Effects of genetic variations in the genes encoding NOD1 and NOD2 on type 2 diabetes mellitus and insulin resistance

Özbayer, Cansu; Kurt, Hülyam; Kebapçı, Medine Nur; Güneş, Hasan Veysi; Çolak, Ertuğrul; Degirmenci, I.

doi:10.1111/jcpt.12482

Cited by 13 publications

(8 citation statements)

References 29 publications

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“…Decreased NOD-like signaling in human fibroblast cells with HG stress were also observed in a previous study (12). Furthermore, genetic variation of NOD1 and NOD2 has been associated with type II DM (23), suggesting the importance of NOD-like signaling in DM-mediated stress. Previous results have suggested that ECM remodeling is important for wound repair, which is in agreement with previous findings (24).…”

Section: Discussionsupporting

confidence: 77%

Nuclear factor-κB signaling negatively regulates high glucose-induced vascular endothelial cell damage downstream of the extracellular signal-regulated kinase/c-Jun N-terminal kinase pathway

Chen

Guo

Zheng

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Diabetes mellitus (DM)-induced high blood sugar severely damages vascular endothelial cells (VECs), which are in direct contact with the blood. Diabetic complications cause difficulties in skin wound healing and VECs are important for this process. Previous studies demonstrated that high blood sugar delayed the repair of wounded VECs, but the underlying mechanism has remained elusive. To explore the effects of diabetic conditions on VEC damage, cells were incubated in a medium with high glucose and then subjected to RNA-sequencing based transcriptome analysis. The results revealed that numerous biological processes were altered by HG stress, including extracellular matrix-receptor interaction, NOD-like receptor signaling and the nuclear factor (NF)-κB pathway. HG treatment increased the levels of phosphorylated inhibitor of NF-κB (IκB-α), the key NF-κB signaling regulator as well as the transcripts of plasminogen activator inhibitor-1 and interleukin-8, two inflammatory response markers. Treatment with extracellular signal-regulated kinase (ERK)-and c-Jun N-terminal kinase (JNK)-specific inhibitors U0126 and sp600125, respectively, led to the activation of IκB-α; however, the inhibitor of IκBα phosphorylation Bay11-7082 did not affect ERK and JNK activity, suggesting that ERK/JNK signaling occurs upstream of NF-κB in VECs. The present study provided useful information regarding the effects of diabetes on VECs, which may provide approaches for therapies of diabetes-associated complications in the future.

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Section: Discussionsupporting

confidence: 77%

Nuclear factor-κB signaling negatively regulates high glucose-induced vascular endothelial cell damage downstream of the extracellular signal-regulated kinase/c-Jun N-terminal kinase pathway

Chen

Guo

Zheng

et al. 2017

Experimental and Therapeutic Medicine

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“…The NOD2 gene has been related to inflammation, since a higher expression of NOD2 may contribute to an increased inflammatory response of immune cells in diet-induced obesity [54]. Genetic variants of NOD2 may also influence the risk of chronic inflammation, insulin resistance, and T2D [55]. The gene FPR2 binds to lipid mediators such as resolvin D1 for promoting resolution of inflammation [56], including the resolution of obesity-induced chronic low-grade inflammation [57].…”

Section: Discussionmentioning

confidence: 99%

Methylome-Wide Association Study in Peripheral White Blood Cells Focusing on Central Obesity and Inflammation

Arpón

Milagro

Ramos-López

et al. 2019

Genes

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Epigenetic signatures such as DNA methylation may be associated with specific obesity traits in different tissues. The onset and development of some obesity-related complications are often linked to visceral fat accumulation. The aim of this study was to explore DNA methylation levels in peripheral white blood cells to identify epigenetic methylation marks associated with waist circumference (WC). DNA methylation levels were assessed using Infinium Human Methylation 450K and MethylationEPIC beadchip (Illumina) to search for putative associations with WC values of 473 participants from the Methyl Epigenome Network Association (MENA) project. Statistical analysis and Ingenuity Pathway Analysis (IPA) were employed for assessing the relationship between methylation and WC. A total of 669 CpGs were statistically associated with WC (FDR < 0.05, slope ≥ |0.1|). From these CpGs, 375 CpGs evidenced a differential methylation pattern between females with WC ≤ 88 and > 88 cm, and 95 CpGs between males with WC ≤ 102 and > 102 cm. These differentially methylated CpGs are located in genes related to inflammation and obesity according to IPA. Receiver operating characteristic (ROC) curves of the top four significant differentially methylated CpGs separated by sex discriminated individuals with presence or absence of abdominal fat. ROC curves of all the CpGs from females and one CpG from males were validated in an independent sample (n = 161). These methylation results add further insights about the relationships between obesity, adiposity-associated comorbidities, and DNA methylation where inflammation processes may be involved.

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“…Inwiefern NOD1 und NOD2 einen genetischen Beitrag zur Fettleibigkeit beim Menschen leisten, ist derzeit nicht bekannt. Gut untersuchte Mutationen, wie der mit Morbus Crohn assoziierte L1008fs-Polymorphismus in NOD2 und der E266K-Austausch in NOD1, scheinen nicht mit T2DM und einer IR assoziiert [53]. Eine Arbeit lässt jedoch eine Assoziation eines Polymorphismus in NOD1 (Glu266Lys) mit der Aufnahme gesättigter Fettsäuren aus der Nahrung und der Insulinsensitivität vermuten [54].…”

Section: Nod1 Und Nod2unclassified

Angeborene Immunität und Adipositas – Die Rolle der Nod-like-Rezeptoren (NLR)

Mirza

Bauer

Kufer

2019

Aktuel Ernahrungsmed

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ZusammenfassungAllgemein wird angenommen, dass die mit Adipositas assoziierten Komorbiditäten, vor allem das metabolische Syndrom, wesentlich durch niederschwellige Entzündungsreaktionen, vorrangig im Fettgewebe, ausgelöst werden. In Mausmodellen spielt hierbei die Freisetzung proinflammatorischer Zytokine wie Interleukin-1 beta (IL-1β) und die Prägung von Immunzellen zu einem proinflammatorischen Phänotyp im Fettgewebe eine wichtige Rolle. Die zugrundeliegenden genetischen und molekularen Determinanten sind jedoch noch nicht im Detail verstanden.Eine Reihe neuer Arbeiten zeigt, dass Proteine der Nod-like-Rezeptoren(NLR)-Familie wichtige Rollen bei der Entstehung und Ausprägung von Adipositas und Adipositas-assoziierten Entzündungsreaktionen spielen. In diesem Artikel betrachten wir den aktuellen Stand der Forschung auf diesem Gebiet und diskutieren offene Fragen zur Relevanz dieser Daten für das Verständnis der Entstehung von Adipositas und des metabolischen Syndroms im Menschen.

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Effects of genetic variations in the genes encoding NOD1 and NOD2 on type 2 diabetes mellitus and insulin resistance

Cited by 13 publications

References 29 publications

Nuclear factor-κB signaling negatively regulates high glucose-induced vascular endothelial cell damage downstream of the extracellular signal-regulated kinase/c-Jun N-terminal kinase pathway

Nuclear factor-κB signaling negatively regulates high glucose-induced vascular endothelial cell damage downstream of the extracellular signal-regulated kinase/c-Jun N-terminal kinase pathway

Methylome-Wide Association Study in Peripheral White Blood Cells Focusing on Central Obesity and Inflammation

Angeborene Immunität und Adipositas – Die Rolle der Nod-like-Rezeptoren (NLR)

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