The sensitivity of adipose tissue visfatin mRNA expression to lipopolysaccharide-induced endotoxemia is increased by ovariectomy in female rats

Iwasa, Takeshi; Matsuzaki, Takashi; Matsui, Shinji; Tungalagsuvd, Altankhuu; Munkhzaya, Munkhsaikhan; Takiguchi, Eri; Kawakita, Takako; Kuwahara, Akira; Irahara, Minoru

doi:10.1016/j.intimp.2016.04.002

Cited by 6 publications

(6 citation statements)

References 23 publications

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“…Like leptin, visfatin plasma levels have been reported to increase during LPS-stimulated systemic inflammation in rats (85) and humans (86) and may induce production of IL-6 and TNFα (16). Our present results confirm that release of visfatin is more pronounced from visceral adipose tissue compared to SAT (24).…”

Section: Discussionmentioning

confidence: 99%

Age-Dependent Changes of Adipokine and Cytokine Secretion From Rat Adipose Tissue by Endogenous and Exogenous Toll-Like Receptor Agonists

et al. 2020

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White adipose tissue but recently also brown adipose tissue have emerged as endocrine organs. Age-associated obesity is accompanied by prolonged and elevated lipopolysaccharide (LPS)-induced sickness symptoms and increased cytokine and adipokine levels in the circulation partially originating from adipose tissue. In the present study, ex vivo fat explants were used to investigate how the exogenous pathogen-associated molecular pattern (PAMP) LPS or the endogenous danger-associated molecular patterns (DAMPs) high mobility group box-1 protein (HMGB1) and biglycan modulate the release of cytokines and adipokines/batokines and, thus, could influence systemic and/or local inflammation. The response of adipose tissue (epididymal, retroperitoneal, subcutaneous, and brown) was compared between young lean and old obese rats (2 vs. 24 months old). LPS induced a strong interleukin (IL)-6 and tumor necrosis factor (TNF) alpha release into the supernatant of all adipose tissue types investigated. HMGB1 (subcutaneous) and biglycan (retroperitoneal) led to an increased release of IL-6 and TNFalpha (HMGB1) and decreased visfatin and adiponectin (biglycan) secretion from epididymal adipose tissue (young rats). Visfatin was also decreased by HMGB1 in retroperitoneal adipose tissue of old rats. We found significantly higher leptin (all fat pads) and adiponectin (subcutaneous) levels in supernatants of adipose tissue from old compared to young rats, whereas visfatin secretion showed the opposite. The expression of the biglycan receptor Toll-like receptor (TLR) 2 as well as the LPS and HMGB1 receptors TLR4 and receptor for advanced glycation end products (RAGE) were reduced with age (TLR4/RAGE) and by stimulation with their ligands (subcutaneous). Overall, we revealed that adipokines/adipose-tissue released cytokines show some modulation of their release caused by mediators of septic (batokines) and Peek et al. Age-Dependent Adipokine and Cytokine Secretion sterile inflammation with potential implication for acute and chronic disease. Moreover, aging may increase or decrease the release of fat-derived mediators. These data show that DAMPS and LPS locally modulate cytokine secretion while only DAMPS but not LPS can locally alter adipokine secretion during inflammation.

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Section: Discussionmentioning

confidence: 99%

Age-Dependent Changes of Adipokine and Cytokine Secretion From Rat Adipose Tissue by Endogenous and Exogenous Toll-Like Receptor Agonists

et al. 2020

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“…It has been reported in mice and rat models that males and ovariectomized females show higher levels of IL-6- and LPS-binding protein (LBP, that promotes a pro-inflammatory cellular response) after LPS-induced endotoxemia [ 20 , 201 ]. An increase in visfatin expression levels (an adipokine with pro-inflammatory properties) has been reported in the serum, liver, and adipose tissue from male and female rats after LPS-induced endotoxemia, and this increase is higher in the adipose tissue of ovariectomized rats that also display a worse outcome and higher levels of mortality than intact animals [ 202 , 203 ]. In contrast, it has been reported that male rats display an early suppressive immune response (decreased levels of TNF-α as compared with females) after LPS injection that is testosterone dependent, confirming an increased susceptibility to sepsis in males as compared with females [ 204 ].…”

Section: Sexual Dimorphism and Bacterial Sepsismentioning

confidence: 99%

Sexual dimorphism in bacterial infections

et al. 2018

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BackgroundSex differences are important epidemiological factors that impact in the frequency and severity of infectious diseases. A clear sexual dimorphism in bacterial infections has been reported in both humans and animal models. Nevertheless, the molecular mechanisms involved in this gender bias are just starting to be elucidated. In the present article, we aim to review the available data in the literature that report bacterial infections presenting a clear sexual dimorphism, without considering behavioral and social factors.Main bodyThe sexual dimorphism in bacterial infections has been mainly attributed to the differential levels of sex hormones between males and females, as well as to genetic factors. In general, males are more susceptible to gastrointestinal and respiratory bacterial diseases and sepsis, while females are more susceptible to genitourinary tract bacterial infections. However, these incidences depend on the population evaluated, animal model and the bacterial species. Female protection against bacterial infections and the associated complications is assumed to be due to the pro-inflammatory effect of estradiol, while male susceptibility to those infections is associated with the testosterone-mediated immune suppression, probably via their specific receptors. Recent studies indicate that the protective effect of estradiol depends on the estrogen receptor subtype and the specific tissue compartment involved in the bacterial insult, suggesting that tissue-specific expression of particular sex steroid receptors contributes to the susceptibility to bacterial infections. Furthermore, this gender bias also depends on the effects of sex hormones on specific bacterial species. Finally, since a large number of genes related to immune functions are located on the X chromosome, X-linked mosaicism confers a highly polymorphic gene expression program that allows women to respond with a more expanded immune repertoire as compared with men.ConclusionNotwithstanding there is increasing evidence that confirms the sexual dimorphism in certain bacterial infections and the molecular mechanisms associated, further studies are required to clarify conflicting data and to determine the role of specific hormone receptors involved in the gender bias of bacterial infections, as well as their potential as therapeutic targets.

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“…Visfatin level in plasma is associated with the amount of fat tissue, type 2 diabetes, and metabolic syndrome [ 31 ]. It has been shown that the concentration of visfatin levels and mRNA levels in a visceral adipose tissue and the liver were increased in a rat model [ 46 ]. Authors have suggested strengthening role of visfatin inflammatory response in the formation of visceral adipose tissue rats [ 46 ].…”

Section: Adipokinesmentioning

confidence: 99%

“…It has been shown that the concentration of visfatin levels and mRNA levels in a visceral adipose tissue and the liver were increased in a rat model [ 46 ]. Authors have suggested strengthening role of visfatin inflammatory response in the formation of visceral adipose tissue rats [ 46 ]. Furthermore, visfatin can induce TNF-α, which is associated with obesity and insulin resistance [ 46 , 47 ].…”

Section: Adipokinesmentioning

confidence: 99%

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The interplay between Th17 and T-regulatory responses as well as adipokines in the progression of non-alcoholic fatty liver disease

Świderska

Jaroszewicz

Stawicka

et al. 2017

ceh

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Non-alcoholic fatty liver disease (NAFLD) is a chronic progressive liver disease, coupled with metabolic syndrome, which may progress to non-alcoholic steatohepatitis (NASH). Diabetes, obesity, hypertension, hypercholesterolemia, and hypertriglyceridemia are considered to be the most common causes leading to the incidence of NAFLD. It is assumed that the accumulation of lipid deposits in hepatocytes leads to production of proinflammatory cytokines that triggers the development of liver inflammation. Regulatory T cells (Tregs) play a critical role in regulating inflammatory processes in NASH, while T helper type 17 (Th17) might functionally oppose Treg-mediated responses. In addition, important mediators of hepatic steatosis are fatty hormones known as adipokines. We aimed to describe the significance and interaction between Treg and Th17-related cytokines as well as adipokines in pathogenesis and its potential use as biomarkers of NAFLD, especially with respect to progression to NASH.

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The sensitivity of adipose tissue visfatin mRNA expression to lipopolysaccharide-induced endotoxemia is increased by ovariectomy in female rats

Cited by 6 publications

References 23 publications

Age-Dependent Changes of Adipokine and Cytokine Secretion From Rat Adipose Tissue by Endogenous and Exogenous Toll-Like Receptor Agonists

Age-Dependent Changes of Adipokine and Cytokine Secretion From Rat Adipose Tissue by Endogenous and Exogenous Toll-Like Receptor Agonists

Sexual dimorphism in bacterial infections

The interplay between Th17 and T-regulatory responses as well as adipokines in the progression of non-alcoholic fatty liver disease

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