scholarly journals Angiogenesis in Adipose Tissue: The Interplay Between Adipose and Endothelial Cells

2021 ◽  
Vol 11 ◽  
Author(s):  
Jacqueline Herold ◽  
Joanna Kalucka
Keyword(s):  
Adipose Tissue ◽  
Cell Number ◽  
Tube Formation ◽  
Angiogenic Factors ◽  
Fat Cell ◽  
Necrosis Factor Alpha ◽  
Functional Link ◽  
Tnf Α ◽  
Factor Alpha ◽  
Endothelial Growth Factor

Obesity is a worldwide health problem, and as its prevalence increases, so does the burden of obesity-associated co-morbidities like type 2 diabetes or cardiovascular diseases (CVDs). Adipose tissue (AT) is an endocrine organ embedded in a dense vascular network. AT regulates the production of hormones, angiogenic factors, and cytokines. During the development of obesity, AT expands through the increase in fat cell size (hypertrophy) and/or fat cell number (hyperplasia). The plasticity and expansion of AT is related to its angiogenic capacities. Angiogenesis is a tightly orchestrated process, which involves endothelial cell (EC) proliferation, migration, invasion, and new tube formation. The expansion of AT is accelerated by hypoxia, inflammation, and structural remodeling of blood vessels. The paracrine signaling regulates the functional link between ECs and adipocytes. Adipocytes can secrete both pro-angiogenic molecules, e.g., tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), or vascular endothelial growth factor (VEGF), and anti-angiogenic factors, e.g., serpins. If the pro-angiogenic molecules dominate, the angiogenesis is dysregulated and the endothelium becomes dysfunctional. However, if anti-angiogenic molecules are overexpressed relative to the angiogenic regulators, the angiogenesis is repressed, and AT becomes hypoxic. Furthermore, in the presence of chronic nutritional excess, endothelium loses its primary function and contributes to the inflammation and fibrosis of AT, which increases the risk for CVDs. This review discusses the current understanding of ECs function in AT, the cross-talk between adipose and ECs, and how obesity can lead to its dysfunction. Understanding the interplay of angiogenesis with AT can be an approach to therapy obesity and obesity-related diseases such as CVDs.

scholarly journals Trehalose 6,6′-Dimycolate (Cord Factor) of Mycobacterium tuberculosis Induces Corneal Angiogenesis in Rats

2000 ◽  
Vol 68 (10) ◽  
pp. 5991-5997 ◽  
Author(s):  
Norio Saita ◽  
Nagatoshi Fujiwara ◽  
Ikuya Yano ◽  
Kazuhiko Soejima ◽  
Kazuo Kobayashi
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Neutralizing Antibodies ◽  
Early Stage ◽  
Vascular Endothelial ◽  
Cytokine Network ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Cord Factor ◽  
Factor Alpha ◽  
Endothelial Growth Factor

ABSTRACT Neovascularization or angiogenesis is required for the progression of chronic inflammation. The mechanism of inflammatory neovascularization in tuberculosis remains unknown. Trehalose 6,6′-dimycolate (TDM) purified from Mycobacterium tuberculosis was injected into rat corneas. TDM challenge provoked a local granulomatous response in association with neovascularization. Neovascularization was seen within a few days after the challenge, with the extent of neovascularization being dose dependent, although granulomatous lesions developed 14 days after the challenge. Cytokines, including tumor necrosis factor alpha (TNF-α), interleukin-8 (IL-8), IL-1β, and vascular endothelial growth factor (VEGF), were found in lesions at the early stage (within a few days after the challenge) and were detectable until day 21. Neovascularization was inhibited substantially by neutralizing antibodies to VEGF and IL-8 but not IL-1β. Treatment with anti-TNF-α antibodies resulted in partial inhibition. TDM possesses pleiotropic activities, and the cytokine network plays an important role in the process of neovascularization.

scholarly journals Tributyrin in Inflammation: Does White Adipose Tissue Affect Colorectal Cancer?

Nutrients ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 110 ◽  
Author(s):  
Luana Amorim Biondo ◽  
Alexandre Abilio S. Teixeira ◽  
Loreana S. Silveira ◽  
Camila O. Souza ◽  
Raquel G. F. Costa ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Colon Carcinogenesis ◽  
Serum Glucose ◽  
Control Group ◽  
Chow Diet ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha

Colorectal cancer affects the large intestine, leading to loss of white adipose tissue (WAT) and alterations in adipokine secretion. Lower incidence of colorectal cancer is associated with increased fibre intake. Fructooligosaccharides (FOS) are fibres that increase production of butyrate by the intestinal microbiota. Tributyrin, a prodrug of butyric acid, exerts beneficial anti-inflammatory effects on colorectal cancer. Our aim was to characterise the effects of diets rich in FOS and tributyrin within the context of a colon carcinogenesis model, and characterise possible support of tumorigenesis by WAT. C57/BL6 male mice were divided into four groups: a control group (CT) fed with chow diet and three colon carcinogenesis-induced groups fed either with chow diet (CA), tributyrin-supplemented diet (BUT), or with FOS-supplemented diet. Colon carcinogenesis decreased adipose mass in subcutaneous, epididymal, and retroperitoneal tissues, while also reducing serum glucose and leptin concentrations. However, it did not alter the concentrations of adiponectin, interleukin (IL)-6, IL-10, and tumour necrosis factor alpha (TNF)-α in WAT. Additionally, the supplements did not revert the colon cancer affected parameters. The BUT group exhibited even higher glucose tolerance and levels of IL-6, VEGF, and TNF-α in WAT. To conclude our study, FOS and butyrate supplements were not beneficial. In addition, butyrate worsened adipose tissue inflammation.

Abstract 1298: Adipocytes Produce The Angiogenesis Inhibitor, Soluble Fms-like Tyrosine Kinase (sflt-1)

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Florian Herse ◽  
Lydia Hering ◽  
Juergen Janke ◽  
Kerstin Gorzcelniak ◽  
Stefan Engeli ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Angiogenesis Inhibitor ◽  
Vascular Endothelial ◽  
Fat Cell ◽  
Tnf Α ◽  
17Β Estradiol ◽  
Low Bmi ◽  
Endothelial Growth Factor ◽  
Necrosis Factor

Vascular endothelial growth factor (VEGF) exerts its effects via receptors, including Flt-1. sFLT-1 is a soluble splice variant that binds VEGF locally so that the molecule cannot signal; sFLT-1 is implicated in preeclampsia, a condition associated with obesity. Adipose tissue has a dense vascular network regulated in part by LYVE-1-expressing macrophages and VEGF. The role of sFLT-1 in adipose tissue angiogenesis has not been investigated. We used RT-PCR and found that sFlt-1 was 2.6-fold upregulated in adipose tissue from preeclamptic women, 2.5-fold in decidua, and 6.9-fold in placenta. Circulating sFlt-1 was 2.4-fold elevated (all compared to pregnant nonpreeclamptic controls; p<0.05). We next cultured human preadi-pocytes and adipocytes to examine sFlt-1 and VEGF. sFlt-1 expression increased 9-fold as preadipocytes matured to adipocytes. Adipocytes actively secreted sFlt-1 into the supernatant. Hypoxia (O2 tension reduced to 3%) did not alter sFlt-1 mRNA, while VEGF expression increased 4-fold. Tumor necrosis factor (TNF)- α (100 ng/ml, 48 h) induced VEGF 2-fold, but reduced sFlt-1 production 4-fold. Angiotensin II, insulin, hydrocortisone, pioglitazone, and 17β-estradiol all had no influcence on adipocyte sFlt-1 expression. In fat tissue biopsies from 69 postmenopausal women, sFlt-1 correlated inversely with BMI (r=-0.36, p=0.002), but directly with adiponectin expression (r=0.33, p=0.01). No significant correlation was found to blood pressure, insulin, or microalbuminuria. Our study shows that sFlt-1 is elevated in the circulation, placenta, and is upregulated in adipose tissue from preeclamptic women. sFlt-1 is expressed and secreted by adipocytes. sFlt-1 is elevated during fat cell differentiation and downregulated by TNF-α. In healthy postmeonopausal women, adipose tissue sFlt-1 correlates with low BMI and high adiponectin expression. We speculate that secreted sFlt-1 from adipocytes may contribute to the vascular damage during preeclampsia. Furthermore, sFlt-1 may play a regulatory role in adipose tissue under other circumstances, perhaps as an angiogenesis regulating factor.

scholarly journals ANALYSIS OF CHANGES IN TNF-Α, IL-6, IL-8 IN PATIENTS WITH INCREASED BODY MASS INDEX AND POLYTRAUMA

2019 ◽  
Vol 19 (1) ◽  
pp. 22-26
Author(s):  
V.V. Kucheryavchenko
Keyword(s):  
Body Mass Index ◽  
Adipose Tissue ◽  
Body Mass ◽  
The Body ◽  
Necrosis Factor Alpha ◽  
Inhibition Of Growth ◽  
Tnf Α ◽  
Initial Body Mass Index ◽  
Factor Alpha ◽  
The Moment

It is known that adipose tissue is the site of the formation of proinflammatory cytokines - tumour necrosis factor alpha (TNF-α) and some interleukins. The aim of our work was to analyze changes in the level of TNF-α, interleukins 6, 8 (IL-6, IL-8) in the blood serum of 224 patients with an increased body mass index who had a polytrauma with different initial body mass index through the period of 1 day – 1 year since the moment of injury. It has been revealed that patients with a BMI of ≤ 29.9 are characterized by an increase in the control numbers of IL-6 from day 1 to day 7, an increase in the level of IL-8 from day 1 to day 3, and an increase in the level of TNF-α from day 1 to day 3. For patients with obesity II - III, an excess of IL-6 was detected from day 1 to day 30, an increase in the level of IL-8 from day 1 to day 3, and an increase in the level of TNF-α from day 1 to day 30. Patients with a BMI ≥ 40.0 demonstrate an increase in the IL-6 control figures during the year from the moment of receiving polytrauma, followed by a decrease to the 360th day, an increase in the level of IL-8 from day 1 to day 3, an increase in the TNF level -α from the day 1 to day 3. It has been found out that the indicators we studied directly reflect the adaptation status of patients with increased body mass index and polytrauma, which presentation depends on the body mass index, that is, on the amount of adipose tissue. It is apparent that it is pro-inflammatory cytokinins - IL-6, IL-8, TNF-α that are able to simulate the expected result, as they determine vigilance, stimulation or inhibition of growth, including immune cells, their differentiation, and functional activation.

scholarly journals Adipose Tissue and Brain Metabolic Responses to Western Diet—Is There a Similarity between the Two?

2020 ◽  
Vol 21 (3) ◽  
pp. 786 ◽  
Author(s):  
Arianna Mazzoli ◽  
Maria Stefania Spagnuolo ◽  
Cristina Gatto ◽  
Martina Nazzaro ◽  
Rosa Cancelliere ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Frontal Cortex ◽  
White Adipose Tissue ◽  
Insulin Signaling ◽  
Metabolic Response ◽  
Western Diet ◽  
Dietary Fats ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha

Dietary fats and sugars were identified as risk factors for overweight and neurodegeneration, especially in middle-age, an earlier stage of the aging process. Therefore, our aim was to study the metabolic response of both white adipose tissue and brain in middle aged rats fed a typical Western diet (high in saturated fats and fructose, HFF) and verify whether a similarity exists between the two tissues. Specific cyto/adipokines (tumor necrosis factor alpha (TNF-α), adiponectin), critical obesity-inflammatory markers (haptoglobin, lipocalin), and insulin signaling or survival protein network (insulin receptor substrate 1 (IRS), Akt, Erk) were quantified in epididymal white adipose tissue (e-WAT), hippocampus, and frontal cortex. We found a significant increase of TNF-α in both e-WAT and hippocampus of HFF rats, while the expression of haptoglobin and lipocalin was differently affected in the various tissues. Interestingly, adiponectin amount was found significantly reduced in e-WAT, hippocampus, and frontal cortex of HFF rats. Insulin signaling was impaired by HFF diet in e-WAT but not in brain. The above changes were associated with the decrease in brain derived neurotrophic factor (BDNF) and synaptotagmin I and the increase in post-synaptic protein PSD-95 in HFF rats. Overall, our investigation supports for the first time similarities in the response of adipose tissue and brain to Western diet.

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