scholarly journals Central Obesity, Inflammation and Angiogenesis in Adult Men

2016 ◽  
Vol 2 (1) ◽  
Author(s):  
Cynthia R Sartika ◽  
Andi Wijaya ◽  
Widjaja Lukito ◽  
Suryani As’ad
Keyword(s):  
Tumor Necrosis Factor ◽  
Central Obesity ◽  
Tumor Necrosis ◽  
Abdominal Circumference ◽  
Low Grade ◽  
High Concentration ◽  
Adult Men ◽  
Obese Subjects ◽  
Low Grade Inflammation ◽  
Necrosis Factor

AbstractObesity is known to link with low-grade inflammation. Experimental studies revealed that inflammation was associated with angiogenesis process in adipose tissue. We investigate the correlation between inflammation and angiogenesis in Indonesian adult men with central obesity. A cross-sectional study was undertaken on 161 healthy Indonesian adult men (age: 23-53 y, waist circumference: 64-125 cm). Clinical parameters; biochemical markers; anthropometric parameters (weight, height and abdominal circumference); inflammatory biomarkers (tumor necrosis factor-α (TNF-α) and its soluble tumor necrosis factor receptor-2 (sTNFR-2), interleukin (IL)-1β); and biomarkers of angiogenesis (leptin, vascular endothelial growth factor (VEGF), angiopoietin (Ang)-1 and Ang-2 were measured. Obese II, Obese I subjects had higher concentrations of fasting blood glucose and triglycerides (P<0.005) than those Non-obese subjects. Obese II subjects had higher concentrations of hsCRP (P<0.05) than obese I subjects; and obese I subjects had higher concentration of hsCRP (P<0.05) than Non-obese subjects. sTNFR-2 correlated positively with leptin and Ang-2 (rs = 0.376, P< 0.001 and rs = 0.281, P = 0.003, respectively) and negatively with Ang-1 in obese subjects. High concentration of sTNFR-2 also correlated with increased concentrations of leptin, VEGF and Ang-2 in all subjects (P= 0.001, P= 0.033, and P= 0.005, respectively). In obese subjects, high concentration of sTNFR-2 had correlated with increased leptin and Ang-2, and decreased Ang-1 (7.4 %, 10.9% and 9.2%, respectively). This study was able to demonstrate the relations between inflammation and angiogenesis in Indonesian adult men with central obesity. Findings of this study suggest that inflammation and angiogenesis were mutually supportive processes contribute to systemic low grade inflammation in central obesity.

scholarly journals Lipopolysaccharide influence on leptin hormone and tumor necrosis factor-alpha release from human adipose tissue

2018 ◽  
Vol 16 ◽  
pp. 205873921877497
Author(s):  
Sa’ad Al-Lahham ◽  
Nidal Jaradat ◽  
Malik Al-Qub ◽  
Abdallah Hamayel ◽  
Abdalrahman Assaassa ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Ex Vivo ◽  
Enzyme Linked Immunosorbent Assay ◽  
Low Grade ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Low Grade Inflammation ◽  
Necrosis Factor

Obesity is associated with low-grade inflammation that originates mainly from adipose tissue. This is implicated in the pathogenesis of type-2 diabetes and cardiovascular diseases. Strong evidence indicates that chronically elevated systemic low-grade lipopolysaccharide (LPS), elicits low-grade inflammation. However, evidence on LPS effect on adipokines’ level, such as leptin, is scarce, and it has never been investigated ex vivo in human subcutaneous adipose tissue (SAT) and therefore we aim to investigate this. To achieve our aim, SAT explants were obtained from 12 patients (50% males) and were treated with/without LPS. Protein concentration was determined by enzyme-linked immunosorbent assay (ELISA). We found that the average age and body mass index (BMI) of included patients were 58.6 years and 28.6 kg/m2, respectively. LPS induced significantly (~3×, P < 0.0001) the secretion of tumor necrosis factor (TNF)-α from SAT, and it was not associated with age or BMI. However, leptin secretion was inhibited slightly (~20%), but significantly. Interestingly, leptin release was significantly inhibited (~50%) in SAT from lean but not from obese patients, and there was an association between leptin response and BMI (R = 0.8), but no association with age. In this study, we found, for the first time, that LPS suppresses the release of leptin hormone from SAT obtained from lean patients, while it induces TNF-α release. Our findings provide extra evidence and confirm earlier studies regarding the role of LPS in low-grade inflammation. Further investigations are essential to identify factors that inhibit LPS passage through intestinal barrier in order to prevent or reduce the development of obesity and its associated chronic diseases.

scholarly journals Dendritic cell maturation in the corneal epithelium with onset of type 2 diabetes is associated with tumor necrosis factor receptor superfamily member 9

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Neil S. Lagali ◽  
Reza A. Badian ◽  
Xu Liu ◽  
Tobias R. Feldreich ◽  
Johan Ärnlöv ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Dendritic Cell ◽  
Tumor Necrosis Factor ◽  
Corneal Epithelium ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Low Grade ◽  
Antigen Presenting ◽  
Necrosis Factor

AbstractType 2 diabetes mellitus is characterized by a low-grade inflammation; however, mechanisms leading to this inflammation in specific tissues are not well understood. The eye can be affected by diabetes; thus, we hypothesized that inflammatory changes in the eye may parallel the inflammation that develops with diabetes. Here, we developed a non-invasive means to monitor the status of inflammatory dendritic cell (DC) subsets in the corneal epithelium as a potential biomarker for the onset of inflammation in type 2 diabetes. In an age-matched cohort of 81 individuals with normal and impaired glucose tolerance and type 2 diabetes, DCs were quantified from wide-area maps of the corneal epithelial sub-basal plexus, obtained using clinical in vivo confocal microscopy (IVCM). With the onset of diabetes, the proportion of mature, antigen-presenting DCs increased and became organized in clusters. Out of 92 plasma proteins analysed in the cohort, tumor necrosis factor receptor super family member 9 (TNFRSF9) was associated with the observed maturation of DCs from an immature to mature antigen-presenting phenotype. A low-grade ocular surface inflammation observed in this study, where resident immature dendritic cells are transformed into mature antigen-presenting cells in the corneal epithelium, is a process putatively associated with TNFRSF9 signalling and may occur early in the development of type 2 diabetes. IVCM enables this process to be monitored non-invasively in the eye.

scholarly journals Tumor necrosis factor/cachectin and lymphotoxin gene expression in lymph nodes from lymphoma patients

Blood ◽  
1990 ◽  
Vol 75 (4) ◽  
pp. 958-962
Author(s):  
AP Sappino ◽  
W Seelentag ◽  
MF Pelte ◽  
P Alberto ◽  
P Vassalli
Keyword(s):  
Gene Expression ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Growth Control ◽  
Low Grade ◽  
Mrna Levels ◽  
Malignant Cells ◽  
Systemic Symptoms ◽  
Tissue Specimens ◽  
Necrosis Factor

We investigated the mRNA content for tumor necrosis factor (TNF)/cachectin and lymphotoxin (LT) in tumoral tissues of a prospective series of 35 non-Hodgkin's (NHL) and 23 Hodgkin's (HL) lymphomas, to assess their postulated contribution to systemic symptoms. Total RNAs were extracted from diagnostic tissue specimens and submitted to Northern blot analysis, using specific TNF and LT cRNA probes. High amounts of TNF mRNA were found exclusively in NHL (12/35). The majority (9/12) of these were low grade B-cell NHL, which contained a uniform population of malignant cells. In contrast, abundant LT mRNA production was detected in most HL (21/23) and in 19 of 35 NHL. The highest LT mRNA levels were observed in high grade NHL and in lymphocytic predominant subtypes of HL specimens. A significant correlation was found between TNF/cachectin and LT gene expression in NHL and the presence of constitutional symptoms. The biologic and prognostic implications of these preliminary findings are presently unknown, but they demonstrate that lymphoma tissues sharing common histologic features are highly heterogeneous in their ability to synthesize cytokines susceptible to playing a role in the growth control of malignant cells. These results suggest that the evaluation of TNF/cachectin and LT production in lymphomas may help to elucidate the mechanisms of tumoral fever and cachexia.

scholarly journals Tumor necrosis factor/cachectin and lymphotoxin gene expression in lymph nodes from lymphoma patients

Blood ◽  
1990 ◽  
Vol 75 (4) ◽  
pp. 958-962 ◽  
Author(s):  
AP Sappino ◽  
W Seelentag ◽  
MF Pelte ◽  
P Alberto ◽  
P Vassalli
Keyword(s):  
Gene Expression ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Growth Control ◽  
Low Grade ◽  
Mrna Levels ◽  
Malignant Cells ◽  
Systemic Symptoms ◽  
Tissue Specimens ◽  
Necrosis Factor

Abstract We investigated the mRNA content for tumor necrosis factor (TNF)/cachectin and lymphotoxin (LT) in tumoral tissues of a prospective series of 35 non-Hodgkin's (NHL) and 23 Hodgkin's (HL) lymphomas, to assess their postulated contribution to systemic symptoms. Total RNAs were extracted from diagnostic tissue specimens and submitted to Northern blot analysis, using specific TNF and LT cRNA probes. High amounts of TNF mRNA were found exclusively in NHL (12/35). The majority (9/12) of these were low grade B-cell NHL, which contained a uniform population of malignant cells. In contrast, abundant LT mRNA production was detected in most HL (21/23) and in 19 of 35 NHL. The highest LT mRNA levels were observed in high grade NHL and in lymphocytic predominant subtypes of HL specimens. A significant correlation was found between TNF/cachectin and LT gene expression in NHL and the presence of constitutional symptoms. The biologic and prognostic implications of these preliminary findings are presently unknown, but they demonstrate that lymphoma tissues sharing common histologic features are highly heterogeneous in their ability to synthesize cytokines susceptible to playing a role in the growth control of malignant cells. These results suggest that the evaluation of TNF/cachectin and LT production in lymphomas may help to elucidate the mechanisms of tumoral fever and cachexia.

scholarly journals Differential effects of anti-tumor necrosis factor monoclonal antibodies on systemic inflammatory responses in experimental endotoxemia in chimpanzees

Blood ◽  
1994 ◽  
Vol 83 (2) ◽  
pp. 446-451 ◽  
Author(s):  
T van der Poll ◽  
M Levi ◽  
SJ van Deventer ◽  
H ten Cate ◽  
BL Haagmans ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Inflammatory Responses ◽  
Tissue Injury ◽  
Peak Plasma ◽  
Plasma Concentrations ◽  
Coagulation System ◽  
Low Grade ◽  
Neutrophil Degranulation ◽  
Necrosis Factor

Abstract Tumor necrosis factor (TNF) is considered to be a pivotal mediator of endotoxin-induced lethality. To assess the intermediate role of TNF in specific systemic inflammatory responses known to contribute to tissue injury in endotoxemia, eight healthy adult chimpanzees were intravenously injected with Escherichia coli endotoxin (4 ng/kg). In four of these animals the administration of endotoxin was followed immediately by a bolus intravenous injection of an anti-TNF monoclonal antibody (15 mg/kg). Treatment with anti-TNF completely prevented the endotoxin-induced increase in serum TNF activity, and profoundly reduced the appearance of interleukin-6 and -8 (both P < .05). Neutrophilia and lymphopenia were not affected by anti-TNF, whereas neutrophil degranulation, as measured by the plasma concentrations of elastase-alpha 1-antitrypsin complexes, was only slightly reduced (peak levels after endotoxin alone 31.0 +/- 3.4 ng/mL, versus 25.5 +/- 3.4 ng/mL after endotoxin with anti-TNF; P < .05). Anti-TNF did not influence endotoxin-induced activation of the coagulation system, as reflected by unchanged increases in the plasma concentrations of the prothrombin fragment F1 + 2 and thrombin-antithrombin III complexes. In contrast, anti-TNF strongly attenuated the activation of the fibrinolytic system, ie, peak plasma levels of plasmin-alpha 2- antiplasmin were 33.8 +/- 11.1 nmol/L after endotoxin alone and 17.0 +/- 2.9 nmol/L after endotoxin with anti-TNF (P < .05). These results suggest that TNF is not the common mediator of systemic inflammatory changes in low-grade endotoxemia. Moreover, the finding that in this mild model anti-TNF specifically inhibited fibrinolysis suggests that treatment with anti-TNF potentially may enhance the tendency towards microvascular thrombosis in sepsis.

Relationship between plasma leptin levels and the tumor necrosis factor-α system in obese subjects

1999 ◽  
Vol 23 (4) ◽  
pp. 355-360 ◽  
Author(s):  
F Corica ◽  
A Allegra ◽  
A Corsonello ◽  
M Buemi ◽  
G Calapai ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Obese Subjects ◽  
Factor Α ◽  
Plasma Leptin ◽  
Necrosis Factor

scholarly journals Plasma Interleukin-8 Concentrations Are Increased in Obese Subjects and Related to Fat Mass and Tumor Necrosis Factor-α System

2002 ◽  
Vol 87 (10) ◽  
pp. 4602-4606 ◽  
Author(s):  
Marek Straczkowski ◽  
Stella Dzienis-Straczkowska ◽  
Agnieszka Stêpieñ ◽  
Irina Kowalska ◽  
Malgorzata Szelachowska ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Fat Mass ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Interleukin 8 ◽  
Obese Subjects ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Correlation Between Adiponectin, Tumor Necrosis Factor-alpha, Insulin Resistance and Atherogenic Dyslipidemia in Non Diabetic Central Obese Males

2010 ◽  
Vol 2 (1) ◽  
pp. 73
Author(s):  
Candra Ninghayu ◽  
Andi Wijaya ◽  
Suryani As'ad
Keyword(s):  
Insulin Resistance ◽  
Tumor Necrosis Factor ◽  
Central Obesity ◽  
Tumor Necrosis ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
Atherogenic Dyslipidemia ◽  
Homa Index ◽  
Tnf Α ◽  
Necrosis Factor

BACKGROUND: Obesity raises the risk for atherosclerotic cardiovascular disease (ASCVD) through many risk factors including atherogenic dyslipidemia. Atherogenic dyslipidemia is characterized by high levels of triglyceride, increased small dense low density lipoprotein particles, and reduced levels of high density lipoprotein cholesterol. The exact mechanisms of central obesity and this atherogenic lipoprotein phenotype (ALP) is not clearly understood. Central obesity is characterized by a state of systemic low grade inflammation and insulin resistance. Adipose tissue has recently been shown to secrete a variety of bioactive peptides, called adipocytokines, that can potentially affect glucose and lipid metabolism. The aim of this study was to observe the role of adiponectin, tumor necrosis factor-α (TNF- α) and insulin resistance in atherogenic dyslipidemia in nondiabetic central obese males.METHODS: This was a cross-sectional study on 75 non-diabetic central obese male subjects (waist circumferences > 90 cm). Adiponectin and TNF-α testing were performed by ELISA; insulin resistance was assessed by the Homeostasis Model Assessment (HOMA) index, triglyceride was assessed by GPO-PAP, HDL cholesterol and small dense LDL were measured by homogenous method. Statistical analysis was done by SPSS for Windows v. 11.5 with a significance level at p < 0.05. The Pearson and Spearman’s Rho correlation coefficient was used to assess the correlation between various anthropometric and biochemical parameters.RESULTS: There were 75 patients aged 38.0±6.3 years, Adiponectin concentration was 3.55±1.38 μg/ml, HOMA index was 2.28±1.63, TNF-α was 12.42±11.25 pg/ml, triglyceride was 185.17±109.00, HDL-cholesterol was 44.15±9.23 mg/dL, small dense LDL 23.22±12.26 mg/dL. This study revealed that there were correlations between adiponectin and triglyceride (r=-0.236, p=0.042), adiponectin and HDL cholesterol (r=0.300, p=0.009), adiponectin and atherogenic dyslipidemia (r=-0.256, p=0.027), whereas there was no correlation between insulin resistance and TNF-α with the atherogenic dyslipidemia.CONCLUSION: Adiponectin might contribute to atherogenic dyslipidemia in central obese non-diabetic males. Advancing our understanding of the function and measurement of adiponectin serum concentration will be useful in clinical diagnosis of obesity related atherogenic dyslipidemia.KEYWORDS: obesity, waist circumference, adiponectin, insulin resistance, TNF-α, atherogenic dyslipidemia

Sign in / Sign up

Export Citation Format

Share Document