IRS-1 pY612 and Akt-1/PKB pT308 Phosphorylation and Antiinflammatory Effect of Diindolylmethane in Adipocytes Cocultured with Macrophages

Lopez-Vazquez, Alfonso; García-Bañuelos, Jesús; González-Garibay, Angélica S; Urzua-Lozano, Pedro E; Toro-Arreola, Susana del; Bueno-Topete, Miriam Ruth; Sánchez‐Enríquez, Sergio; Muñoz‐Valle, José Francisco; Jave-Suárez, Luis F; Armendáriz‐Borunda, Juan; Bastidas-Ramírez, Blanca Estela

doi:10.2174/1573406413666170922095011

Cited by 10 publications

(9 citation statements)

References 45 publications

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“…These results show that LGAL and SG both improve insulin sensitivity. It has also been shown that phosphorylation of IRS and Akt has an anti-inflammatory effect [20].…”

Section: Resultsmentioning

confidence: 99%

“…Increasing evidence shows that JNK and ERK are involved in inflammation. The activation of JNK and ERK signaling plays an important role in modulation of inflammatory responses and regulation of macrophage phenotype [20]. Nuclear factor kappa-light-chain enhancer of activated B cells (NF-κB) is a crucial transcription factor that is rapidly activated by various stimuli, increasing expression of proinflammatory cytokines (e.g., MCP-1 and TNF-α) and inducible nitric oxide synthase (iNOS), and it participates in inflammation [21].…”

Section: Resultsmentioning

confidence: 99%

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Effects of Left Gastric Artery Ligation Versus Sleeve Gastrectomy on Obesity-Induced Adipose Tissue Macrophage Infiltration and Inflammation in Diet-Induced Obese Rats

et al. 2019

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BackgroundBariatric procedures such as left gastric artery ligation (LGAL) and sleeve gastrectomy (SG) have emerged as important procedures for treating morbid obesity. In this study, we compared the effects of LGAL vs. SG on obesity-induced adipose tissue macrophage infiltration and inflammation in diet-induced obese rats.Material/MethodsSprague-Dawley (SD) rats were fed a high-fat diet (HFD) for 16 weeks to induce obesity. SG, GLAL, or corresponding sham surgeries were performed in anesthetized rats. Inflammatory factor expression in serum and epididymal and retroperitoneal adipose tissues were analyzed 4 weeks after surgery. Macrophage infiltration and phenotype transformation were also assessed with Western blot analysis and immunofluorescence.ResultsBoth LGAL and SG strongly attenuated high-fat diet (HFD)-induced fat accumulation in retroperitoneal and epididymal tissues. The expressions of inflammatory cytokines such as tumor necrosis factor (TNF)-agr;, interleukin (IL)-6, and monocyte chemoattractant protein (MCP)-1 were downregulated after LGAL and after SG by promoting activation of M2 macrophages, despite continued exposure to HFD. Furthermore, both LGAL and SG resulted in increased macrophage infiltration, but did not contribute to phenotype transformation of macrophages to M1.ConclusionsLGAL and SG both reduced fat accumulation caused by HFD feeding. Therapies designed to ameliorate the inflammatory response by promoting activation of M2 macrophages may be valuable.

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“…These results show that LGAL and SG both improve insulin sensitivity. It has also been shown that phosphorylation of IRS and Akt has an anti-inflammatory effect [20].…”

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Effects of Left Gastric Artery Ligation Versus Sleeve Gastrectomy on Obesity-Induced Adipose Tissue Macrophage Infiltration and Inflammation in Diet-Induced Obese Rats

et al. 2019

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“…Finally, reverse transcriptase was inactivated by incubation for 10 min at 95°C, storing the complementary DNA (cDNA) at -20°C. 12…”

Section: Rna Isolation and Synthesis Of Complementary Dnamentioning

confidence: 99%

“…This proinflammatory profile is evidenced by monocyte chemoattractant protein-1 (MCP-1), interleukin 6 (IL-6), IL-1b, and tumor necrosis factor a (TNF-a) increase, simultaneously with adiponectin and anti-inflammatory adipokines diminution, among other molecules. [6][7][8][9][10] MCP-1 induces macrophage recruitment increasing the proinflammatory gene expression and impairing insulin signaling 11,12 ; IL-1b leads to insulin signaling blockage and progressive loss of the insulin-producing pancreatic b cell 13 ; IL-6 and TNF-a contribute to insulin signaling pathway disruption, and are negatively associated with adiponectin expression, an insulin-sensitizing adipokine. [14][15][16] Hyperinsulinemia constitutes an underlying factor of obesity-related comorbidities and its role in initiating, sustaining, and expanding IR, a T2D hallmark, is relevant.…”

Section: Introductionmentioning

confidence: 99%

“…[26][27][28]32 UA targets multiple proinflammatory transcription factors, kinases, proinflammatory cytokines and enzymes, chemokines, and adhesion molecules promoting its anti-inflammatory action. 21,33 As inflammation is considered one of the pivotal causes of IR and hyperinsulinemia in obesity, [6][7][8][9][10][11][12][13][14][15] the aim of this study was to assess whether UA may improve proinflammatory adipokines expression, IR, and hyperinsulinemia in rats with diet-induced obesity.…”

Section: Introductionmentioning

confidence: 99%

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Effect of Ursolic Acid on Insulin Resistance and Hyperinsulinemia in Rats with Diet-Induced Obesity: Role of Adipokines Expression

González-Garibay

Lopez-Vazquez

García-Bañuelos

et al. 2020

Journal of Medicinal Food

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Excess of visceral adipose tissue (VAT) characteristic of obesity leads to a proinflammatory state disrupting the insulin signaling pathway, triggering insulin resistance (IR) and inflammation, the main processes contributing to obesity comorbidities. Ursolic acid (UA), a pentacyclic triterpenoid occurring in a variety of plant foods, exhibits anti-inflammatory properties. The aim of this study was to evaluate UA effects on IR, hyperinsulinemia, and inflammation in experimental dietinduced obesity. Forty male Wistar rats were randomly assigned to eight groups (n = 5). One group was used for time 0. Three groups were labeled as OBE (control): receiving high-fat diet (HFD; fat content 45.24% of energy) during 3, 6, or 9 weeks; three groups UA-PREV: exposed to simultaneous HFD and UA during 3, 6, or 9 weeks to evaluate UA preventive effects; one group UA-REV: receiving HFD for 6 weeks, followed by simultaneous HFD and UA for three additional weeks to analyze UA reversal effects. Measurements were performed after 3, 6, or 9 weeks of treatment. Adiposity was calculated by weighing VAT after sacrifice. Serum markers were quantified through colorimetric and enzyme-linked immunosorbent assay methods. VAT adipokines RNAm expression was evaluated by quantitative reverse transcriptase-polymerase chain reaction. Data were analyzed by Kruskal-Wallis and Mann-Whitney U tests. UA significantly decreased adiposity, IR, hyperinsulinemia, triacylglycerides, and cholesterol levels, and also VAT mRNA expression of MCP-1 (monocyte chemoattractant protein-1), IL (interleukin)-1b and IL-6, concomitantly increasing adiponectin levels. UA metabolic effects demonstrated in this study support its potential therapeutic utility to improve IR, hyperinsulinemia, and inflammation observed in obesity and diabetes.

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Naturally occurring glucosinolates and isothiocyanates as a weapon against chronic pain: potentials and limits

et al. 2022

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Investigation into glucosinolates (GLs) therapeutic effects boasts a long history, which began with the evidence that their hydrolysis-derived isothiocyanates (ITCs) could exert cytoprotective effects through the modulation of both the inflammatory response (NF-kB pathway) and the oxidative stress (Nrf2/ARE pathway), two processes largely involved in the pathogenesis of chronic pain syndromes. GLs and ITCs are also able to modulate the activity and the expression of several targets involved in pain regulation, like opioid receptors. Recently, ITCs turned out to be slow-H2S donors in vivo, able to directly modulate the activity of a subtype of KV7 potassium channels involved in the transmission of painful stimuli, providing a further incentive to their employment in pain management. Nevertheless, some controversies exist in the use of ITCs for pain relief considering their ability to positively modulate the activity of TRPA1 receptors. This review focuses on the preclinical and clinical evidence attesting the beneficial effects of GLs and their derivatives ITCs in chronic inflammatory and neuropathic conditions. In this context, the mechanisms underlying the ability of GLs and ITCs to modulate pain perception and, besides, to prevent the establishment of chronic pain will be described along with their pharmacokinetics and toxicological profile. Finally, other possible mechanisms hidden behind GLs efficacy on pain will be discussed.

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IRS-1 pY612 and Akt-1/PKB pT308 Phosphorylation and Antiinflammatory Effect of Diindolylmethane in Adipocytes Cocultured with Macrophages

Cited by 10 publications

References 45 publications

Effects of Left Gastric Artery Ligation Versus Sleeve Gastrectomy on Obesity-Induced Adipose Tissue Macrophage Infiltration and Inflammation in Diet-Induced Obese Rats

Effects of Left Gastric Artery Ligation Versus Sleeve Gastrectomy on Obesity-Induced Adipose Tissue Macrophage Infiltration and Inflammation in Diet-Induced Obese Rats

Effect of Ursolic Acid on Insulin Resistance and Hyperinsulinemia in Rats with Diet-Induced Obesity: Role of Adipokines Expression

Naturally occurring glucosinolates and isothiocyanates as a weapon against chronic pain: potentials and limits

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