scholarly journals Free Fatty Acids Activate Renin-Angiotensin System in 3T3-L1 Adipocytes through Nuclear Factor-kappa B Pathway

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Jia Sun ◽  
Jinhua Luo ◽  
Yuting Ruan ◽  
Liangchang Xiu ◽  
Bimei Fang ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Signaling Pathway ◽  
Molecular Mechanisms ◽  
Renin Angiotensin System ◽  
Toll Like Receptor 4 ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Ras Activation ◽  
Tlr4 Signaling Pathway

The activity of a local renin-angiotensin system (RAS) in the adipose tissue is closely associated with obesity-related diseases. However, the mechanism of RAS activation in adipose tissue is still unknown. In the current study, we found that palmitic acid (PA), one kind of free fatty acid, induced the activity of RAS in 3T3-L1 adipocytes. In the presence of fetuin A (Fet A), PA upregulated the expression of angiotensinogen (AGT) and angiotensin type 1 receptor (AT1R) and stimulated the secretion of angiotensin II (ANG II) in 3T3-L1 adipocytes. Moreover, the activation of RAS in 3T3-L1 adipocytes was blocked when we blocked Toll-like receptor 4 (TLR4) signaling pathway using TAK242 or NF-κB signaling pathway using BAY117082. Together, our results have identified critical molecular mechanisms linking PA/TLR4/NF-κB signaling pathway to the activity of the local renin-angiotensin system in adipose tissue.

scholarly journals Expression of Renin-Angiotensin System Components in the Taste Organ of Mice

Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 2251 ◽  
Author(s):  
Noriatsu Shigemura ◽  
Shingo Takai ◽  
Fumie Hirose ◽  
Ryusuke Yoshida ◽  
Keisuke Sanematsu ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Taste Receptor ◽  
Renin Angiotensin System ◽  
Α Subunit ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Salt Taste ◽  
Taste Cells ◽  
Taste Organ

The systemic renin-angiotensin system (RAS) is an important regulator of body fluid and sodium homeostasis. Angiotensin II (AngII) is a key active product of the RAS. We previously revealed that circulating AngII suppresses amiloride-sensitive salt taste responses and enhances the responses to sweet compounds via the AngII type 1 receptor (AT1) expressed in taste cells. However, the molecular mechanisms underlying the modulation of taste function by AngII remain uncharacterized. Here we examined the expression of three RAS components, namely renin, angiotensinogen, and angiotensin-converting enzyme-1 (ACE1), in mouse taste tissues. We found that all three RAS components were present in the taste buds of fungiform and circumvallate papillae and co-expressed with αENaC (epithelial sodium channel α-subunit, a salt taste receptor) or T1R3 (taste receptor type 1 member 3, a sweet taste receptor component). Water-deprived mice exhibited significantly increased levels of renin expression in taste cells (p < 0.05). These results indicate the existence of a local RAS in the taste organ and suggest that taste function may be regulated by both locally-produced and circulating AngII. Such integrated modulation of peripheral taste sensitivity by AngII may play an important role in sodium/calorie homeostasis.

scholarly journals Identification of miRNAs Mediating Effects of the Renin Angiotensin System in Adipose Tissue (P21-076-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Kalhara Menikdiwela ◽  
Latha Ramalingam ◽  
Halima Bensmail ◽  
Mostafa Abbas ◽  
Nishan Kalupahana ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
Molecular Mechanisms ◽  
Metabolic Diseases ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
High Fat ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Physiological Processes

Abstract Objectives Renin angiotensin system (RAS) classically known to regulate blood pressure, is also involved in several metabolic disorders including obesity. Interestingly, RAS components are highly expressed in adipose tissue; however, mechanisms underlying RAS-obesity interactions are still ambiguous and limited information is available about RAS regulation in adipose tissue. We identified previously that RAS overactivation induces ER stress and inflammation, and our goal is to characterize additional mechanisms linking RAS to obesity. Hence, we hypothesized that overactivation of angiotensinogen (Agt, precursor protein in RAS), modulates processes linked to metabolic diseases such as oxidative stress, apoptosis and autophagy in adipocytes. Methods mRNA and small RNA profiling were performed in adipose tissues of male wild type B6 mice (Wt) and transgenic mice (Agt-Tg) overexpressing Agt which were either fed a low fat (LF) or a high fat (HF) diet with or without RAS inhibitor captopril, an angiotensin converting enzyme inhibitor. Results We identified 18 miRNAs and 5 miRNAs, which were significantly either up or downregulated respectively in Tg compared to Wt mice. Of these, we validated expression of mir195 and 690 which were significantly higher in Tg compared to Wt mice. Furthermore, these miRNAs were significantly reduced in high fat-fed Tg mice treated with captopril compared to non-treated high fat fed mice, indicating the role of angiotensin II in regulation of these miRNAs. Additionally, we identified and validated several genes involved in physiological processes such as oxidative stress and autophagy, some of which were direct targets of the above miRNAs. Mitogen-activated protein kinases including Mapk4, Map3k4, and Map3k7; Caspase 3, 8 and 9; autophagic genes such as autophagy 5 (Atg5), Atg14 and beclin1 were all significantly higher in Tg compared to Wt mice. Additional mechanistic studies are ongoing in cultured adipocytes to further dissect molecular mechanisms linking RAS to obesity. Conclusions Overexpression of RAS in adipose tissue alters various physiological processes such as oxidative stress, apoptosis and autophagy, which could be mediated, in part through regulatory miRNAs. These pathways and miRNAs could be potential therapeutic targets to reduce RAS-associated metabolic diseases. Funding Sources American Heart Association.

scholarly journals Sympathoexcitation Associated with Renin-Angiotensin System in Metabolic Syndrome

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Takuya Kishi ◽  
Yoshitaka Hirooka
Keyword(s):  
Metabolic Syndrome ◽  
Animal Studies ◽  
Renin Angiotensin System ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Ras Activation ◽  
Sympathetic Nervous ◽  
The Brain

Renin-angiotensin system (RAS) is activated in metabolic syndrome (MetS), and RAS inhibitors are preferred for the treatments of hypertension with MetS. Although RAS activation is important for the therapeutic target, underlying sympathetic nervous system (SNS) activation is critically involved and should not be neglected in the pathogenesis of hypertension with MetS. In fact, previous studies have suggested that SNS activation has the interaction with RAS activation and/or insulin resistance. As a novel aspect connecting the importance of SNS and RAS activation, we and other investigators have recently demonstrated that angiotensin II type 1 receptor (AT1R) blockers (ARBs) improve SNS activation in patients with MetS. In the animal studies, SNS activation is regulated by the AT1R-induced oxidative stress in the brain. We have also demonstrated that orally administered ARBs cause sympathoinhibition independent of the depressor effects in dietary-induced hypertensive rats. Interestingly, these benefits on SNS activation of ARBs in clinical and animal studies are not class effects of ARBs. In conclusion, SNS activation associated with RAS activation in the brain should be the target of the treatment, and ARBs could have the potential benefit on SNS activation in patients with MetS.

Effects of Sleeve Gastrectomy on the Metabolic Profile and on the Expression of Renin-Angiotensin System in Adipose Tissue of Obese Rats

2017 ◽  
Vol 24 (9) ◽  
Author(s):  
Thaisa Soares Crespo ◽  
Joao Marcus Oliveira Andrade ◽  
Alanna Fernandes Paraiso ◽  
Deborah de Farias Lelis ◽  
Pablo Vinicyus Ferreira Chagas ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Sleeve Gastrectomy ◽  
Metabolic Profile ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Obese Rats

Celecoxib Modulates the Renin-Angiotensin System in the Adipose Tissue of Obese Mice

2018 ◽  
Vol 14 (3) ◽  
pp. 203-209
Author(s):  
Jamille Fernandes Lula ◽  
Toni Ramos Alves de Souza ◽  
Keila Lopes Mendes ◽  
Alanna Fernandes Paraíso ◽  
Deborah de Farias Lelis ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Renin Angiotensin System ◽  
Obese Mice ◽  
Angiotensin System ◽  
Renin Angiotensin

Epicardial adipose tissue: the genetics behind an emerging cardiovascular marker

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J.A Sousa ◽  
M.G Serrao ◽  
M Temtem ◽  
A Pereira ◽  
M Santos ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Cardiovascular Risk ◽  
Genetic Risk ◽  
Epicardial Adipose Tissue ◽  
Genetic Risk Score ◽  
Renin Angiotensin System ◽  
Epicardial Fat ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Genetic Burden

Abstract Background Increasing evidence points epicardial adipose tissue (EAT) as an emerging cardiovascular risk marker. Whether genetic polymorphisms are associated with a higher EAT burden is still unknow. Genetic risk score (GRS) is an emerging method that attempts to establish correlation between single nucleotide polymorphisms (SNPs) and clinical phenotypes. Aim Evaluate the role of genetic burden and its association to EAT. Methods 996 patients (mean age 59±8, 78% male) were prospectively enrolled in a single center. EAT was measured on cardiac CT using a modified simplified method. Patients were divided into 2 groups (above vs. below the median EAT volume). We studied different polymorphisms across the following gene-regulated pathways: oxidation, renin-angiotensin system, cellular, diabetes/obesity and dyslipidemia pathways. Genotyping was performed by TaqMan allelic discrimination assay. A multiplicative genetic risk score (mGRS) was constructed and represents the genetic burden of the different polymorphisms studied. To evaluate the relation between genetics and EAT volume, we compared both groups by: global mGRS, gene cluster/axis mGRS and individual SNPs. Results Patients with above-median EAT volume were older, had higher body mass index (BMI) and higher prevalence of hypertension, diabetes and dyslipidemia (p&lt;0.05). Patients with higher EAT volumes presented a higher global mean GRS (p&lt;0.001), with the latter remaining an independent predictor for higher EAT volumes (OR 1.3, 95% CI 1.2–1.5), alongside age and BMI. In the analysis by gene clusters, patients with more epicardial fat consistently presented a higher polymorphism burden (translated by a higher mGRS level) across numerous pathways: oxidation, renin-angiotensin system, cellular, diabetes/obesity and dyslipidemia. After adjusting for confounders and other univariate predictors of higher fat volume, the following have emerged as independently related to higher EAT volumes: mGRS comprising the genes of different clusters, age and BMI. Amongst the 33 genes analyzed, only MTHFR677 polymorphisms (a gene with a critical role in regulating plasma homocysteine levels) emerged as significantly related to higher EAT volumes in our population (OR 1.4, 95% CI: 1.100–1.684, p=0.005). Conclusion Patients with a higher polymorphism burden in genes involved in the oxidation, renin-angiotensin, cellular, diabetes/obesity and dyslipidemia pathways present higher levels of epicardial fat. This potential association seems to be independent from the expected association between epicardial fat and cardiovascular risk factors. To our knowledge, this is the first time such genetic profiling has been done, casting further insight into this complex matter. Funding Acknowledgement Type of funding source: None

UPREGULATION OF RENIN ANGIOTENSIN SYSTEM IN TYPE 1 DIABETES MELLITUS ASSOCIATED WITH HYPERTENSION

2011 ◽  
Vol 29 ◽  
pp. e377-e378
Author(s):  
L. Morais ◽  
I. Watanabe ◽  
M. Franco ◽  
D. Arita ◽  
M. Gabbay ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Type 1 Diabetes Mellitus ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

Downregulation of the renin-angiotensin system in streptozotocin-diabetic rats

1992 ◽  
Vol 262 (1) ◽  
pp. E105-E109 ◽  
Author(s):  
L. A. Cassis
Keyword(s):  
Adipose Tissue ◽  
Replacement Therapy ◽  
White Adipose Tissue ◽  
Plasma Concentrations ◽  
Renin Angiotensin System ◽  
Diabetic Rats ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Brown Adipose ◽  
Insulin Replacement

To determine if insulin has the ability to regulate components of the renin-angiotensin system, renin and angiotensinogen mRNA and plasma concentrations were determined in 4-wk streptozotocin (STZ)-diabetic rats. In another group of STZ-diabetic rats, replacement insulin therapy was given over the 4-wk period, and the above parameters were examined. In STZ-diabetic rats, there was a significant regression of white adipose tissue that was accompanied by an increase in the yield of RNA obtained. Changes in white adipose tissue were reversed by insulin replacement therapy in STZ-diabetic rats. There were no changes in brown adipose tissue weight or RNA yield in STZ-diabetic rats. Plasma renin activity (PRA) was significantly decreased in STZ-diabetic rats; however, plasma angiotensinogen concentration was not significantly affected by diabetes. PRA was restored to control levels in STZ-diabetic rats with insulin replacement. Kidney renin mRNA as well as liver, epididymal, and interscapular fat angiotensinogen mRNA were significantly decreased in STZ-diabetic rats. Renin and angiotensinogen mRNA were not significantly different from control in all tissues examined in STZ-diabetic rats with insulin replacement therapy. Results from this study suggest a downregulation of the renin-angiotensin system in 4-wk STZ-diabetic rats at the level of mRNA expression that is restored by replacement therapy with insulin; therefore, insulin may directly or indirectly regulate the renin-angiotensin system.

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