Stress in Obesity and Associated Metabolic and Cardiovascular Disorders

Holvoet, Paul

doi:10.6064/2012/205027

Cited by 37 publications

(39 citation statements)

References 201 publications

(204 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Meanwhile, TNF-α activates CD4 + Th 1 cells and CD8 + effector T cells, leading to proinflmmatory macrophage stimulation (Holvoet, 2012;Lafontan, 2014). This study found that RAW 264.7 macrophages treated with exosomes isolated from ob/ob mice led to higher production of IL-6 and TNF-α when compared to +/+ mice.…”

Section: Discussionmentioning

confidence: 65%

“…During obesity, adipocytes secrete exosomes, which are absorbed by monocytes, and the monocytes further migrate into adipose tissues and differentiate into macrophages (Hajer et al, 2008;Holvoet, 2012). Meanwhile, TNF-α activates CD4 + Th 1 cells and CD8 + effector T cells, leading to proinflmmatory macrophage stimulation (Holvoet, 2012;Lafontan, 2014).…”

Section: Discussionmentioning

confidence: 99%

“…Large adipocytes release fatty acids which can bind to macrophage toll-like receptor-4 (TLR-4), resulting in NF-κB activation and TNF-α production consequently (Hajer et al, 2008). Monocytes from blood migrate into adipose tissues and differentiate into macrophages by MCP-1/CCR2 and intracellular adhesion molecule-1 (ICAM-1) stimulation (Hajer et al, 2008;Holvoet, 2012 (Lolmede et al, 2011;Holvoet, 2012;Lafontan, 2014). Besides, adipose where receptors and signaling protein (including GPI-anchored proteins, cavin and caveolin) accumulate and signal (Boscher & Nabi, 2012).…”

Section: Dysfunctional Adipose Tissues Caused By Obesitymentioning

confidence: 99%

“…Interaction between dysfunctional adipose tissues, activated T cells, and chemokines leads to dysregulation of adipokines (Holvoet, 2012), by overexpression of resistin, leptin and reduction of adiponectin levels (Holvoet, 2012;Torres-Leal et al, 2012). Another mechanism of dysfunctional adipose tissues leading to insulin resistance is involved in oxidative stress and cell apoptosis (Holvoet, 2012). The summary of dysfunctional adipocytes during obesity is shown in fig.…”

Section: Dysfunctional Adipose Tissues Caused By Obesitymentioning

confidence: 99%

“…Changes in adipocyte during obesity lead to insulin resistance (Holvoet, 2012) derived exosomes could be accompanied by molecules produced specially in adipocytes.…”

Section: Figmentioning

confidence: 99%

See 4 more Smart Citations

Adiponectin is partially associated with exosomes in mouse serum

Phoonsawat

Aoki-Yoshida

Tsuruta

et al. 2014

Biochemical and Biophysical Research Communications

View full text Add to dashboard Cite

Previous studies suggest that adipocyte-derived exosomes play a role in cell-to-cell communication during the development of metabolic diseases. However, the characteristics and function of exosomes released from adipocytes in vivo remain to be elucidated. Clearly, exosomes released from adipocytes could exist in the circulation. In addition, because the composition of exosomes is heterogenic, depending on the cellular origin of the exosome, adipocyte-derived exosomes could be accompanied by molecules produced specifically in adipocytes. In this context, this study postulated that such molecules associated with exosomes in the serum could be markers for adipocyte-derived exosomes in vivo. This study particularly focused on secretory proteins produced specifically in adipocytes, namely adipocytokines including adiponectin, leptin, and resistin. Serum adiponectin is partially associated with exosomesBased on western blotting, CD63, a well-known protein marker of exosomes, was concentrated in the pellet of mouse serum after ultracentrifugation, suggesting successful isolation of exosomes. Western blotting detected adiponectin but no leptin and only trace amounts of resistin in the exosome fraction. After ultracentrifugation on a discontinuous gradient, both adiponectin and CD63 were detected in a fraction at a density of 1.17 g/mL, consistent with the density of exosomes. The adiponectin signal in the exosome fraction was decreased by proteinase K treatment and completely quenched by a combination of proteinase K and Triton X-100. These results suggest that a portion of adiponectin exists as a transmembrane protein in the exosomes in mouse serum. showed that the concentration of adiponectin in the serum and the ratio of adiponectin to total protein in the exosome fraction were lower in obese mice than in lean mice.In conclusion, this study showed that serum adiponectin is partially associated with exosomes in mice. Considering that adiponectin is produced exclusively by adipocytes, adiponectin-associated exosomes in serum could be derived from adipocytes. This study proposes that adiponectin could be a marker for exosomes released from adipocytes in vivo.iii

show abstract

Section: Discussionmentioning

confidence: 65%

Section: Discussionmentioning

confidence: 99%

Section: Dysfunctional Adipose Tissues Caused By Obesitymentioning

confidence: 99%

Section: Dysfunctional Adipose Tissues Caused By Obesitymentioning

confidence: 99%

“…Changes in adipocyte during obesity lead to insulin resistance (Holvoet, 2012) derived exosomes could be accompanied by molecules produced specially in adipocytes.…”

Section: Figmentioning

confidence: 99%

See 3 more Smart Citations

Adiponectin is partially associated with exosomes in mouse serum

Phoonsawat

Aoki-Yoshida

Tsuruta

et al. 2014

Biochemical and Biophysical Research Communications

View full text Add to dashboard Cite

show abstract

A novel chi‐square statistic for detecting group differences between pathways in systems epidemiology

Yuan

Zhang

et al. 2016

Statistics in Medicine

View full text Add to dashboard Cite

Traditional epidemiology often pays more attention to the identification of a single factor rather than to the pathway that is related to a disease, and therefore, it is difficult to explore the disease mechanism. Systems epidemiology aims to integrate putative lifestyle exposures and biomarkers extracted from multiple omics platforms to offer new insights into the pathway mechanisms that underlie disease at the human population level. One key but inadequately addressed question is how to develop powerful statistics to identify whether one candidate pathway is associated with a disease. Bearing in mind that a pathway difference can result from not only changes in the nodes but also changes in the edges, we propose a novel statistic for detecting group differences between pathways, which in principle, captures the nodes changes and edge changes, as well as simultaneously accounting for the pathway structure simultaneously. The proposed test has been proven to follow the chi-square distribution, and various simulations have shown it has better performance than other existing methods. Integrating genome-wide DNA methylation data, we analyzed one real data set from the Bogalusa cohort study and significantly identified a potential pathway, Smoking → SOCS3 → PIK3R1, which was strongly associated with abdominal obesity. The proposed test was powerful and efficient at identifying pathway differences between two groups, and it can be extended to other disciplines that involve statistical comparisons between pathways. The source code in R is available on our website. Copyright © 2016 John Wiley & Sons, Ltd.

show abstract

High Sucrose Intake Ameliorates the Accumulation of Hepatic Triacylglycerol Promoted by Restraint Stress in Young Rats

Corona-Pérez

Dı́az-Muñoz

Rodríguez

et al. 2015

Lipids

View full text Add to dashboard Cite

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disorder. Stress promotes the onset of the NAFLD with a concomitant increment in the activity of the hepatic 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD-1). However, the interaction between the stress and a carbohydrate-enriched diet for the development of NAFLD in young animals is unknown. In the present study, we evaluated the impact of chronic stress on the hepatic triacylglycerol level of young rats fed or not with a high sucrose-diet. For doing this, 21-day old male Wistar rats were allocated into 4 groups: control (C), chronic restraint stress (St), high-sucrose diet (S30), and chronic restraint stress plus a 30 % sucrose diet (St + S30). Chronic restraint stress consisted of 1-hour daily session, 5 days per week and for 4 weeks. Rats were fed with a standard chow and tap water (C group) or 30 % sucrose diluted in water (S30 group). The St + S30 groups consumed less solid food but had an elevated visceral fat accumulation in comparison with the St group. The St group showed a high level of serum corticosterone and a high activity of the hepatic 11β-HSD-1 concomitantly to the augmentation of hepatic steatosis signs, a high hepatic triacylglycerol content, and hepatic oxidative stress. Conversely, the high-sucrose intake in stressed rats (St + S30 group) reduced the hepatic 11β-HSD-1 activity, the level of serum corticosterone, and the hepatic triacylglycerol content. Present findings show that a high-sucrose diet ameliorates the triacylglycerol accumulation in liver promoted by the restraint stress in young male rats.

show abstract

Stress in Obesity and Associated Metabolic and Cardiovascular Disorders

Cited by 37 publications

References 201 publications

Adiponectin is partially associated with exosomes in mouse serum

Adiponectin is partially associated with exosomes in mouse serum

A novel chi‐square statistic for detecting group differences between pathways in systems epidemiology

High Sucrose Intake Ameliorates the Accumulation of Hepatic Triacylglycerol Promoted by Restraint Stress in Young Rats

Contact Info

Product

Resources

About