Quercetin reduces obesity-associated ATM infiltration and inflammation in mice: a mechanism including AMPKα1/SIRT1

Dong, Jing; Zhang, Xian; Zhang, Lei; Bian, Huixi; Xu, Na; Bao, Bin; Liu, Jian

doi:10.1194/jlr.m038786

Cited by 228 publications

(164 citation statements)

References 55 publications

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“…In our study, HFD feeding induced body weight gain and visceral obesity, hyperglycemia, insulin resistance and dyslipidemia. It has been described that quercetin possesses anti-insulin resistance properties, ameliorating insulin sensitivity and glucose intolerance [26,27]. Our results corroborate the modulatory capacity of quercetin on glucose homeostasis through the improvement of glucose tolerance and insulin sensitivity despite the high fat diet intake, as previously described in an in vivo model of obesity in rats [16].…”

Section: Discussionsupporting

confidence: 80%

Protective effect of quercetin on high-fat diet-induced non-alcoholic fatty liver disease in mice is mediated by modulating intestinal microbiota imbalance and related gut-liver axis activation

Porras

Nistal

Martínez‐Flórez

et al. 2017

Free Radical Biology and Medicine

370

233

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Abbreviations: ALT, alanine aminotransferase; C/EBPα, CCAAT/enhancer binding protein alpha; CHOP, CCAAT-enhancer-binding protein homologous protein; CYP2E1, cytochrome P450 2E1; DAMPs, danger-associated molecular patterns; FABP1, fatty acid binding protein 1; FAS, fatty acid synthase; FAT/CD36, fatty acid translocase CD36; FFA, free fatty acid; FOXA1, forkhead box protein A1; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; GRP78, 78 kDa glucose-regulated protein; HFD, high fat diet; HOMA-IR, homeostasis model assessment of insulin resistance; IAP, intestinal phosphatase alkaline; IL-6, interleukin 6; LPO, lipid peroxidation; LPS, lipopolysaccharide; LXRα, liver X receptor alpha; NAFLD, non-alcoholic fatty liver disease; NAS, NAFLD activity score; NASH, non-alcoholic steatohepatitis; NF-B , nuclear factor kappa B; NLRP3, NOD-like receptor family pyrin domain containing 3;PAMPs, pathogen-associated molecular patterns; PRRs, pattern recognition receptors; SCFAs, short-chain fatty acids; SREBP-1c, sterol regulatory element binding protein 1c; TG, triglycerides; TLR, Toll-like receptor; TNF-αtumor necrosis factor; UPR, unfolded protein response. AbstractGut microbiota is involved in obesity, metabolic syndrome and the progression of nonalcoholic fatty liver disease (NAFLD). It has been recently suggested that the flavonoid quercetin may have the ability to modulate the intestinal microbiota composition, suggesting a prebiotic capacity which highlights a great therapeutic potential in NAFLD. The present study aims to investigate benefits of experimental treatment with quercetin on gut microbial balance and related gut-liver axis activation in a nutritional animal model of NAFLD associated to obesity. C57BL/6J mice were challenged with high fat diet (HFD) supplemented or not with quercetin for 16 weeks.

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Section: Discussionsupporting

confidence: 80%

Protective effect of quercetin on high-fat diet-induced non-alcoholic fatty liver disease in mice is mediated by modulating intestinal microbiota imbalance and related gut-liver axis activation

Porras

Nistal

Martínez‐Flórez

et al. 2017

Free Radical Biology and Medicine

370

233

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“…Conversely, polyunsaturated fatty acids suppress these inflammatory effects on monocytes/macrophages (15)(16)(17)(18)(19)(20). A recent study ascribed this protection to activation of AMP-activated protein kinase (AMPK) 6 (21), and, indeed, AMPK activation in vitro and in vivo correlates with macrophage skewing toward an M2 phenotype (22)(23)(24).…”

mentioning

confidence: 99%

Palmitoleate Reverses High Fat-induced Proinflammatory Macrophage Polarization via AMP-activated Protein Kinase (AMPK)

Chan

Pillon

Sivaloganathan

et al. 2015

Journal of Biological Chemistry

155

164

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Background: Elevated saturated fats during obesity activate proinflammatory pathways in macrophages, contributing to insulin resistance. Results: The monounsaturated fatty acid cis-palmitoleate antagonizes saturated fat-induced proinflammatory macrophage polarization through an AMPK-dependent mechanism. Conclusion: Palmitoleate is a lipid mediator that confers an anti-inflammatory macrophage phenotype. Significance: Understanding lipid-mediated macrophage polarization is critical to develop nutritional or cell-based strategies to combat insulin resistance.

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“…RAW264.7 cells and PCMs were planted in 24-well plates and pretreated with vehicle, 20 μmol/l LU or 2 mmol/l of the AMPKα1 activator AICAR (5-aminoimidazole-4-carboxamide 1-β-D-ribofuranoside; Sigma-Aldrich, St. Louis, MO, USA) for 12 h. To examine the effects of LU on macrophage M1 polarisation, the cells were stimulated with 100 ng/ml LPS (Sigma-Aldrich) according to previously published reports [14,25]. The MMe phenotype polarisation method was performed according to the procedures described by Kratz et al [14].…”

Section: Methodsmentioning

confidence: 99%

“…At 15 and 25 weeks of age, the mice were fasted overnight and a GTT and insulin tolerance test were performed as previously described [15]. At 25 weeks of age, all mice were killed with CO 2 and their blood and adipose tissues were harvested and stored at −80°C, as previously described [25]. All experimental procedures were approved by the Standing Committee on Animals of Hefei University of Technology.…”

Section: Methodsmentioning

confidence: 99%

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Luteolin reduces obesity-associated insulin resistance in mice by activating AMPKα1 signalling in adipose tissue macrophages

et al. 2016

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Aims/hypothesis Inflammatory polarisation of adipose tissue macrophages (ATMs) plays a critical role in the development of obesity-associated metabolic diseases such as insulin resistance and diabetes. Our previous study indicated that dietary luteolin (LU) could prevent the establishment of insulin resistance in mice fed a high-fat diet (HFD). Here, we further investigated the effects of LU, which is a natural flavonoid, on pre-established insulin resistance and obesityassociated ATM polarisation in mice. Methods Five-week-old C57/BL6 mice were fed on a low-fat diet or HFD for 20 weeks, with some mice receiving supplementation with 0.01% LU from weeks 1 or 10 of the HFD to assess the actions of LU on insulin resistance and ATM polarisation. Furthermore, the role of LU in metabolicdysfunction-associated macrophage phenotypes was investigated in vitro. Results Dietary LU supplementation, either for 20 weeks or from weeks 10 to 20 of an HFD, significantly improved insulin resistance in HFD-fed mice. In addition, inflammatory macrophage infiltration and polarisation were suppressed in mouse epididymal adipose tissues. Furthermore, LU treatment directly reversed lipopolysaccharide-stimulated and metabolism-regulated molecules, and induced inflammatory polarisation in mouse RAW264.7 cells and peritoneal cavity resident macrophages. Finally, using the selective AMPactivated protein kinase (AMPK) inhibitor compound C and Ampkα1 (also known as Prkaa1) silencing with siRNA, we found that LU activated AMPKα1 in macrophages to inhibit their inflammatory polarisation and enhanced insulin signals in adipocytes that were stimulated with macrophageconditioned media. Conclusions/interpretation Dietary LU ameliorated insulin resistance in diet-induced obese mice by promoting AMPKα1 signalling in ATMs.

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Quercetin reduces obesity-associated ATM infiltration and inflammation in mice: a mechanism including AMPKα1/SIRT1

Cited by 228 publications

References 55 publications

Protective effect of quercetin on high-fat diet-induced non-alcoholic fatty liver disease in mice is mediated by modulating intestinal microbiota imbalance and related gut-liver axis activation

Protective effect of quercetin on high-fat diet-induced non-alcoholic fatty liver disease in mice is mediated by modulating intestinal microbiota imbalance and related gut-liver axis activation

Palmitoleate Reverses High Fat-induced Proinflammatory Macrophage Polarization via AMP-activated Protein Kinase (AMPK)

Luteolin reduces obesity-associated insulin resistance in mice by activating AMPKα1 signalling in adipose tissue macrophages

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