IL-6 Promotes Islet <i>β</i>-Cell Dysfunction in Rat Collagen-Induced Arthritis

Jin, Huan; Ning, Y.N.; Zhou, Haotong; Wang, Youlian

doi:10.1155/2016/7592931

Cited by 5 publications

(4 citation statements)

References 25 publications

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“…Consistently, there are increased levels of serum inflammatory markers, IL-6, in patients with type 2 diabetes, which can induce beta-cell apoptosis [ 19 , 31 – 33 ]. Our previous study also showed that the abnormal glucose metabolism was accompanied by the increased IL-6 expression [ 34 ]. Furthermore, in line with increased IL-6 expression, the apoptosis related enzyme Caspase-3 was also markedly increased in β cell.…”

Section: Inflammation and Abnormal Glucose Metabolismmentioning

confidence: 99%

Abnormal Glucose Metabolism in Rheumatoid Arthritis

Zhou

Jin

et al. 2017

BioMed Research International

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The incidence of abnormal glucose metabolism in patients with rheumatoid arthritis was considerably higher than the general population. The persistent systemic inflammatory state in rheumatoid arthritis might be associated with the glucose metabolism dysfunction. In this context, insulin resistance, islet β cell apoptosis, inflammatory cytokines, and other aspects which were linked with abnormal glucose metabolism in rheumatoid arthritis were reviewed. This review will be helpful in understanding the abnormal glucose metabolism mechanism in patients with rheumatoid arthritis and might be conducive to finding an effective treatment.

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Section: Inflammation and Abnormal Glucose Metabolismmentioning

confidence: 99%

Abnormal Glucose Metabolism in Rheumatoid Arthritis

Zhou

Jin

et al. 2017

BioMed Research International

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“…Interestingly, IL-6 levels were reduced in both CP and LPP groups by PPD90, concomitant with the return of glucose tolerance to control values. Some studies have found that high concentrations of IL-6 could promote β-cell apoptosis and contribute to glucose intolerance (Jin et al 2016). However, since β-cell area did not change at any time point after parturition in LPP mice, it is more likely that IL-6 is exerting effects on non-islet tissues.…”

Section: Journal Of Endocrinologymentioning

confidence: 89%

Altered pancreas remodeling following glucose intolerance in pregnancy in mice

Szlapinski

Botros

Donegan

et al. 2020

Journal of Endocrinology

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Gestational diabetes mellitus increases the risk of dysglycemia postpartum, in part, due to pancreatic β-cell dysfunction. However, no histological evidence exists comparing endocrine pancreas after healthy and glucose-intolerant pregnancies. This study sought to address this knowledge gap, in addition to exploring the contribution of an inflammatory environment to changes in endocrine pancreas after parturition. We used a previously established mouse model of gestational glucose intolerance induced by dietary low protein insult from conception until weaning. Pancreas and adipose samples were collected at 7, 30 and 90 days postpartum for histomorphometric and cytokine analyses, respectively. Glucose tolerance tests were performed prior to euthanasia and blood was collected via cardiac puncture. Pregnant female mice born to dams fed a low protein diet previously shown to develop glucose intolerance at late gestation relative to controls continued to be glucose intolerant until 1 month postpartum. However, glucose tolerance normalized by 3 months postpartum. Glucose intolerance at 7 days postpartum was associated with lower beta- and alpha-cell fractional areas and higher adipose levels of pro-inflammatory cytokine, interleukin-6. By 3 months postpartum, a compensatory increase in the number of small islets and a higher insulin to glucagon ratio likely enabled euglycemia to be attained in the previously glucose-intolerant mice. The results show that impairments in endocrine pancreas compensation in hyperglycemic pregnancy persist after parturition and contribute to prolonged glucose intolerance. These impairments may increase the susceptibility to development of future type 2 diabetes.

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“…The literature proves that potential targets can interact with each other. To explore the possible mechanism of the rheumatoid arthritis- (RA-) related abnormal glucose metabolism, researchers showed that the apoptosis-related enzyme Caspase-3 was significantly increased with upregulation of IL-6 expression [ 31 ]. MMP9 released after nerve injury is involved in the activation of microglia, leading to the release of IL-6 by microglia [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

Network Pharmacology-Based Strategy for Exploring the Pharmacological Mechanism of Honeysuckle (Lonicer japonica Thunb.) against Newcastle Disease

Huang

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Objective. Newcastle disease causes huge economic losses in the global poultry industry. An efficient treatment is needed to deal with the variable immunogenicity of the Newcastle disease virus (NDV). This study utilized network pharmacology to study the potential therapeutic targets of Honeysuckle (Lonicer japonica Thunb.) against Newcastle disease. Methods. Venny online analysis was used to analyze the potential overlapping targets of Honeysuckle and Newcastle disease. Hub genes were obtained using the STRING database and Cytoscape 3.8.2 software. Gene Ontology (GO) functions and Kyoto Encyclopedia of Genes and Genomics (KEGG) pathway enrichment analysis using the DAVID online tool were performed on these targets. Results. Twenty-five overlapping targets were identified. The PPI network construction results included 23 nodes of 25 genes and 95 edges. It was found that the IL-6 node had the largest degree. STAT1 and IRF1, CASP9, and CASP3 had the same as well as strongest interaction strengths. GO functions, such as “cytokine activity,” had a regulatory effect on NDV. The “Toll-like receptor signaling Pathway” “Nod-like receptor signaling pathway,” “RIG-I-like receptor signaling pathway,” and “Apoptosis,” which were obtained using KEGG analysis, also indicated that these pathways can act on NDV to enhance immune function. Conclusions. In this study, the potential targets and mechanisms of action of Honeysuckle against Newcastle disease were explored through network pharmacology, which provided a theoretical basis for the treatment of Newcastle disease and provided new ideas for the development of traditional Chinese medicine for the poultry industry.

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IL-6 Promotes Islet β-Cell Dysfunction in Rat Collagen-Induced Arthritis

Cited by 5 publications

References 25 publications

Abnormal Glucose Metabolism in Rheumatoid Arthritis

Abnormal Glucose Metabolism in Rheumatoid Arthritis

Altered pancreas remodeling following glucose intolerance in pregnancy in mice

Network Pharmacology-Based Strategy for Exploring the Pharmacological Mechanism of Honeysuckle (Lonicer japonica Thunb.) against Newcastle Disease

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