarding the role played by ACE2 in COVID-19 in terms of degree of infection and disease outcomes. The greater risk of infection that may hypothetically derive from enhanced ACE2 expression is not clear since the functionality of the enzyme seems to be as important as the abundance. Thus, the greater abundance of ACE2 in adipose tissue of obese subjects may be counterbalanced by its lower activation. In addition, a protective role of ACE2 overexpression has also been suggested, associated with the increase in anti-inflammatory factors that it may produce.

scholarly journals Macrophage infiltration into adipose tissue may promote angiogenesis for adipose tissue remodeling in obesity

2008 ◽  
Vol 295 (2) ◽  
pp. E313-E322 ◽  
Author(s):  
Can Pang ◽  
Zhanguo Gao ◽  
Jun Yin ◽  
Jin Zhang ◽  
Weiping Jia ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Adipose Tissue ◽  
Tube Formation ◽  
Macrophage Infiltration ◽  
Platelet Derived Growth Factor ◽  
Angiogenic Factor ◽  
Vascular Density ◽  
Adipose Tissue Macrophages ◽  
Adipose Tissue Remodeling

The biological role of macrophage infiltration into adipose tissue in obesity remains to be fully understood. We hypothesize that macrophages may act to stimulate angiogenesis in the adipose tissue. This possibility was examined by determining macrophage expression of angiogenic factor PDGF (platelet-derived growth factor) and regulation of tube formation of endothelial cells by PDGF. The data suggest that endothelial cell density was reduced in the adipose tissue of ob/ob mice. Expression of endothelial marker CD31 was decreased in protein and mRNA. The reduction was associated with an increase in macrophage infiltration. In the obese mice, PDGF concentration was elevated in the plasma, and its mRNA expression was increased in adipose tissue. Macrophages were found to be a major source of PDGF in adipose tissue, as deletion of macrophages led to a significant reduction in PDGF mRNA. In cell culture, PDGF expression was induced by hypoxia, and tube formation of endothelial cells was induced by PDGF. The PDGF activity was dependent on S6K, as inhibition of S6K in endothelial cells led to inhibition of the PDGF activity. We conclude that, in response to the reduced vascular density, macrophages may express PDGF in adipose tissue to facilitate capillary formation in obesity. Although the PDGF level is elevated in adipose tissue, its activity in angiogenesis is dependent on the availability of sufficient endothelial cells. The study suggests a new function of macrophages in the adipose tissue in obesity.

scholarly journals SUN-603 Electronic Cigarette Exposure Induces Pro-Inflammatory Changes in Adipose Tissue in Apolipoprotein E (APOE) Knockout Mice

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Jorge Espinoza-Derout ◽  
Xuesi M Shao ◽  
Jocelyn Molina-Mancio ◽  
Kamrul M Hasan ◽  
Norma Mtume ◽  
...  
Keyword(s):  
Metabolic Disease ◽  
Adipose Tissue ◽  
Electronic Cigarettes ◽  
Transcriptional Response ◽  
Cigarette Use ◽  
Inflammatory Phenotype ◽  
Apoe Knockout Mice ◽  
Apoe Ko Mice ◽  
Inflammatory Changes

Abstract Electronic nicotine delivery systems or electronic cigarettes (e-cigarettes) are becoming exceptionally popular in the world as an alternative to conventional nicotine cigarettes, both in smokers and people who have never smoked. Nicotine can induce lipolysis in adipose tissue, leading to increased serum free fatty acids (FFA). Increased levels of FFA are one of the key elements in inducing a pro-inflammatory response and lead to ectopic lipid accumulation, lipotoxicity, mitochondrial dysfunction and metabolic disease. Our laboratory has shown that chronic e-cigarette exposure induces cardiac dysfunction, atherosclerosis and hepatic steatosis in the ApoE knockout (KO) model associated with increased levels of serum FFA. In this study, we investigated the role of adipose tissue in the metabolic changes associated with e-cigarette exposure. ApoE KO mice were exposed to saline, e-cigarette without nicotine [e-cigarette (0%)] and e-cigarette with 2.4% nicotine [e-cigarette (2.4%)] aerosol for 12 weeks. Western blot analyses from adipose tissue showed that mice treated with e-cigarette (2.4%) had decrease levels of SIRT1 when compared to mice treated with saline or e-cigarette (0%). Transcriptomic analysis of the differentially expressed genes shows a differential transcriptional response to e-cigarette (2.4%) in adipose tissue in comparison with e-cigarette (0%) or saline. The RNA-seq examination using ingenuity pathway analysis (IPA) software, revealed dysregulation of fibrosis, agranulocyte and granulocyte adhesion and diapedesis pathways in e-cigarette (2.4%) -exposed adipose tissue. Overall, we found an inflammatory phenotype associated with decreased levels of SIRT1 in adipose tissue of mice treated with e-cigarette (2.4%). Understanding the consequences of e-cigarette use on metabolic disease is directly relevant to the development of policies related to e-cigarette use.

Telmisartan attenuates progression of steatohepatitis in mice: role of hepatic macrophage infiltration and effects on adipose tissue

2009 ◽  
Vol 29 (7) ◽  
pp. 988-996 ◽  
Author(s):  
Hiroshi Kudo ◽  
Yutaka Yata ◽  
Terumi Takahara ◽  
Kengo Kawai ◽  
Yasuhiro Nakayama ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Macrophage Infiltration ◽  
Hepatic Macrophage

scholarly journals A Unique Role of Monocyte Chemoattractant Protein 1 among Chemokines in Adipose Tissue of Obese Subjects

2005 ◽  
Vol 90 (10) ◽  
pp. 5834-5840 ◽  
Author(s):  
Ingrid Dahlman ◽  
Maria Kaaman ◽  
Tommy Olsson ◽  
Garry D. Tan ◽  
Alex S. T. Bickerton ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Unique Role ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Obese Subjects

scholarly journals Serum Resistin (FIZZ3) Protein Is Increased in Obese Humans

2003 ◽  
Vol 88 (11) ◽  
pp. 5452-5455 ◽  
Author(s):  
Mikako Degawa-Yamauchi ◽  
Jason E. Bovenkerk ◽  
Beth Elisa Juliar ◽  
William Watson ◽  
Kimberly Kerr ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Significant Positive Correlation ◽  
Human Adipose Tissue ◽  
Model Assessment ◽  
Homeostasis Model Assessment ◽  
Obese Subjects ◽  
Isolated Adipocytes ◽  
Resistance Score

Abstract The role of resistin in obesity and insulin resistance in humans is controversial. Therefore, resistin protein was quantitated by ELISA in serum of 27 lean [13 women/14 men, body mass index (BMI) 21.7 ± 0.4 kg/m2, age 33 ± 2 yr] and 50 obese (37 women/13 men, BMI 49.8 ± 1.5 kg/m2, age 47 ± 1 yr) subjects. There was more serum resistin protein in the obese (mean ± sem: 5.3 ± 0.4 ng/ml; range 1.8–17.9) than lean subjects (3.6 ± 0.4 ng/ml; range 1.5–9.9; P = 0.001). The elevation of serum resistin in obese humans was confirmed by Western blot as was expression of resistin protein in human adipose tissue and isolated adipocytes. There was a significant positive correlation between resistin and BMI (r = 0.37; P = 0.002). Multiple regression analysis with predictors BMI and resistin explained 25% of the variance in homeostasis model assessment of insulin resistance score. BMI was a significant predictor of insulin resistance (P = 0.0002), but resistin adjusted for BMI was not (P = 0.11). The data demonstrate that resistin protein is present in human adipose tissue and blood, and that there is significantly more resistin in the serum of obese subjects. Serum resistin is not a significant predictor of insulin resistance in humans.

Do adipose tissue macrophages promote insulin resistance or adipose tissue remodelling in humans?

2014 ◽  
Vol 20 (1) ◽  
Author(s):  
Leonie K. Heilbronn ◽  
Bo Liu
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Tissue Expansion ◽  
Macrophage Infiltration ◽  
Low Grade ◽  
Tissue Remodelling ◽  
Inflammatory Phenotype ◽  
Inflammatory State ◽  
Caloric Excess

AbstractIn diet induced and genetically obese rodent models, adipose tissue is associated with macrophage infiltration, which promotes a low grade inflammatory state and the development of insulin resistance. In humans, obesity is also closely linked with macrophage infiltration in adipose tissue, a pro-inflammatory phenotype and insulin resistance. However, whether macrophage infiltration is a direct contributor to the development of insulin resistance that occurs in response to weight gain, or is a later consequence of the obese state is unclear. There are a number of concomitant changes that occur during adipose tissue expansion, including the number and size of adipocytes, the vasculature and the extracellular matrix. In this review, we will examine evidence for and against the role of macrophage recruitment into adipose tissue in promoting the development of insulin resistance in rodents and humans, as well as discuss the emerging role of macrophages in mediating healthy adipose tissue expansion during periods of caloric excess.

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