Targeting innate immune mediators in type 1 and type 2 diabetes

Donath, Marc Y.; Dinarello, Charles A.; Mandrup‐Poulsen, Thomas

doi:10.1038/s41577-019-0213-9

Cited by 276 publications

(247 citation statements)

References 162 publications

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“…In obesity, chronic rise in circulating nutrients such as glucose and free fatty acids (FFAs) resulted in over-expression of IL-1β in pancreatic β-cells (Maedler et al, 2002;Böni-Schnetzler et al, 2008;Fei et al, 2008;Böni-Schnetzler et al, 2009). It is now clear that IL-1β is a key cytokine in the etiology of T2D since it has been implicated in IR, β-cell dysfunction, and death (Eizirik and Mandrup-Poulsen, 2001;Donath et al, 2008Donath et al, , 2019. IL-1β alters the insulin sensitivity of AT by suppressing insulin signaling; exposure to IL-1β of murine and human adipocytes decreases insulin-stimulated glucose uptake and lipogenesis (Lagathu et al, 2006;Jager et al, 2007;Fève and Bastard, 2009), reduces glucose transporter type 4 (GLUT4) expression, and inhibits GLUT4 translocation to the plasma membrane (Jager et al, 2007;Ballak et al, 2015).…”

Section: Molecular Pathways Linking Obesity-induced Inflammation and Irmentioning

confidence: 99%

Chronic Adipose Tissue Inflammation Linking Obesity to Insulin Resistance and Type 2 Diabetes

et al. 2020

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Section: Molecular Pathways Linking Obesity-induced Inflammation and Irmentioning

confidence: 99%

Chronic Adipose Tissue Inflammation Linking Obesity to Insulin Resistance and Type 2 Diabetes

et al. 2020

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“…20 GLMD is associated with neuroendocrine disorders, insulin resistance, oxidative stress, chronic inflammatory responses, and intestinal flora disorders. [21][22][23] In COVID-19 patient, over activation of T cells lead to the severe immune injury. 24 Severe COVID-19 patients had higher concentrations of pro-inflammatory cytokines than non-severe patients, suggesting that the cytokine storm was associated with disease severity.…”

Section: Glucolipid Metabolic Disorders Induce Cytokine Stormsmentioning

confidence: 99%

Effects of hypertension, diabetes and coronary heart disease on COVID-19 diseases severity: a systematic review and meta-analysis

Chen

Gong

Wang

et al. 2020

Preprint

127

115

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Background COVID-19 patients with chronic diseases such as hypertension, diabetes and coronary heart diseases is more likely to worsen, but with mixed results for COVID-19 severity. This meta-analysis is to analyze the correlation between hypertension, diabetes, coronary heart disease and COVID-19 disease severity.Methods Available data from PubMed, Web of Science, China National Knowledge Infrastructure Database, WanFang Database and VIP Database, were analyzed using a fixed effects model meta-analysis to derive overall odds ratios (OR) with 95% CIs. Funnel plots and Begg's were used to assess publication bias.Findings Of 182 articles found following our initial search, we assessed 34 full-text articles, of which 9 articles with 1936 COVID-19 patients met all selection criteria for our meta-analysis. No significant heterogeneity between studies. There were significant correlations between severity and hypertension [OR=2.3 [95% CI (1.76, 3.00), P<0.01], diabetes [OR=2.67, 95% CI (1.91, 3.74), P<0.01], coronary heart disease [OR=2.85 [95% CI (1.68, 4.84), P<0.01]. Most of the studies in the funnel plot are on the upper part and few on the base part, and are roughly symmetrical left and right. Begg's test: hypertension (Z=-0.1, P=1.0), diabetes (Z=0.73, P=0.466), coronary heart disease (Z=0.38, P=0.707), all found no publication bias.Interpretation Hypertension, diabetes, and coronary heart disease can affect the severity of COVID-19. It may be related to the imbalance of angiotensin-converting enzyme 2 (ACE2) and the cytokine storm induced by Glucolipid metabolic disorders (GLMD).

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“…Thus, it is conceivable that local cytokines derived from platelets act in combination with glucose to induce the recruitment of inflammatory cells into the dermis, and to inhibit the angiogenesis required during wound healing and tissue regeneration. It is also conceivable that local presence of high glucose levels induces the activation and cytokine production from tissue and immune cells as it is traditionally known in the context of diabetes (Donath et al, 2019). The requirement of glucose in anticoagulants and preservative solutions have been stablished to avoid lysis of erythrocytes during storage of these cells for transfusion (Mollison, 2000).…”

Section: Discussionmentioning

confidence: 99%

Anticoagulants Interfere With the Angiogenic and Regenerative Responses Mediated by Platelets

Oneto

Zubiry

Schattner

et al. 2020

Front. Bioeng. Biotechnol.

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Background and aims: Platelet rich plasma (PRP) obtained from blood anticoagulated with acid-citrate-dextrose (ACD) or sodium-citrate (SC) is used for regenerative medicine as source of platelet-derived growth factors. Allergic reactions against citrate were reported in patients after local injection of PRP allowing us to hypothesize that anticoagulants exert a harmful and local effect that interferes with the regenerative proprieties of platelets. Herein we test this hypothesis by analyzing the effect of ACD and SC on angiogenic and regenerative responses mediated by platelets. Methods: PRP was obtained from SC-or ACD-anticoagulated blood; platelets were lysed to release growth factors; and PRP releasates (PRPr) were used to induce in vitro endothelial proliferation and 2D-migration, and regeneration of mouse skin wounds. Results: We first compared proliferation and migration of endothelial cells mediated by anticoagulated-PRPr supplemented or not with CaCl 2. Alteration of endothelial adhesion and impediment of proliferation and migration was observed without CaCl 2. Although endothelial morphology was normalized in SC-and ACD-PRPr after calcium restitution, angiogenic responses were only markedly induced by SC-PRPr. In vivo studies revealed a delay in mouse skin regeneration after treatment with anticoagulated-PRPr without CaCl 2. Healing was only induced after calcium restitution in SC-but ACD-PRPr. Moreover, the development of inflammatory intradermal papules was evidenced after injection of ACD-PRPr. Supplementation of SC-PRPr with the equivalent concentration of dextrose (D-Glucose, 18 mM) present in ACD-PRPr resulted in reduction of endothelial proliferation and migration, delay of mouse skin regeneration and development of intradermal papules. Finally, collecting blood with half amount of SC significantly improved all the angiogenic and regenerative responses mediated by PRPr. In contrast, the delay of skin regeneration and the development of inflammatory papules remained stable after dilution of ACD. Conclusion: Our findings indicate that (1) calcium restitution is required to impair the cellular and tissue alterations induced by citrated-anticoagulants contained in PRP; (2) ACD-derived dextrose confers anti-angiogenic, anti-regenerative and pro-inflammatory proprieties to PRP; and (3) half concentration of SC improves the angiogenesis and regeneration mediated by PRP.

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Targeting innate immune mediators in type 1 and type 2 diabetes

Cited by 276 publications

References 162 publications

Chronic Adipose Tissue Inflammation Linking Obesity to Insulin Resistance and Type 2 Diabetes

Chronic Adipose Tissue Inflammation Linking Obesity to Insulin Resistance and Type 2 Diabetes

Effects of hypertension, diabetes and coronary heart disease on COVID-19 diseases severity: a systematic review and meta-analysis

Anticoagulants Interfere With the Angiogenic and Regenerative Responses Mediated by Platelets

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