scholarly journals Visceral adipose tissue activated macrophage content and inflammatory adipokine secretion is higher in pre-eclampsia than in healthy pregnancys

2017 ◽  
Vol 131 (13) ◽  
pp. 1529-1540 ◽  
Author(s):  
Shahzya S. Huda ◽  
Fiona Jordan ◽  
Jack Bray ◽  
Gillian Love ◽  
Reba Payne ◽  
...  

Obesity increases pre-eclampsia (PE) risk. Adipose tissue inflammation may contribute to the clinical syndrome of PE. We compared adipose tissue macrophage infiltration and release of pro-inflammatory adipokines in PE and healthy pregnancy. Subcutaneous and visceral adipose tissue biopsies were collected from healthy (n=13) and PE (n=13) mothers. Basal and lipopolysaccharide (LPS) stimulated adipocyte TNFα, IL-6, CCL-2, and CRP release was measured. Adipose tissue cell densities of activated (cfms+) and total (CD68+) macrophages were determined. In PE only, visceral adipose tissue TNFα release was increased after LPS stimulation (57 [76] versus 81 [97] pg/ml/µg DNA, P=0.030). Basal TNFα release was negatively correlated insulin sensitivity of visceral adipocytes (r = −0.61, P=0.030) in PE. Visceral adipocyte IL-6 release was increased after LPS stimulation in PE only (566 [696] versus 852 [914] pg/ml/µg DNA, P=0.019). Visceral adipocyte CCL-2 basal (67 [61] versus 187 [219] pg/ml/µgDNA, P=0.049) and stimulated (46 [46] versus 224 [271] pg/ml/µg DNA, P=0.003) release was greater than in subcutaneous adipocytes in PE only. In PE, median TNF mRNA expression in visceral adipose tissue was higher than controls (1.94 [1.13–4.14] versus 0.8 [0.00–1.27] TNF/PPIA ratio, P=0.006). In visceral adipose tissue, CSF1R (a marker of activated macrophages) mRNA expression (24.8[11.0] versus 51.0[29.9] CSF1R/PPIA ratio, P=0.011) and activated (cfms+) macrophage count (6.7[2.6] versus 15.2[8.8] % cfms+/adipocyte, P=0.031) were higher in PE than in controls. In conclusion, our study demonstrates dysregulation of inflammatory pathways predominantly in visceral adipose tissue in PE. Inflammation of visceral adipose tissue may mediate many of the adverse metabolic effects associated with PE.

Obesity Facts ◽  
2012 ◽  
Vol 5 (3) ◽  
pp. 452-459 ◽  
Author(s):  
Thais Ortiz Hammes ◽  
Cíntia dos Santos Costa ◽  
Francieli Rohden ◽  
Rogério Margis ◽  
Jussara Carnevale de Almeida ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Todd Hulgan ◽  
M. Sean Boger ◽  
Diana H. Liao ◽  
Grace A. McComsey ◽  
Christine A. Wanke ◽  
...  

Chronic inflammation is a hallmark of HIV infection. Eicosanoids reflect inflammation, oxidant stress, and vascular health and vary by sex and metabolic parameters. Raltegravir (RAL) is an HIV-1 integrase inhibitor that may have limited metabolic effects. We assessed urinary F2-isoprostanes (F2-IsoPs), prostaglandin E2(PGE-M), prostacyclin (PGI-M), and thromboxane B2(TxB2) in HIV-infected women switching to RAL-containing antiretroviral therapy (ART). Thirty-seven women (RAL = 17; PI/NNRTI = 20) with a median age of 43 years and BMI 32 kg/m2completed week 24. TxB2increased in the RAL versus PI/NNRTI arm (+0.09 versus −0.02;P=0.06). Baseline PGI-M was lower in the RAL arm (P=0.005); no other between-arm cross-sectional differences were observed. In the PI/NNRTI arm, 24-week visceral adipose tissue change correlated with PGI-M (rho=0.45;P=0.04) and TxB2(rho=0.44;P=0.005) changes, with a trend seen for PGE-M (rho=0.41;P=0.07). In an adjusted model, age ≥ 50 years (N=8) was associated with increased PGE-M(P=0.04). In this randomized trial, a switch to RAL did not significantly affect urinary eicosanoids over 24 weeks. In women continuing PI/NNRTI, increased visceral adipose tissue correlated with increased PGI-M and PGE-M. Older age (≥50) was associated with increased PGE-M. Relationships between aging, adiposity, ART, and eicosanoids during HIV-infection require further study.


2008 ◽  
Vol 93 (12) ◽  
pp. 4969-4973 ◽  
Author(s):  
Blerina Kola ◽  
Mirjam Christ-Crain ◽  
Francesca Lolli ◽  
Giorgio Arnaldi ◽  
Gilberta Giacchetti ◽  
...  

Objective: Features of the metabolic syndrome such as central obesity with insulin resistance and dyslipidemia are typical signs of Cushing’s syndrome and common side effects of prolonged glucocorticoid treatment. AMP-activated protein kinase (AMPK), a key regulatory enzyme of lipid and carbohydrate metabolism as well as appetite, is involved in the development of the deleterious metabolic effects of excess glucocorticoids, but no data are available in humans. In the current study, we demonstrate the effect of high glucocorticoid levels on AMPK activity of human adipose tissue samples from patients with Cushing’s syndrome. Methods: AMPK activity and mRNA expression of genes involved in lipid metabolism were assessed in visceral adipose tissue removed at abdominal surgery of 11 patients with Cushing’s syndrome, nine sex-, age-, and weight-matched patients with adrenal incidentalomas, and in visceral adipose tissue from four patients with non-endocrine-related abdominal surgery. Results: The patients with Cushing’s syndrome exhibited a 70% lower AMPK activity in visceral adipose tissue as compared with both incidentalomas and control patients (P = 0.007 and P < 0.001, respectively). Downstream targets of AMPK fatty acid synthase and phosphoenol-pyruvate carboxykinase were up-regulated in patients with Cushing’s syndrome. AMPK activity was inversely correlated with 0900 h serum cortisol and with urinary free cortisol. Conclusions: Our data suggest that glucocorticoids inhibit AMPK activity in adipose tissue, suggesting a novel mechanism to explain the deposition of visceral adipose tissue and the consequent central obesity observed in patients with iatrogenic or endogenous Cushing’s syndrome.


2019 ◽  
Vol 37 (7_suppl) ◽  
pp. 571-571
Author(s):  
Wen-Hao Xu ◽  
Yuan-Yuan Qu ◽  
Jun Wang ◽  
Hai-Liang Zhang ◽  
Dingwei Ye

571 Background: Growing evidence has proved obesity one of the confirmed important etiologic indicators for renal cell carcinoma (RCC). CD36 is underpinned to be involved in adipose absorption, but its role in clear cell renal cell carcinoma (ccRCC) remains unclear. This study aimed to investigate the mRNA expression of CD36 in anthropometric measures of adipose tissue and defining its value in predicting prognosis in ccRCC patients. Methods: Real-Time qPCR was detected from 367 paired ccRCC and adjacent normal tissues. Distributions of categorical clinical-pathological data together with levels of CD36 expression were compared with χ2-test. Subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) were measured by MRI. Pearson’s correlation coefficient was utilized to quantify relations between body mass index (BMI), VAT%, SAT and CD36 expression respectively. Cox regression analysis were developed to address the influence of independent factors on prognostic value. Gene Set Enrichment Analysis (GSEA) was performed to select related genes and pathways from TCGA database. Results: In the current study, we demonstrated that CD36 mRNA was highly expressed in ccRCC tissues, and was found significantly increased in patients with advanced TNM stage ( p= 0.003, p< 0.001, p< 0.001), and high VAT% ( p= 0.004). Pearson’s correlation coefficient indicated CD36 amplification positively correlated with BMI ( r= 0.117, p= 0.025), VAT% ( r= 0.465, p< 0.001), while negatively with SAT ( r= -0.296, p= 0.002). Furthermore, ccRCC patients with elevated CD36 expression held shorter PFS and OS, with HR of 4.873 (3.300-7.196, p< 0.001) and 4.610 (2.956-7.189, p< 0.001). In 104 cases whose MRI scans were available, VAT was significantly correlated with poor PFS and OS. Significant genes were obtained from GSEA, and CD36 was found involved in the most significant pathways including fatty acid metabolism, angiogenesis and TGF-β signaling pathways. Conclusions: In conclusion, our study first reveal that elevated CD36 mRNA expression is positively correlated to distribution of abdominal adipose, particularly VAT%, which, in addition, notably predicts poor prognosis in ccRCC patients.


2007 ◽  
Vol 293 (4) ◽  
pp. E958-E964 ◽  
Author(s):  
Gregory R. Steinberg ◽  
Bruce E. Kemp ◽  
Matthew J. Watt

We have investigated the gene and protein expression of adipose triglyceride lipase (ATGL) and triglyceride (TG) lipase activity from subcutaneous and visceral adipose tissue of lean and obese subjects. Visceral and subcutaneous adipose tissue was obtained from 16 age-matched lean and obese subjects during abdominal surgery. Tissues were analyzed for mRNA expression of lipolytic enzymes by real-time quantitative PCR. ATGL protein content was assessed by Western blot and TG lipase activity by radiometric assessment. Subcutaneous and visceral adipose tissue of obese subjects had elevated mRNA expression of PNPLA2 (ATGL) and other lipases including PNPLA3, PNPLA4, CES1, and LYPLAL1 ( P < 0.05). Surprisingly, ATGL protein expression and TG lipase activity were reduced in subcutaneous adipose tissue of obese subjects. Immunoprecipitation of ATGL reduced total TG lipase activity in adipose lysates by 70% in obese and 83% in lean subjects. No significant differences in the ATGL activator CGI-58 mRNA levels ( ABHD5) were associated with obesity. These data demonstrate that ATGL is important for efficient TG lipase activity in humans. They also demonstrate reduced ATGL protein expression and TG lipase activity despite increased mRNA expression of ATGL and other novel lipolytic enzymes in obesity. The lack of correlation between ATGL protein content and in vitro TG lipase activity indicates that small decrements in ATGL protein expression are not responsible for the reduction in TG lipase activity observed here in obesity, and that posttranslational modifications may be important.


2020 ◽  
Author(s):  
Jiao Li ◽  
Xu-Fang Liang ◽  
Muhammad Shoaib Alam ◽  
Haocan Luo ◽  
Yanpeng Zhang ◽  
...  

Abstract Background: Chinese perch, a carnivorous fish, can accept artificial diet after domestication nowadays, and this farm way will gain high economic interest and sustainability. However, the high content and high quality requirement of dietary protein make it need the high cost in Chinese perch. Therefore, the aim of this study was to explore the effect of fish meal replacement by low- or high-rapeseed meal on growth performance, feeding, lipid and glucose metabolism. Methods: Three experimental diets were formulated with 0, 10% and 30% rapeseed meal, named as control, RSL and RSH, groups respectively. After the 8-week of feeding trial, growth performance, lipid metabolism and AMPK-mTOR-signal pathways were measured. Results: Chinese perch fed with RSH and RSL diets showed significantly decreased WG, SGR, BFR, VSI, MSI and the whole-body crude lipid compared to those fed with the control diet (P < 0.05). Fish in RSL group decreased feed intake, serum LDL-C, hepatic mRNA expression of LPL, PEPCK and phosphorylated Grb10 (P < 0.05). In visceral adipose tissue, mRNA expression of FAS, SREBP1, ACC1, HL, CPT1 and PEPCK were all significantly down-regulated (P < 0.05). Fish in RSH group showed phosphorylated AMPK, hepatic mRNA expression of SREBP1, ACC1, FAS, PPARα and CPT1 were down-regulated, while HSL, G6PD and PC were up-regulated (P < 0.05). In visceral adipose tissue, mRNA expressions of SREBP1, LPL, CPT1 and PEPCK were down-regulated, while mRNA expression of HSL was up-regulated (P < 0.05). Conclusions: Chinese perch fed with RSL and RSH diets showed decreased fat deposition in viscera. Fish fed with low level of rapeseed meal diet ate less diet, which caused inhibited lipid metabolism in the liver and visceral adipose tissues.Fish fed with high level of rapeseed meal diet inhibited hepatic FA synthesis, activated lipolysis, hence reducing Acetyl-CoA pool. In turn, β-oxidation were inhibited, glycolysis was activated, thus lipid accumulation was decreased. In visceral adipose tissue, lipid uptake was inhibited, caused inhibited FA synthesis, β-oxidation, glycerol synthesis, and improved lipolysis.


2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Annelie Shami ◽  
Suzanne Aarts ◽  
Christina Bürger ◽  
Pascal Kusters ◽  
Susan van den Berg ◽  
...  

Introduction: The co-stimulatory dyad CD40-CD40L plays a central role in fine-tuning immune reactions in atherosclerosis, obesity-induced inflammation and multiple sclerosis (MS). Inhibition of CD40 in atherosclerosis and experimental autoimmune encephalomyelitis (EAE) ameliorates disease outcome, whereas CD40-deficiency in a diet induced obesity (DIO) model worsens insulin resistance and induces excessive adipose tissue inflammation. Although inhibition of CD40 has powerful effects, we do not know which CD40 expressing cell-type is responsible for the amelioration/aggravation of disease. As myeloid CD40 is known to play a role in leukocyte trafficking, which is important in atherosclerosis, obesity and neuro-inflammation, we hypothesize that myeloid CD40 is important in these disease modalities. Methods: To investigate the role of myeloid CD40 in atherosclerosis, obesity and EAE we have generated macrophage specific LysM-CD40flfl - (ApoE-/-), and dendritic cell/adipose tissue macrophage specific CD11C-CD40flfl). Atherosclerosis was induced by aging the LysM-CD40flfl - ApoE-/- mice until 30 weeks. EAE was induced in LysM-CD40flfl mice by subjecting them to myelin oligodendrocyte glycoprotein peptide (MOG35-55), and LysM-CD40flfl and CD11c-CD40flfl mice were subjected to a 60% high fat diet for 18 wks. Results: LysM-CD40flfl - ApoE-/- mice showed a significant reduction in atherosclerotic plaque area, with a reduced macrophage accumulation. Loss of macrophage CD40 in EAE results in a significant decrease in the neurological symptoms of EAE, and a majority of the LysM-CD40flfl mice were fully protected against EAE. LysM-CD40flfl mice subjected to DIO showed an increase in macrophage accumulation in the visceral adipose tissue, but did not affect adipose tissue mass, insulin tolerance, or plasma triglyceride concentrations. The CD11CcreCD40flfl mice exhibited a decrease in visceral adipose tissue weight, an increased lipid content in the liver and slightly decreases leukocyte numbers and pro-inflammatory gene expression in the adipose tissue. Conclusions: Macrophage CD40 is an important driver of atherosclerosis and EAE. Macrophage CD40 is protective in obesity-induced inflammation, but is probably not the key player.


2011 ◽  
Vol 164 (4) ◽  
pp. 539-547 ◽  
Author(s):  
Ximena Terra ◽  
Yunuen Quintero ◽  
Teresa Auguet ◽  
Jose Antonio Porras ◽  
Mercé Hernández ◽  
...  

ObjectiveThe adipocyte/macrophage fatty acid-binding protein 4 (FABP4) has been described as a biomarker for adiposity and metabolic syndrome (MS). The aims of this study were to assess the relationship between FABP4 and inflammatory cytokines related to obesity, and to evaluate FABP4 mRNA expression in visceral and subcutaneous adipose tissue in non-diabetic morbidly obese women versus healthy lean women.MethodsWe analyzed circulating levels of FABP4 in 81 Spanish women: 38 lean (body mass index (BMI)<25 kg/m2) and 43 morbidly obese (BMI>40 kg/m2). We took 30 follow-up blood samples at 6 and 12 months after bariatric surgery. We assessed FABP4 gene expression in samples of subcutaneous abdominal and visceral adipose tissue. Adipose tissue mRNA expression was determined by real-time RT-PCR.ResultsIn morbidly obese women, plasma FABP4 levels were significantly higher than in non-obese patients. These levels positively correlated with BMI, homeostasis model assessment of insulin resistance (HOMA2-IR), and plasma glucose and insulin levels. Post-operative FABP4 levels decreased by a maximum of 30% after 12 months. We also found an inverse association between FABP4 and adiponectin levels, and positive correlations between FABP4 and circulating leptin, tumor necrosis factor (TNF) receptors, C-reactive protein (CRP) and interleukin 6 levels. Linear regression analysis revealed that FABP4 was more closely related to HOMA2-IR than adiponectin, CRP, TNF-RI, or leptin. Furthermore, high circulating FABP4 levels were associated with the presence of MS. FABP4 mRNA expression in visceral adipose tissue was related to its circulating levels in morbidly obese women.ConclusionsOur results indicate that serum FABP4 is associated with inflammatory factors related to obesity and MS in non-diabetic morbidly obese women.


2014 ◽  
Vol 9 (S 01) ◽  
Author(s):  
T Wohland ◽  
D Schleinitz ◽  
M Kern ◽  
M Prellberg ◽  
J Breitfeld ◽  
...  

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