A novel mechanism of diabetic vascular endothelial dysfunction: Hypoadiponectinemia-induced NLRP3 inflammasome activation

Zhang, Jinglong; Xia, Linying; Zhang, Fen; Zhu, Di; Xin, Chao; Wang, Helin; Zhang, Fuyang; Guo, Xiaorong; Lu, Yan; Zhang, Ling; Wang, Shan; Guo, Xiong; Huang, Chong; Gao, Feng; Liu, Yi; Tao, Ling

doi:10.1016/j.bbadis.2017.02.012

Cited by 60 publications

(44 citation statements)

References 46 publications

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“…Thus, it is conceivable that FSTL1 levels may not only reflect the MU state, but may also activate the NLRP3 inflammasome in macrophages infiltrating VAT, thereby resulting in an MU state with more adverse inflammatory profiles as mediators of increasing metabolic risk. Furthermore, low levels of adiponectin from adipocyte showing the FSTL1 as a marker of metabolic unhealth inverse correlation with the cardiovascular disease [30] also induced activation of the NLRP3 inflammasome [31,32]. Taken altogether, these findings indicate that additional investigations to identify the relationships between adiponectin and FSTL1 are necessary.…”

Section: Discussionmentioning

confidence: 88%

High circulating follistatin-like protein 1 as a biomarker of a metabolically unhealthy state

et al. 2019

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The inflammatory biomarkers that fully characterize the metabolically unhealthy (MU) state-which is a risk factor for cardiovascular disease (CVD)-remain unclear. Recent studies suggest follistatin-like protein 1 (FSTL1) could be used as a biomarker for inflammation and CVD, however there is little information on FSTL1 levels in the MU state. We aimed to evaluate the associations between FSTL1, the presence of MU state and subclinical coronary atherosclerosis. In a cross-sectional study, we evaluated FSTL1 levels and their relationship with the presence of MU state and coronary artery plaques in 230 Korean patients. Significant increase in FSTL1 levels was observed in subjects with MU state (p = 0.020), but not those with obesity state according to body mass index criteria (p = 0.790). After adjusting for confounders, the odd ratio (OR) for the MU state among patients in the highest FSTL1 tertile (T3) was higher in comparison with the lowest tertile (T1) (OR = 3.60, 95% confidence interval [95% CI] = 1.20-10.83). In a subgroup (n = 66), FSTL1 levels were also marginally higher in patients with plaques (p = 0.098). The OR for plaque presence in patients with T3 was significantly higher in comparison with T1 after adjusting for confounders (OR = 12.51, 95% CI = 1.15-135.73). Plasma FSTL1 may be a useful biomarker for the risk of MU state and CVD.

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Section: Discussionmentioning

confidence: 88%

High circulating follistatin-like protein 1 as a biomarker of a metabolically unhealthy state

et al. 2019

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“…We and others reported the increased superoxide anion production, lipid peroxidation, and NADPH oxidase activity in the plasma and tissue of type 2 diabetic mice . It is well established that oxidative stress is involved in the development and progression of diabetes mellitus and diabetic complications.…”

Section: Discussionmentioning

confidence: 61%

The opposite effects of nitric oxide donor, S‐nitrosoglutathione, on myocardial ischaemia/reperfusion injury in diabetic and non‐diabetic mice

Liu

Chen

Wang

et al. 2017

Clin Exp Pharma Physio

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Nitric oxide is a potent anti-apoptotic and cardioprotective molecule in healthy animals. However, recent study demonstrates that overexpression of eNOS exacerbates the liver injury in diabetic animals. whether diabetes may also alter NO's biologic activity in ischaemic/reperfused heart remains unknown. The present experiment was designed to determine whether the nitric oxide donor, S-nitrosoglutathione, may exert different effects on diabetic and non-diabetic myocardial ischaemia/reperfusion (MI/R) injury. Diabetic state was induced in mice by multiple intraperitoneal injections of low-dose streptozotocin (STZ). The control or diabetic mice were subjected to 30 minutes ischaemia and 3 or 24 hours reperfusion. At 10 minutes before reperfusion, diabetic and non-diabetic mice were received an intraperitoneal injection of S-nitrosoglutathione (GSNO, a nitric oxide donor, 1 μmol/kg). GSNO attenuated MI/R injury in non-diabetic mice, as measured by improved cardiac function, reduced infarct size and decreased cardiomyocyte apoptosis. In contrast, GSNO failed to attenuate but, rather, aggravated the MI/R injury in diabetic mice. Mechanically, the diabetic heart exhibited an increased nitrative/oxidative stress level, as measured by peroxynitrite formation, compared with non-diabetic mice. Co-administration of GSNO with EUK134 (a peroxynitrite scavenger) or MnTE-2-PyP5 (a superoxide dismutase mimetic) or Apocynin (a NADPH oxidase inhibitor) 10 minutes before reperfusion significantly decreased the MI/R-induced peroxynitrite formation and the MI/R injury. Collectively, the present study for the first time demonstrated that diabetes may cause superoxide overproduction, increase NO inactivation and peroxynitrite formation, and thus convert GSNO from a cardioprotective molecule to a cardiotoxic molecule.

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“…The study of our laboratory also found that anthocyanin protected against diabetes-related endothelial dysfunction [16]. On the other hand, hypoadiponectinemia-induced in ammasome activation may be the molecular mechanism for diabetic vascular endothelial dysfunction [19]. Basic and clinical studies have identi ed the anti-atherogenic function of adiponectin [20] and its positive effect on vascular in ammation and endothelial function [21].…”

Section: Possible Mechanismmentioning

confidence: 71%

Anthocyanins increase serum adiponectin in newly diagnosed diabetes but not in prediabetes: a randomized controlled trial

Yang¹,

Liu²,

Qiu³

et al. 2020

Preprint

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Background Epidemiological studies have suggested that adiponectin is associated with the development of insulin resistance and type 2 diabetes. This study first examined the effect of purified anthocyanins, a group of dietary flavonoids, on serum adiponectin in patients with prediabetes and newly diagnosed diabetes.Methods A total of 160 patients with prediabetes (n=90) or newly diagnosed diabetes (n=70) were randomly assigned to either the anthocyanins group or the placebo group for 12 weeks of intervention. Serum adiponectin, a set of biomarkers related to glucolipid metabolism, anthropometric parameters, dietary intake and physical activity were measured before and after intervention.Results Anthocyanins increased serum adiponectin compared with placebo (net change 0.46 µg/mL, 95% CI [0.03, 0.90], p=0.038) in the subjects with newly diagnosed diabetes. No significant difference in the change in adiponectin was observed between the two groups either in the overall subjects (0.02 µg/mL [-0.32, 0.36], p=0.906) or in prediabetes (-0.35 µg/mL [-0.85, 0.16], p=0.174). Anthocyanins also decreased fasting glucose (-0.5 mmol/L [-1, -0.04], p=0.035) in the subjects with newly diagnosed diabetes, but no such change was observed in those with prediabetes.Conclusions Anthocyanins supplementation for 12 weeks improved serum adiponectin and fasting glucose in patients with newly diagnosed diabetes, but not in patients with prediabetes.

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A novel mechanism of diabetic vascular endothelial dysfunction: Hypoadiponectinemia-induced NLRP3 inflammasome activation

Cited by 60 publications

References 46 publications

High circulating follistatin-like protein 1 as a biomarker of a metabolically unhealthy state

High circulating follistatin-like protein 1 as a biomarker of a metabolically unhealthy state

The opposite effects of nitric oxide donor, S‐nitrosoglutathione, on myocardial ischaemia/reperfusion injury in diabetic and non‐diabetic mice

Anthocyanins increase serum adiponectin in newly diagnosed diabetes but not in prediabetes: a randomized controlled trial

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