scholarly journals The Relationships of Plasma Adiponectin with a Favorable Lipid Profile, Decreased Inflammation, and Less Ectopic Fat Accumulation Depend on Adiposity

2006 ◽  
Vol 52 (10) ◽  
pp. 1934-1942 ◽  
Author(s):  
Konstantinos Kantartzis ◽  
Killian Rittig ◽  
Bernd Balletshofer ◽  
Jürgen Machann ◽  
Fritz Schick ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Endothelial Function ◽  
Visceral Adipose Tissue ◽  
Hdl Cholesterol ◽  
Ectopic Fat ◽  
Fat Accumulation ◽  
Plasma Adiponectin ◽  
Markers Of Inflammation ◽  
Visceral Adipose ◽  
The Relationship

Abstract Background: The metabolic effects of adiponectin, including insulin sensitivity, seem to become stronger with increasing adiposity. Adiposity may also affect the relationship of adiponectin concentrations with serum lipid profile; markers of inflammation, atherosclerosis, and endothelial function; and ectopic fat accumulation. Methods: We measured plasma adiponectin concentrations, serum lipids, and serum markers of inflammation, atherosclerosis, and endothelial function in 242 Caucasians without type 2 diabetes. We also measured visceral adipose tissue with magnetic resonance tomography and liver and intramyocellular fat with 1H magnetic resonance spectroscopy. Results: We divided the study participants into 2 groups: lean [mean (SE) total body fat, 26% (0.6%); n = 119] and obese [36% (0.6%); n = 123]. In the obese group, plasma adiponectin concentrations showed a strong positive association with concentrations of HDL cholesterol (P <0.0001) and negative associations with LDL cholesterol, triglycerides, high-sensitivity C-reactive protein, interleukin 6, apolipoprotein B100, soluble E-selectin, soluble vascular cellular adhesion molecule 1, plasminogen activator inhibitor 1, leukocyte count, and liver and intramyocellular fat (all P <0.03). In the lean group, adiponectin showed a less strong association with HDL cholesterol (P = 0.005) and liver fat (P = 0.03) and no significant associations with the other variables (all P >0.10). High visceral adipose tissue was a strong predictor of low adiponectin concentrations, particularly in the obese group, and attenuated many of the significant relationships. Conclusions: High adiponectin plasma concentrations are associated with favorable lipid profiles, decreased subclinical inflammation, decreased markers of atherosclerosis and endothelial function, and low ectopic fat accumulation, particularly in obese persons. Adiponectin may also have a concentration-related effect on the relationship between visceral adipose tissue and these metabolic characteristics, especially in obese persons.

scholarly journals Vascular Adhesion Protein 1 Mediates Gut Microbial Flagellin-Induced Inflammation, Leukocyte Infiltration, and Hepatic Steatosis

Sci ◽  
2021 ◽  
Vol 3 (1) ◽  
pp. 13
Author(s):  
Raine Toivonen ◽  
Sanja Vanhatalo ◽  
Maija Hollmén ◽  
Eveliina Munukka ◽  
Anniina Keskitalo ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Hepatic Steatosis ◽  
Visceral Adipose Tissue ◽  
Leukocyte Infiltration ◽  
Fat Accumulation ◽  
Adhesion Protein ◽  
Hepatic Fat ◽  
Vascular Adhesion ◽  
Visceral Adipose ◽  
Vascular Adhesion Protein 1

Toll-like receptor 5 ligand, flagellin, and vascular adhesion protein 1 (VAP-1) are involved in non-alcoholic fatty liver disease. This study aimed to determine whether VAP-1 mediates flagellin-induced hepatic fat accumulation. The effects of flagellin on adipocyte VAP-1 expression were first studied in vitro. Then, flagellin (100 ng/mouse) or saline was intraperitoneally injected into C57BL/6J (WT) and C57BL/6-Aoc3-/- (VAP-1 KO) mice on a high-fat diet twice a week every 2 weeks for 10 weeks. After that, the effects on inflammation, insulin signaling, and metabolism were studied in liver and adipose tissues. Hepatic fat was quantified histologically and biochemically. Because flagellin challenge increased VAP-1 expression in human adipocytes, we used VAP-1 KO mice to determine whether VAP-1 regulates the inflammatory and metabolic effects of flagellin in vivo. In mice, VAP-1 mediated flagellin-induced inflammation, leukocyte infiltration, and lipolysis in visceral adipose tissue. Consequently, an increased release of glycerol led to hepatic steatosis in WT, but not in KO mice. Flagellin-induced hepatic fibrosis was not mediated by VAP-1. VAP-1 KO mice harbored more inflammation-related microbes than WT mice, while flagellin did not affect the gut microbiota. Our results suggest that by acting on visceral adipose tissue, flagellin increased leukocyte infiltration that induced lipolysis. Further, the released glycerol participated in hepatic fat accumulation. In conclusion, the results describe that gut microbial flagellin through VAP-1 induced hepatic steatosis.

Non-HDL cholesterol relates to pro-inflammatory status of human visceral adipose tissue

2016 ◽  
Vol 252 ◽  
pp. e182
Author(s):  
R. Poledne ◽  
I. Kralova Lesna ◽  
A. Kralova ◽  
A. Sekerkova ◽  
J. Fronek
Keyword(s):  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Hdl Cholesterol ◽  
Inflammatory Status ◽  
Visceral Adipose

scholarly journals IRGMGene Variants Modify the Relationship Between Visceral Adipose Tissue and NAFLD in Patients With Crohn’s Disease

2018 ◽  
Vol 24 (10) ◽  
pp. 2247-2257 ◽  
Author(s):  
Tracey G Simon ◽  
Kimberley W J Van Der Sloot ◽  
Samantha B Chin ◽  
Amit D Joshi ◽  
Paul Lochhead ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Visceral Adipose Tissue ◽  
Visceral Adipose ◽  
The Relationship

scholarly journals Chronic inflammation in psoriasis promotes visceral adipose tissue association with lipid-rich necrotic core through atherogenic myeloid score

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
G A Manyak ◽  
N H Patel ◽  
A K Dey ◽  
M Svirydava ◽  
P Parel ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Adipose Tissue ◽  
Coronary Artery ◽  
High Risk ◽  
Visceral Adipose Tissue ◽  
Myeloid Cells ◽  
Necrotic Core ◽  
Artery Disease ◽  
Visceral Adipose ◽  
The Relationship

Abstract Background/Introduction Psoriasis is a chronic inflammatory condition associated with adipose dysfunction and high-risk coronary artery disease features, including non-calcified coronary burden (NCB) and lipid-rich necrotic core (LRNC). Visceral adipose tissue (VAT) is a metabolically-active depot that secretes inflammatory and proatherogenic factors, and is associated with increased NCB. Additionally, an atherogenic myeloid score (AMS) comprised of classical monocytes, low-density granulocytes, and platelets was shown to associate with psoriasis severity and NCB. Purpose To investigate the relationship between VAT and high-risk plaque features and test whether this relationship was potentially mediated by myeloid cells. Methods A cohort of 131 psoriasis patients were included in this study. Atherogenic myeloid score components were calculated using complete blood count data (platelets) and by flow cytometry (monocytes, LDGs). Coronary NCB and LRNC were quantified using QAngio and vascuCAP respectively. VAT was defined as intra-abdominal fat and was quantified using an automated contouring software with abdominal CT scans. Statistical analyses were performed using STATA 12. Results The cohort was middle-aged 50 (42–61) (median (IQR)), and predominantly male (61%). High VAT vs low VAT groups differed significantly in their NCB ((0.910±0.279) vs (1.431±0.517)); p<0.001), (mean ± SD). After adjustment for cardiovascular risk factors, VAT associated with the atherogenic myeloid score (β=0.221, p=0.044), with LRNC (β=0.128, p=0.047), and atherogenic myeloid score associated with LRNC (β=0.161, p=0.003). The relationship of VAT to LRNC was partially mediated by atherogenic myeloid score (25.14%, p=0.029) (Figure 1). Conclusions VAT associated with LRNC, and this relationship was partially mediated by the atherogenic myeloid score. These findings suggest that bioactive VAT may impart risk on coronary artery disease in part through myeloid cells. FUNDunding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): National Heart, Lung, and Blood Institute Intramural Research Program in Bethesda, Maryland Figure 1. Log-transformed atherogenic myeloid score partially mediates the relationship between VAT and log-transformed LRNC. Adjusted by Framingham Risk Score, PASI score, biologic therapy, statin therapy, type 2 diabetes, hyperlipidemia, and subcutaneous adipose tissue volume. Red arrow: represents indirect effect; Beta: standard regression coefficient.

scholarly journals Adipocyte differentiation impairment as well as lipid metabolism and transport problems – major causes of genetic lipodystrophies

2019 ◽  
Vol 73 ◽  
pp. 741-761
Author(s):  
Agnieszka Dettlaff-Pokora
Keyword(s):  
Adipose Tissue ◽  
Primary Care Physicians ◽  
Adipocyte Differentiation ◽  
Plasma Cholesterol ◽  
Correct Diagnosis ◽  
Hdl Cholesterol ◽  
Diagnostic Methods ◽  
Tissue Loss ◽  
Ectopic Fat ◽  
Fat Accumulation

Lipodystrophies are heterogenic group of adipose tissue disorders with its general or partial atrophy. In case of congenital lipodystrophies disturbances of adipogenesis or/and alterations of adipocyte differentiation often occur leading to thermogenic adipocytes formation. Basic adipocyte functions can be perturbed, including improper synthesis of triacylglycerols and phospholipids of lipid droplet, but also impaired fatty acids release and intracellular lipid traffic. Lipodystrophy can result from weakening of adipose tissue structure, but also from improper function of both cytoskeleton and nuclear lamina leading to cell dysfunction. Lack of adipose tissue leads to a) increased plasma triacylglycerols level and ectopic fat accumulation in other tissues; b) total plasma cholesterol increase; c) plasma HDL-cholesterol decrease. Ectopic fat accumulation in liver can cause fatty liver and with time can lead to hepatomegaly and liver cirrhosis. Dysfunctions are proportional to the extent of fat tissue loss with generalized lipodystrophies patients developing complications at early ages. Diabetes and insulin resistance are common comorbidities. Improvement of diagnostic methods of medical genetics allows precise determination of their genotypes and correct diagnosis of patients suffering from lipodystrophy. For that reason number of described cases increased in recent years, also in Poland. New lipodystrophy types were described. Therefore there is a need to bring lipodystrophy syndromes for the attention of primary care physicians, pediatricians and endocrinologists.

Abstract P206: Estimation of Directly Quantified Visceral Adipose Tissue Using Cardiometabolic Biomarkers

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Tiffany M Powell-Wiley ◽  
Josh Hasan ◽  
Parasuram Krishnamoorthy ◽  
Elizabeth Weiner ◽  
Jenny Dave ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
High Sensitivity ◽  
Visceral Adiposity ◽  
Anthropometric Measures ◽  
Linear Regression Modeling ◽  
Inferior Border ◽  
Visceral Adipose ◽  
The Relationship

Background: Visceral adipose tissue (VAT) has been linked to increased cardiovascular (CV) risk. Furthermore, there is limited data on how anthropometric measures and known markers of cardiometabolic disease (CMD) relate to the presence of VAT. Therefore, the aim of this study was to define how CMD biomarkers relate to directly-quantified volume-based measures of VAT using computed tomography (CT) scan measurements in a well-phenotyped sample of patients from an ongoing cohort study of inflammation and CMD. Methods and Results: We evaluated the relationship between directly measured VAT, anthropometric measures [body mass index (BMI), waist circumference (WC), waist-to-hip ratio (WHR)] and CMD biomarkers [lipoproteins, lipoprotein particle size, high sensitivity C-reactive protein (hsCRP), insulin resistance markers] in a longitudinal study of CV risk predictors in chronic inflammation (NCT: NCT01778569). Patients underwent blood testing and CT to measure the sum of visceral adipose tissue between the diaphragm and the inferior border of the urinary bladder (slice 50-150 SumVAT) during a single baseline visit in 2012-2013 (N=42), resulting in a validated, volume-based measurement of VAT. Linear regression modeling was used to understand the relationship between VAT, anthropometric measures and CMD biomarkers. Those with higher levels of visceral adiposity were more likely to be male (p=0.05) and have higher BMI. Adjusting for age, sex, race, physical activity, smoking, and CV risk factors, HDL, hsCRP, insulin, and HOMA-IR were independent predictors of 50-150 SumVAT (Table). Conclusions: Markers of lipid metabolism, inflammation, and insulin resistance serve as independent predictors of visceral adiposity and may be useful surrogates to estimate VAT when volume-based CT measures are not possible. Therefore, these biomarkers may be used to evaluate cardio-metabolic risk in areas with limited access to imaging for defining visceral adiposity, particularly community-based settings.

scholarly journals Overproduction of endothelin-1 impairs glucose tolerance but does not promote visceral adipose tissue inflammation or limit metabolic adaptations to exercise

2019 ◽  
Vol 317 (3) ◽  
pp. E548-E558 ◽  
Author(s):  
Thomas J. Jurrissen ◽  
Zachary I. Grunewald ◽  
Makenzie L. Woodford ◽  
Nathan C. Winn ◽  
James R. Ball ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Glucose Tolerance ◽  
Visceral Adipose Tissue ◽  
Wheel Running ◽  
Obese Mice ◽  
Endothelin 1 ◽  
Markers Of Inflammation ◽  
Metabolic Adaptations ◽  
Wide Range ◽  
Visceral Adipose

Endothelin-1 (ET-1) is a potent vasoconstrictor and proinflammatory peptide that is upregulated in obesity. Herein, we tested the hypothesis that ET-1 signaling promotes visceral adipose tissue (AT) inflammation and disrupts glucose homeostasis. We also tested if reduced ET-1 is a required mechanism by which exercise ameliorates AT inflammation and improves glycemic control in obesity. We found that 1) diet-induced obesity, AT inflammation, and glycemic dysregulation were not accompanied by significantly increased levels of ET-1 in AT or circulation in wild-type mice and that endothelial overexpression of ET-1 and consequently increased ET-1 levels did not cause AT inflammation yet impaired glucose tolerance; 2) reduced AT inflammation and improved glucose tolerance with voluntary wheel running was not associated with decreased levels of ET-1 in AT or circulation in obese mice nor did endothelial overexpression of ET-1 impede such exercise-induced metabolic adaptations; 3) chronic pharmacological blockade of ET-1 receptors did not suppress AT inflammation in obese mice but improved glucose tolerance; and 4) in a cohort of human subjects with a wide range of body mass indexes, ET-1 levels in AT, or circulation were not correlated with markers of inflammation in AT. In aggregate, we conclude that ET-1 signaling is not implicated in the development of visceral AT inflammation but promotes glucose intolerance, thus representing an important therapeutic target for glycemic dysregulation in conditions characterized by hyperendothelinemia. Furthermore, we show that the salutary effects of exercise on AT and systemic metabolic function are not contingent on the suppression of ET-1 signaling.

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