Give a NOD to insulin resistance

Schertzer, Jonathan D.; Klip, Amira

doi:10.1152/ajpendo.00362.2011

Cited by 25 publications

(21 citation statements)

References 16 publications

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“…2e, f). The expression of two other NLRs, NOD1 and NOD2, which are not involved in the inflammasome pathway but might play a role in the pathophysiology of type 2 diabetes [35,36], was also similar in the SAT and VAT of lean and obese participants (ESM Fig. 1).…”

Section: Resultsmentioning

confidence: 86%

Obesity phenotype is related to NLRP3 inflammasome activity and immunological profile of visceral adipose tissue

et al. 2013

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Aims/hypothesis Obesity is a heterogeneous condition comprising both individuals who remain metabolically healthy (MHO) and those who develop metabolic disorders (metabolically unhealthy, MUO). Adipose tissue is also heterogeneous in that its visceral component is more frequently associated with metabolic dysfunction than its subcutaneous component. The development of metabolic disorders is partly mediated by the NLR family pyrin domain containing-3 (NLRP3) inflammasome, which increases the secretion of inflammatory cytokines via activation of caspase-1. We compared the immunological profile and NLRP3 activity in adipose tissue between MUO and MHO individuals. Methods MHO and MUO phenotypes were defined, respectively, as the absence and the presence of the metabolic syndrome. Cellular composition and intrinsic inflammasome activity were investigated by flow cytometry, quantitative RT-PCR and tissue culture studies in subcutaneous and visceral adipose tissue from 23 MUO, 21 MHO and nine lean individuals.Results We found significant differences between the three study groups, including an increased secretion of IL-1β, increased expression of IL1B and NLRP3, increased number of adipose tissue macrophages and decreased number of regulatory T cells in the visceral adipose tissue of MUO patients compared with MHO and lean participants. In macrophages derived from visceral adipose tissue, both caspase-1 activity and IL-1β levels were higher in MUO patients than in MHO patients. Furthermore, caspase-1 activity was higher in CD11c + CD206 + adipose tissue macrophages than in CD11c − CD206 + cells. Conclusions/interpretation The MUO phenotype seems to be associated with an increased activation of the NLPR3 inflammasome in macrophages infiltrating visceral adipose tissue, and a less favourable inflammatory profile compared with the MHO phenotype.

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Section: Resultsmentioning

confidence: 86%

Obesity phenotype is related to NLRP3 inflammasome activity and immunological profile of visceral adipose tissue

et al. 2013

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“…NOD2 is a key receptor in the inflammation reaction, which has been associated with insulin resistance in previous studies (26,28). These physiological functions are similar to those of resistin, therefore the links between resistin and NODs were investigated in the current study.…”

Section: Discussionmentioning

confidence: 94%

“…NOD1 and NOD2 induce the recruitment of receptor-interacting serine/threonine-protein kinase 2 (RIP2), which promotes NF-κB-mediated proinflammatory gene expression when exposed to signal molecules (25). Previous research showed that activation of NOD1 or NOD2 contributes to insulin resistance and a proinflammatory response (26)(27)(28). On this basis, the current study explored the relationship between resistin and NOD receptors.…”

Section: Introductionmentioning

confidence: 97%

Resistin increases the expression of NOD2 in mouse monocytes

Ren

Taomei

Zuo

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Previous studies have indicated that resistin, a type of adipokine, contributes to the development of insulin resistance and type 2 diabetes mellitus, and mediates inflammatory reactions. However, a specific receptor for resistin has not yet been identified. In this study, the relationship between resistin and nucleotide-binding oligomerization domain-like receptors, as well as resistin signal transduction, was examined through transfection, quantitative polymerase chain reaction, western blot analysis and ELISA. The mRNA expression of nucleotide-binding oligomerization domain-containing protein 2 (NOD2), a key immune receptor related to insulin resistance, was significantly increased by resistin treatment at concentrations of 100, 150 and 200 ng/ml (P<0.05, P<0.01 and P<0.01, respectively). The mRNA expression of downstream signaling molecules in the NOD2 signaling pathway, receptor-interacting serine/threonine-protein kinase 2 (RIP2; P<0.01 at 6, 12 and 24 h) and inhibitor of NF-κB kinase subunit beta (P<0.01 at 3, 6, 12 and 24 h) were significantly increased by resistin treatment compared with the control. The mRNA expression of key proinflammatory cytokines, tumor necrosis factor α, IL (interleukin)-6 and IL-1β, were also significantly increased by resistin treatment compared with the control (P<0.01). NOD2 knockdown by small interfering RNA (siRNA) significantly decreased the expression of NOD2 and RIP2 (P<0.01), and there was no significant increase in the levels of cytokines, as compared with treatment with control siRNA. These findings indicate that the inflammatory reaction induced by resistin involves the NOD2-nuclear factor (NF)-κB signaling pathway. The inhibition of NF-κB significantly decreased the secretion of key inflammatory cytokines (P<0.01), suggesting that NF-κB signaling mechanisms are essential to the resistin-induced inflammatory response.

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“…Gut microbiota may have a critical function in the regulation of gut permeability, contributing to endotoxemia, through the endocannabinoid system (eCB) and LPS regulatory loop Like TLRs, nucleotide oligomerization domain (NOD)-1 and -2 proteins are intracellular pattern recognition receptors that sense bacterial cell wall peptidoglycan (PGN) moieties, which induce stress and inflammation pathways [37]. Several studies have associated NOD1-and NOD2-activating bacterial motifs with insulin resistance [38].…”

Section: The Role Of Gut Microbiota In the Pathogenesis Of T2dm (I) Smentioning

confidence: 99%

Gut Microbiota and Type 2 Diabetes Mellitus : What is The Link ?

Ibrahim

2018

Afro-Egyptian Journal of Infectious and Endemic Diseases

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Abstract:The rapid increase of cases of type 2 diabetes mellitus (T2DM) in the past decades has made it a widespread metabolic disorder. In addition to well-established risk factors for T2DM, including genetic predisposition, poor physical activity, fetal programming and obesity, an altered configuration of the microbial community in our gut -the microbiota -has emerged as a new candidate that may be linked to T2DM. The aim of this review is to focus the light on the role of gut microbiota as a novel key organ involved in metabolism, and discussing the putative mechanisms linking gut microbiota and T2DM, as well as the therapeutic perspective of intestinal microbiota modulation for T2DM.

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Give a NOD to insulin resistance

Cited by 25 publications

References 16 publications

Obesity phenotype is related to NLRP3 inflammasome activity and immunological profile of visceral adipose tissue

Obesity phenotype is related to NLRP3 inflammasome activity and immunological profile of visceral adipose tissue

Resistin increases the expression of NOD2 in mouse monocytes

Gut Microbiota and Type 2 Diabetes Mellitus : What is The Link ?

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