Deactivation of the NLRP3 inflammasome in infiltrating macrophages by duodenal-jejunal bypass surgery mediates improvement of beta cell function in type 2 diabetes

Wu, Dong; Yan, Zhibo; Cheng, Yugang; Zhong, Maiying; Liu, Shao-zhuang; Hu, Sanyuan

doi:10.1016/j.metabol.2017.10.015

Cited by 33 publications

(21 citation statements)

References 46 publications

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“…In vivo , the NLRP3 inflammasome is required for IL-1β processing, with caspase -1 and ASC oligomerization mediating IL-1β maturation and secretion. As a crucial element of the innate immune system, the NLRP3 inflammasome is not only an important component in host defense against pathogens (Allen et al, 2009; Wang et al, 2018; Negash et al, 2019) but is also involved in the progression of several inflammatory human diseases, such as gout and type 2 diabetes (So and Martinon, 2017; Wu et al, 2018). Additionally, DENV infection triggers the assembly of the NLRP3 inflammasome in platelets, further contributing to increased vascular permeability by synthesis and release of IL-1β (Hottz et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Dengue Virus Infection Activates Interleukin-1β to Induce Tissue Injury and Vascular Leakage

et al. 2019

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Dengue virus (DENV) infection causes several diseases ranging from dengue fever to life-threatening dengue hemorrhagic fever and dengue shock syndrome characterized by endothelial dysfunction, vascular leakage, and shock. Here, we identify a potential mechanism by which DENV induces tissue injury and vascular leakage by promoting the activation of interleukin (IL)-1β. DENV facilitates IL-1β secretion in infected patients, mice, human peripheral blood mononuclear cells (PBMCs), mouse bone marrow-derived macrophages (BMDMs), and monocyte-differentiated macrophages (THP-1) via activating the NLRP3 inflammasome. The accumulated data suggest that IL-1β probably induces vascular leakage and tissue injury in interferon-alpha/beta receptor 1 deficient C57BL/6 mice (IFNAR–/– C57BL/6), whereas IL-1 receptor antagonist (IL-1RA) alleviates these effects of IL-1β. Finally, administration of recombinant IL-1β protein results in vascular leakage and tissue injury in C57BL/6 mice. Together, the accumulated results demonstrate that IL-1β contributes to DENV-associated pathology and suggest that IL-1RA acts as a potential agent for the treatment of DENV-associated diseases.

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Section: Discussionmentioning

confidence: 99%

Dengue Virus Infection Activates Interleukin-1β to Induce Tissue Injury and Vascular Leakage

et al. 2019

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“…been shown that DJB surgery improved glucose metabolism and insulin secretion by suppressing the glucose uptake by the downregulation of glucose transporters, activating the insulin signaling pathway, and inhibiting the inflammatory signals which induced beta cell apoptosis (Jurowich et al, 2013;Wu et al, 2018;Li et al, 2020), but, a recent study indicated that the new biliopancreatic diversion (NBPD) was a main contributing factor to the glucose-lowering effects of DJB compared with simple duodenal-jejunal exclusion and SHAM surgery in T2DM (Weng et al, 2017). However, the DJB-sa procedure we performed achieved the same hypoglycemic effect without the NBPD.…”

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confidence: 99%

Single-Anastomosis Duodenal Jejunal Bypass Improve Glucose Metabolism by Regulating Gut Microbiota and Short-Chain Fatty Acids in Goto-Kakisaki Rats

Zhang

et al. 2020

Front. Microbiol.

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In recent years, bariatric surgery has emerged as a promising treatment for type 2 diabetes. Bariatric surgery is known to cause alterations in the relative abundance and composition of gut microbiota, which may lead to alterations in the levels of Short-Chain Fatty Acids (SCFAs) that are produced during fermentation by gut microbes. However, little is known about the mechanism of improved glucose metabolism mediated by gut microbiota following bariatric surgery. The aim of our study was to explore whether changes in gut microbiota and in fecal SCFA could be detected following singleanastomosis duodenal jejunal bypass (DJB-sa) surgery, a type of bariatric surgery, and whether these alterations might be related to the improvement of glucose metabolism. To this end, we performed DJB-sa or SHAM surgery on Goto-Kakisaki (GK) rats. We then compared the glucose metabolism as well as changes in gut microbiota and SCFAs levels between both groups. Our results showed that DJB-sa surgery was associated with a significant decrease in fasting blood glucose (FBG), intraperitoneal glucose tolerance test (IPGTT), and fasting serum insulin (FSI). And, DJB-sa led to a change in the composition of gut microbiota including an increase in the relative abundance of SCFA-producing bacteria (Bifidobacterium and Subdoligranulum). Moreover, the levels of six SCFAs in feces, as well as the intestinal expression of SCFA receptors including G-protein-coupled receptor 41 (GPR41), G-protein-coupled receptor 43 (GPR43), and G-protein-coupled receptor 109A (GPR109A), and the expression of Glucagon-like peptide-1 (GLP-1) displayed a significant increase following DJB-sa compared with the Sham group. Thus, the gut microbiota may contribute to the improvement of glucose metabolism in type 2 diabetes following DJB-sa. In conclusion, our study shows that DJB-sa improves glucose metabolism by modulating gut microbiota and by increasing short-chain fatty acid production.

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“…Additionally, the model must be inexpensive and easy access. The rat models described in the current study including rats injected with low or high dose STZ [12]; rats injected with nicotinamide and STZ [13]; and rats received high-fat diet and STZ injection [14]. We attempted to identify a suitable non-genetic rat model to mimics the pathogenesis and clinical features of diabetes for further research.…”

Section: Discussionmentioning

confidence: 99%

Study on optimization and stability of a single dose streptozotocin-induced diabetic modeling in rats

Zhang

Hong

et al. 2020

Preprint

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BackgroundOptimization of experimental conditions in streptozotocin induced diabetic model in Sprague Dawley (SD) rats to evaluate the stability of the model.MethodsMale and female SD rats were randomly divided into control group, STZ 45 group (STZ: 45 mg / kg), STZ 65 group (STZ: 65 mg / kg), STZ 85 group (STZ: 85 mg / kg), high fat diet with STZ 45 group (STZ: 45 mg / kg), high fat diet with STZ 65 group (STZ: 65 mg / kg), high fat diet with STZ 85 group (STZ: 85 mg / kg). N = 6 in each group. The changes of body weight and blood glucose were observed dynamically.ResultsThere was no significant difference in blood glucose or body weight between the STZ 45 group and the control group in both male and female rats, whether or not they were on a high-fat diet. However, there were significant differences in blood glucose between the high-dose STZ group and the control group in both male and female rats, regardless of whether the rats were on a high-fat diet or not (P < 0.05 or P < 0.01). Compared with the control group, there were significant differences in blood glucose levels (P < 0.05 or P < 0.01) and higher blood glucose levels in the male rats fed with the normal diet than that in those fed with the high-fat diet.ConclusionsIn this study, male rats fed with ordinary feed and injected STZ dose of 65 mg / kg were the most stable and ideal diabetic rat.

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Deactivation of the NLRP3 inflammasome in infiltrating macrophages by duodenal-jejunal bypass surgery mediates improvement of beta cell function in type 2 diabetes

Cited by 33 publications

References 46 publications

Dengue Virus Infection Activates Interleukin-1β to Induce Tissue Injury and Vascular Leakage

Dengue Virus Infection Activates Interleukin-1β to Induce Tissue Injury and Vascular Leakage

Single-Anastomosis Duodenal Jejunal Bypass Improve Glucose Metabolism by Regulating Gut Microbiota and Short-Chain Fatty Acids in Goto-Kakisaki Rats

Study on optimization and stability of a single dose streptozotocin-induced diabetic modeling in rats

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