Mo1747 Adipose Tissue From Visceral Fat Has Much Higher Expression of IBD Susceptibility Genes Compared to Subcutaneous Fat

2015 ◽  
Vol 148 (4) ◽  
pp. S-701
Author(s):  
Maneesh Dave ◽  
Fabio Cominelli ◽  
Farren B. Briggs
2015 ◽  
Vol 9 (11-12) ◽  
pp. 795 ◽  
Author(s):  
Ilker Akarken ◽  
Hüseyin Tarhan ◽  
Rahmi Gökhan Ekin ◽  
Özgür Çakmak ◽  
Gökhan Koç ◽  
...  

Introduction: We examined the relationship between stone disease and the amount of visceral adipose tissue measured with unenhanced computed tomography (CT).Methods: We included 149 patients with complaints of flank pain and kidney stones detected by CT, from August 2012 to April 2013. In addition, as the control group we included 139 healthy individuals, with flank pain within the same time period, with no previous history of urological disease and no current kidney stones identified by CT. Patients were analyzed for age, gender, body mass index, amount of visceral and subcutaneous adipose tissue, and serum level of low-density lipoprotein and triglyceride.Results: There were no differences between groups in terms of gender and age (p = 0.27 and 0.06, respectively). Respective measurements for the stone and control groups for body mass index were 29.1 and 27.6 kg/m2; for visceral fat measurement 186.0 and 120.2 cm2; and for subcutaneous fat measurements 275.9 and 261.9 cm2 (p = 0.01; 0.01 and 0.36, respectively). Using multivariate analysis, the following factors were identified as increasing the risk of kidney stone formation: hyperlipidemia (p = 0.003), hypertension (p = 0.001), and ratio of visceral fat tissue to subcutaneous fat tissue (p = 0.01). Our study has its limitations, including its retrospective nature, its small sample size, possible selection bias, and missing data. The lack of stone composition data is another major limitation of our study.Conclusion: The ratio of visceral to subcutaneous adipose tissue, in addition to obesity, hyperlipidemia, and hypertension, was identified as an emerging factor in the formation of kidney stones.


2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Christine Vrakas ◽  
Sheri E Keleman ◽  
Rosario Scalia ◽  
Michael V Autieri

Uncontrolled inflammation leads to many of the chronic diseases associated with obesity. Due to a lack of oxygen in the tissue, expanding adipose tissue becomes hypoxic and pro-inflammatory. Adipocytes release pro-angiogenic factors in an effort to restore blood flow to the tissue. Presently, little is known about the potential for endogenously expressed anti-inflammatory cytokines to attenuate inflammation and also provide pro-angiogenic effects. IL-19 is uniquely anti-inflammatory, pro-angiogenic and is both expressed by and targets various cells types. IL-19 expression in adipocytes and stromal vascular cells is increased in visceral compared to subcutaneous fat, and is also increased in visceral fat on high fat diet (HFD) compared to normal chow diet. There is no known mechanism to explain the role of IL-19 in adipose tissue expansion, and we hypothesized that IL-19 may have pro-angiogenic and anti-inflammatory properties in expanding adipose tissue. We have identified a gene regulatory factor, Interleukin Enhancer-Binding Factor 3 (ILF3) that is induced in adipocytes and stromal vascular cells by HFD and IL-19 treatment. We found that both IL-19 and VEGF induce ILF3 expression in cultured human endothelial cells (hECs). Proliferation is significantly reduced when ILF3 is knocked down using siRNA in hECs. Furthermore, when ILF3 is knocked down and hECs are stimulated with VEGF several angiogenic cytokines are also decreased. Through immunohistochemistry we found that ILF3 translocates from the nucleus to the cytoplasm in visceral fat of C57BL/6 mice fed a HFD, and remains in the nucleus when fed a normal chow diet. In summary IL-19 may be a unique HFD responsive adipokine functioning to reduce inflammation and increase angiogenesis in expanding adipose tissue. The angiogenic function of IL-19 may work through induction of the gene regulatory factor, ILF3.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Eung Ju Kim ◽  
Hong Seog Seo ◽  
Sungeun Kim ◽  
Jin Oh Na ◽  
Jae Hyoung Park ◽  
...  

Background: Visceral adipose tissue is thought to confer increased cardiovascular risk through leukocyte infiltration and increased adipose macrophage activity. Previous positron emission tomography (PET) studies using fluorodeoxyglucose (FDG) demonstrated that increased FDG uptake could reflect the severity of inflammation in atherosclerotic plaque. We hypothesized that active atherosclerotic change in the major arteries would accompany increased inflammation within visceral fat and it could be detected in humans using combined FDG PET/computed tomography (CT). Methods: We observed 44 consecutive subjects with cardiovascular disease. For all of them, an one-hour PET/CT (from brain to foot) was performed after injection of FDG (370–555 MBq). FDG uptake in the aorta or its major branches was evaluated visually and semiquantitatively. Maximal standard uptake values (SUV) of the highest regions of interest were calculated in the subcutaneous fat and visceral fat area, separately. Results: Significant FDG uptake in the arterial wall was noted in 21 patients (plaque positive; PP group), all of whom have experienced acute cardiovascular events (acute coronary syndrome or ischemic stroke) within a week. The other 23 patients (plaque negative; PN group) had chronic stable angina or asymptomatic carotid stenosis. Visceral fat SUV was significantly higher as compared to subcutaneous fat SUV (0.49± 0.15 vs. 0.15± 0.05, p< 0.001) in PP group, whereas there was no significant difference in PN group (0.18± 0.07 vs. 0.16± 0.03, p= 0.622). When we compared two groups, PP group showed higher visceral fat SUV than PN group (p< 0.001). In terms of subcutaneous fat SUV, the results were similar in two groups (p= 0.773). Conclusions: We demonstrated that atherosclerotic plaque inflammation was associated with increased inflammation within visceral fat. Our results need to be confirmed by comparison with histologic or other imaging findings. Further evaluation to determine whether metabolic activity of visceral adipose tissue is a marker or mediator of vascular inflammation is also needed.


2007 ◽  
Vol 293 (1) ◽  
pp. E316-E326 ◽  
Author(s):  
Haifei Shi ◽  
April D. Strader ◽  
Stephen C. Woods ◽  
Randy J. Seeley

White adipose tissue is the principal site for lipid accumulation. Males and females maintain distinctive white adipose tissue distribution patterns. Specifically, males tend to accumulate relatively more visceral fat, whereas females accumulate relatively more subcutaneous fat. The phenomenon of maintaining typical sex-specific fat distributions suggests sex-specific mechanisms that regulate energy balance and adiposity. We used two distinct approaches to reduce fat mass, caloric restriction (CR), and surgical fat removal (termed lipectomy) and assessed parameters involved in the regulation of energy balance. We found that male and female mice responded differentially to CR- and to lipectomy-induced fat loss. Females decreased energy expenditure during CR or after lipectomy. In contrast, males responded by eating more food during food return after CR or after lipectomy. Female CR mice conserved subcutaneous fat, whereas male CR mice lost adiposity equally in the subcutaneous and visceral depots. In addition, female mice had a reduced capability to restore visceral fat after fat loss. After CR, plasma leptin levels decreased in male but not in female mice. The failure to increase food intake after returning to ad libitum intake in females could be due to the relatively stable levels of leptin. In summary, we have found sexual dimorphisms in the response to fat loss that point to important underlying differences in the strategies by which male and female mice regulate body weight.


Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1855
Author(s):  
A. Al-Dibouni ◽  
R. Gaspar ◽  
S. Ige ◽  
S. Boateng ◽  
F. R. Cagampang ◽  
...  

Obesity is a major risk factor for a plethora of metabolic disturbances including diabetes and cardiovascular disease. Accumulating evidence is showing that there is an adipose tissue depot-dependent relationship with obesity-induced metabolic dysfunction. While some adipose depots, such as subcutaneous fat, are generally metabolically innocuous, others such as visceral fat, are directly deleterious. A lesser known visceral adipose depot is the pericardial adipose tissue depot. We therefore set out to examine its transcriptional and morphological signature under chow and high-fat fed conditions, in comparison with other adipose depots, using a mouse model. Our results revealed that under chow conditions pericardial adipose tissue has uncoupling-protein 1 gene expression levels which are significantly higher than classical subcutaneous and visceral adipose depots. We also observed that under high-fat diet conditions, the pericardial adipose depot exhibits greatly upregulated transcript levels of inflammatory cytokines. Our results collectively indicate, for the first time, that the pericardial adipose tissue possesses a unique transcriptional and histological signature which has features of both a beige (brown fat-like) but also pro-inflammatory depot, such as visceral fat. This unique profile may be involved in metabolic dysfunction associated with obesity.


Author(s):  
Thomas Später ◽  
Julia E. Marschall ◽  
Lea K. Brücker ◽  
Ruth M. Nickels ◽  
Wolfgang Metzger ◽  
...  

Abstract Background: Adipose tissue-derived microvascular fragments (MVF) represent effective vascularization units for tissue engineering. Most experimental studies in rodents exclusively use epididymal adipose tissue as a visceral fat source for MVF isolation. However, in future clinical practice, MVF may be rather isolated from liposuctioned subcutaneous fat tissue of patients. Therefore, we herein compared the vascularization characteristics of MVF isolates from visceral and subcutaneous fat tissue of murine origin. Methods: MVF isolates were generated from visceral and subcutaneous fat tissue of donor mice using two different enzymatic procedures. For in vivo analyses, the MVF isolates were seeded onto collagen-glycosaminoglycan scaffolds and implanted into full-thickness skin defects within dorsal skinfold chambers of recipient mice. Results: By means of the two isolation procedures, we isolated a higher number of MVF from visceral fat tissue when compared to subcutaneous fat tissue, while their length distribution, viability and cellular composition were comparable in both groups. Intravital fluorescence microscopy as well as histological and immunohistochemical analyses revealed a significantly reduced vascularization of implanted scaffolds seeded with subcutaneous MVF isolates when compared to implants seeded with visceral MVF isolates. Light and scanning electron microscopy showed that this was due to high amounts of undigested connective tissue within the subcutaneous MVF isolates, which clogged the scaffold pores and prevented the interconnection of individual MVF into new microvascular networks. Conclusion: These findings indicate the need for improved protocols to generate connective tissue-free MVF isolates from subcutaneous fat tissue for future translational studies.


Author(s):  
Chen-Yu Liao ◽  
Oona M P Kummert ◽  
Amanda M Bair ◽  
Nora Alavi ◽  
Josef Alavi ◽  
...  

Abstract Autophagy, a process catabolizing intracellular components to maintain energy homeostasis, impacts aging and metabolism. Spermidine, a natural polyamine and autophagy activator, extends lifespan across a variety of species, including mice. In addition to protecting cardiac and liver tissue, spermidine also affects adipose tissue through unexplored mechanisms. Here, we examined spermidine in the links between autophagy and systemic metabolism. Consistently, daily injection of spermidine delivered even at late life is sufficient to cause a trend in lifespan extension in wild type mice. We further found that spermidine has minimal metabolic effects in young and old mice under normal nutrition. However, spermidine counteracts HFD (high-fat diet)-induced obesity by increasing lipolysis in visceral fat. Mechanistically, spermidine increases the hepatokine FGF21 expression in liver without reducing food intake. Spermidine also modulates FGF21 in adipose tissues, elevating FGF21 expression in subcutaneous fat, but reducing it in visceral fat. Despite this, FGF21 is not required for spermidine action, since Fgf21  -/- mice were still protected from HFD. Furthermore, the enhanced lipolysis by spermidine was also independent of autophagy in adipose tissue, given that adipose-specific autophagy deficient (Beclin-1  flox/+  Fabp4-cre) mice remained spermidine-responsive under HFD. Our results suggest that the metabolic effects of spermidine occurs through systemic changes in metabolism, involving multiple mechanistic pathways.


2013 ◽  
Vol 10 (2) ◽  
pp. 23-27
Author(s):  
T N Markova ◽  
V A Kichigin ◽  
V N Diomidova ◽  
D S Markov ◽  
O V Petrova

We performed an estimation of body fat using ultrasound, magnetic resonance imaging (MRI) and anthropometry in 60 patients with different types of body weight (BW). Correlation of waist circumference (WC), thickness of subcutaneous fat and visceral fat with components of the metabolic syndrome was studied comparatively between ultrasound and MRI measurements. We noted a preferential increase in the thickness of visceral fat compared with subcutaneous with increasing degree of BW. Significant increase in adipose tissue and the development of metabolic disorders occurs in overweight, making it the state close to obesity. During a routine ultrasound of the abdomen it is advisable to determine the thickness of subcutaneous and visceral fat separately.


2013 ◽  
Vol 60 (3) ◽  
pp. 25-30 ◽  
Author(s):  
A. Djuric-Stefanovic ◽  
D. Vasin ◽  
S. Jovanovic ◽  
Lj. Lazic ◽  
J. Kovac ◽  
...  

Visceral fat is considered a key factor in the development of metabolic syndrome and other pathological conditions and diseases associated with obesity. Therefore, analysis of the dynamics of reducing the amount of abdominal visceral fat is important for evaluating the therapeutic effects of different modalities of obesity treatment, including bariatric surgery. In 53 obese patients visceral and subcutaneous abdominal adipose tissue was measured by ultrasonography (US) before and after bariatric surgery, in the period of 1, 3, 6 months. At the same time, standard anthropometric parameters were assessed: body mass (m), BMI, waist circumference (WC), and hip circumference (HC). Five diameters of the visceral abdominal fat (VAF) were measured: IAFT (Intraabdominal Fat Thickness), LV (Lienal Vein), VF (Visceral Fat), MES sum (Mesenterial leafs) and Max PFT (Maximal Preperitoneal Fat Thickness), and three diameters of the subcutaneous abdominal adipose tissue (SCAF): Min SFT (Minimal Subcutaneous Fat), and MaxSFTa and MaxSFTb (Maximal Subcutaneous Fat Thickness a and b). Statistically significant decrease in all anthropometric parameters, except HC was registered 1, 3 and 6 months after the surgery. We registered the decline of almost all US diameters of abdominal adipose tissue in the follow-up period, but statistically significant decrease were found only in the diameters of visceral adipose tissue: IAFT after 1 and 3 months (p=0.031 and p=0.027); VF after 1 month (p=0.031), LV after 6 months (p=0.011), and MESsum after 3 and 6 months (p=0.001 and p=0.028), as well as MaxSFTb, at 1 month follow-up (p=0.015). In the short- term follow-up period after the bariatric surgery, there was a significant decrease in body mass, BMI and WC, and ultrasonography revealed a significant reduction in the diameters of the visceral abdominal fat.


2016 ◽  
Vol 310 (3) ◽  
pp. E238-E247 ◽  
Author(s):  
Almudena Veiga-Lopez ◽  
Jacob Moeller ◽  
Rohit Sreedharan ◽  
Kanakadurga Singer ◽  
Carey Lumeng ◽  
...  

Among potential contributors for the increased incidence of metabolic diseases is the developmental exposure to endocrine-disrupting chemicals such as bisphenol A (BPA). BPA is an estrogenic chemical used in a variety of consumer products. Evidence points to interactions of BPA with the prevailing environment. The aim of this study was to assess the effects of prenatal exposure to BPA on postnatal metabolic outcomes, including insulin resistance, adipose tissue distribution, adipocyte morphometry, and expression of inflammatory markers in adipose tissue as well as to assess whether postnatal overfeeding would exacerbate these effects. Findings indicate that prenatal BPA exposure leads to insulin resistance in adulthood in the first breeder cohort ( study 1), but not in the second cohort ( study 2), which is suggestive of potential differences in genetic susceptibility. BPA exposure induced adipocyte hypertrophy in the visceral fat depot without an accompanying increase in visceral fat mass or increased CD68, a marker of macrophage infiltration, in the subcutaneous fat depot. Cohens effect size analysis found the ratio of visceral to subcutanous fat depot in the prenatal BPA-treated overfed group to be higher compared with the control-overfed group. Altogether, these results suggest that exposure to BPA during fetal life at levels found in humans can program metabolic outcomes that lead to insulin resistance, a forerunner of type 2 diabetes, with postnatal obesity failing to manifest any interaction with prenatal BPA relative to insulin resistance and adipocyte hypertrophy.


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