scholarly journals Systemic Oxidative Stress and Visceral Adipose Tissue Mediators of NLRP3 Inflammasome and Autophagy Are Reduced in Obese Type 2 Diabetic Patients Treated with Metformin

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 892
Author(s):  
Zaida Abad-Jiménez ◽  
Sandra López-Domènech ◽  
Rubén Díaz-Rúa ◽  
Francesca Iannantuoni ◽  
Segundo Ángel Gómez-Abril ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Nlrp3 Inflammasome ◽  
Molecular Mechanisms ◽  
Diabetic Patients ◽  
Low Grade ◽  
Obese Patients ◽  
Visceral Adipose

Obesity is a low-grade inflammatory condition affecting a range of individuals, from metabolically healthy obese (MHO) subjects to type 2 diabetes (T2D) patients. Metformin has been shown to display anti-inflammatory properties, though the underlying molecular mechanisms are unclear. To study whether the effects of metformin are mediated by changes in the inflammasome complex and autophagy in visceral adipose tissue (VAT) of obese patients, a biopsy of VAT was obtained from a total of 68 obese patients undergoing gastric bypass surgery. The patients were clustered into two groups: MHO patients and T2D patients treated with metformin. Patients treated with metformin showed decreased levels of all analyzed serum pro-inflammatory markers (TNFα, IL6, IL1β and MCP1) and a downwards trend in IL18 levels associated with a lower production of oxidative stress markers in leukocytes (mitochondrial ROS and myeloperoxidase (MPO)). A reduction in protein levels of MCP1, NFκB, NLRP3, ASC, ATG5, Beclin1 and CHOP and an increase in p62 were also observed in the VAT of the diabetic group. This downregulation of both the NLRP3 inflammasome and autophagy in VAT may be associated with the improved inflammatory profile and leukocyte homeostasis seen in obese T2D patients treated with metformin with respect to MHO subjects and endorses the cardiometabolic protective effect of this drug.

scholarly journals Visceral Adipose Tissue of Prediabetic and Diabetic Females Shares a Set of Similarly Upregulated microRNAs Functionally Annotated to Inflammation, Oxidative Stress and Insulin Signaling

Antioxidants ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 101
Author(s):  
Justyna Strycharz ◽  
Adam Wróblewski ◽  
Andrzej Zieleniak ◽  
Ewa Świderska ◽  
Tomasz Matyjas ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Insulin Signaling ◽  
Diagnostic Value ◽  
Low Grade ◽  
Mirnas Expression ◽  
Visceral Adipose ◽  
And Oxidative Stress

Hypertrophic and hypoxic visceral adipose tissue (VAT) secretes proinflammatory cytokines promoting insulin resistance (IR), prediabetes and type 2 diabetes (T2DM) microRNAs (miRNAs) are markers of metabolic disorders regulating genes critical for e.g., inflammation, glucose metabolism, and antioxidant defense, with raising diagnostic value. The aim of the current study was to evaluate whether hyperglycemia is able to affect the expression of selected miRNAs in VAT of prediabetic (IFG) and diabetic (T2DM) patients vs. normoglycemic (NG) subjects using qPCR. Statistical analyses suggested that miRNAs expression could be sex-dependent. Thus, we determined 15 miRNAs as differentially expressed (DE) among NG, T2DM, IFG females (miR-10a-5p, let-7d-5p, miR-532-5p, miR-127-3p, miR-125b-5p, let-7a-5p, let-7e-5p, miR-199a-3p, miR-365a-3p, miR-99a-5p, miR-100-5p, miR-342-3p, miR-146b-5p, miR-204-5p, miR-409-3p). Majority of significantly changed miRNAs was similarly upregulated in VAT of female T2DM and IFG patients in comparison to NG subjects, positively correlated with FPG and HbA1c, yet, uncorrelated with WHR/BMI. Enrichment analyses indicated involvement of 11 top DE miRNAs in oxidative stress, inflammation and insulin signaling. Those miRNAs expression changes could be possibly associated with low-grade chronic inflammation and oxidative stress in VAT of hyperglycemic subjects.

Monoamine oxidase is a source of oxidative stress in obese patients with chronic inflammation

2019 ◽  
Vol 97 (9) ◽  
pp. 844-849 ◽  
Author(s):  
Adrian Sturza ◽  
Sorin Olariu ◽  
Mihaela Ionică ◽  
Oana M. Duicu ◽  
Adrian O. Văduva ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Mesenteric Artery ◽  
Vascular Reactivity ◽  
Ros Production ◽  
Obese Patients ◽  
Quantitative Real Time Pcr ◽  
Mao A ◽  
Visceral Adipose

Obesity is an important preventable risk factor for morbidity and mortality from cardiometabolic disease. Oxidative stress (including in visceral adipose tissue) and chronic low-grade inflammation are the major underlying pathomechanisms. Monoamine oxidase (MAO) has recently emerged as an important source of cardiovascular oxidative stress. The present study was conducted to evaluate the role of MAO as contributor to reactive oxygen species (ROS) production in white adipose tissue and vessels harvested from patients undergoing elective abdominal surgery. To this aim, visceral adipose tissue and mesenteric artery branches were isolated from obese patients with chronic inflammation and used for organ bath, ROS production, quantitative real-time PCR, and immunohistology studies. The human visceral adipose tissue and mesenteric artery branches contain mainly the MAO-A isoform, as shown by the quantitative real-time PCR and immunohistology experiments. A significant upregulation of MAO-A, the impairment in vascular reactivity, and increase in ROS production were found in obese vs. non-obese patients. Incubation of the adipose tissue samples and vascular rings with the MAO-A inhibitor (clorgyline, 30 min) improved vascular reactivity and decreased ROS generation. In conclusion, MAO-A is the predominant isoform in human abdominal adipose and vascular tissues, is overexpressed in the setting of inflammation, and contributes to the endothelial dysfunction.

Proteomic analysis of visceral adipose tissue in pre-obese patients with type 2 diabetes

2013 ◽  
Vol 376 (1-2) ◽  
pp. 99-106 ◽  
Author(s):  
Mora Murri ◽  
Maria Insenser ◽  
Maria Rosa Bernal-Lopez ◽  
Pablo Perez-Martinez ◽  
Hector F. Escobar-Morreale ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Proteomic Analysis ◽  
Obese Patients ◽  
Visceral Adipose

scholarly journals Mechanisms of SGLT2 (Sodium-Glucose Transporter Type 2) Inhibition-Induced Relaxation in Arteries From Human Visceral Adipose Tissue

Hypertension ◽  
2020 ◽  
Author(s):  
Alessandro De Stefano ◽  
Manfredi Tesauro ◽  
Nicola Di Daniele ◽  
Giuseppina Vizioli ◽  
Francesca Schinzari ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Glucose Transporter ◽  
Ex Vivo ◽  
Cardiovascular Effects ◽  
Tissue Perfusion ◽  
Obese Patients ◽  
High Potassium ◽  
Visceral Adipose

As novel drug treatments for diabetes have shown favorable cardiovascular effects, interest has mounted with regard to their possible vascular actions, particularly in relation to visceral adipose tissue perfusion and remodeling in obesity. The present study tested the vasorelaxing effect of the SGLT2 (sodium-glucose transporter type 2) inhibitor canagliflozin in arteries from visceral adipose tissue of either nonobese or obese humans and investigated the underlying mechanisms. Also, the vasorelaxing effect of canagliflozin and the GLP-1 (glucagon-like peptide 1) agonist liraglutide were compared in arteries from obese patients. To these purposes, small arteries (116–734 μm) isolated from visceral adipose tissue were studied ex vivo in a wire myograph. Canagliflozin elicited a higher concentration-dependent vasorelaxation in arterioles from obese than nonobese individuals ( P =0.02). The vasorelaxing response to canagliflozin was not modified ( P =0.93) by inhibition of nitric oxide synthase (L-NAME) or prostacyclin (indomethacin), or by H 2 O 2 scavenging (catalase); also, canagliflozin-induced relaxation was similar ( P =0.23) in endothelium-intact or -denuded arteries precontracted with high potassium concentration, thereby excluding an involvement of endothelium-derived hyperpolarizing factors. The vasorelaxing response to canagliflozin was similar to that elicited by the Na + /H + exchanger 1 inhibitor BIX ( P =0.67), but greater than that to the Na + /Ca ++ exchanger inhibitor SEA 0400 ( P =0.001), hinting a role of Na + /H + exchanger inhibition in canagliflozin-induced relaxation. In arterioles from obese patients, the vasorelaxing response to canagliflozin was greater than that to liraglutide ( P =0.004). These findings demonstrate that canagliflozin induces endothelium-independent vasorelaxation in arterioles from human visceral adipose tissue, thereby suggesting that SGLT2 inhibition might favorably impact the processes linking visceral adipose burden to vascular disease in obesity.

Expression of Syntaxin 8 in Visceral Adipose Tissue Is Increased in Obese Patients with Type 2 Diabetes and Related to Markers of Insulin Resistance and Inflammation

2015 ◽  
Vol 46 (1) ◽  
pp. 47-53 ◽  
Author(s):  
Andoni Lancha ◽  
Santiago López-Garrido ◽  
Amaia Rodríguez ◽  
Victoria Catalán ◽  
Beatriz Ramírez ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Obese Patients ◽  
Visceral Adipose

scholarly journals Monocyte chemoattractant protein 1: a possible link between visceral adipose tissue-associated inflammation and subclinical echocardiographic abnormalities in uncomplicated obesity

2005 ◽  
Vol 153 (6) ◽  
pp. 871-877 ◽  
Author(s):  
Alexis E Malavazos ◽  
Emanuele Cereda ◽  
Lelio Morricone ◽  
Calin Coman ◽  
Massimiliano M Corsi ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Visceral Fat ◽  
Left Ventricular ◽  
Low Grade ◽  
Obese Patients ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Visceral Adipose

Objective: Obesity can be considered a state of chronic, low-grade inflammation. Particularly, visceral adipose tissue (VAT) seems to be an active compartment in pro-inflammatory molecule secretion. Adipocytes and VAT are able to produce large amounts of monocyte chemoattractant protein 1 (MCP-1), a chemokine directly involved in ventricular remodeling. Design: In this study, the possible existence of a correlation between MCP-1, abdominal fat accumulation and echocardiographic abnormalities in uncomplicated obesity was investigated. Methods: Echocardiographic parameters, MCP-1 and C-reactive protein (CRP) levels were assessed in 27 normotensive obese women of fertile age (body mass index 43.5 ± 4.8 kg/m2, mean ± s.d.) and 15 normal weight women. Visceral fat (VAT) in the obese group was assessed by computed tomography. Results: Obese patients had higher MCP-1 (P < 0.0001) and CRP (P < 0.0001) levels than controls. MCP-1 levels were correlated with VAT area (r = 0.57, P < 0.0001), CRP (P < 0.0001), left ventricular mass (LVM) (P < 0.02), LVM indexed for height (P < 0.03), end-diastolic posterior wall (P < 0.005), relative wall thickness (P < 0.01), early diastolic filling wave velocity (P < 0.01), isovolumetric relaxation time (P < 0.001) and deceleration time (P < 0,01). Obese patients with greater amounts of VAT (> 130 cm2) presented higher MCP-1 (P < 0.0001) and CRP levels (P < 0.04) than those with a lower degree of abdominal adiposity. Conclusions: MCP-1 levels and visceral adipose tissue seem to be associated with some morphological and functional echocardiographic abnormalities and support a role for visceral fat in predisposing the subject to cardiac dysfunction, possibly through a low-grade state of inflammation.

Overexpression of hepatic 5α-reductase and 11β-hydroxysteroid dehydrogenase type 1 in visceral adipose tissue is associated with hyperinsulinemia in morbidly obese patients

Metabolism ◽  
2011 ◽  
Vol 60 (12) ◽  
pp. 1775-1780 ◽  
Author(s):  
René Baudrand ◽  
José Miguel Domínguez ◽  
Cristian A. Carvajal ◽  
Arnoldo Riquelme ◽  
Carmen Campino ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Hydroxysteroid Dehydrogenase ◽  
Morbidly Obese ◽  
Obese Patients ◽  
Visceral Adipose

scholarly journals Chemotactic cytokines, obesity and type 2 diabetes:in vivoandin vitroevidence for a possible causal correlation?

2009 ◽  
Vol 68 (4) ◽  
pp. 378-384 ◽  
Author(s):  
Henrike Sell ◽  
Jürgen Eckel
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Low Grade ◽  
Obese Patients ◽  
Tissue Mass ◽  
Tissue Biology ◽  
Wide Range ◽  
Adipose Tissue Mass

A strong causal link between increased adipose tissue mass and insulin resistance in tissues such as liver and skeletal muscle exists in obesity-related disorders such as type 2 diabetes. Increased adipose tissue mass in obese patients and patients with diabetes is associated with altered secretion of adipokines, which also includes chemotactic proteins. Adipose tissue releases a wide range of chemotactic proteins including many chemokines and chemerin, which are interesting targets for adipose tissue biology and for biomedical research in obesity and obesity-related diseases. This class of adipokines may be directly linked to a chronic state of low-grade inflammation and macrophage infiltration in adipose tissue, a concept intensively studied in adipose tissue biology in recent years. The inflammatory state of adipose tissue in obese patients may be the most important factor linking increased adipose tissue mass to insulin resistance. Furthermore, chemoattractant adipokines may play an important role in this situation, as many of these proteins possess biological activity beyond the recruitment of immune cells including effects on adipogenesis and glucose homeostasis in insulin-sensitive tissues. The present review provides a summary of experimental evidence of the role of adipose tissue-derived chemotactic cytokines and their function in insulin resistancein vivoandin vitro.

Sign in / Sign up

Export Citation Format

Share Document