Increased expression of toll-like receptor 4 and inflammatory cytokines, interleukin-6 in particular, in islets from a mouse model of obesity and type 2 diabetes

Apmis ◽  
2012 ◽  
Vol 121 (6) ◽  
pp. 531-538 ◽  
Author(s):  
Mette Ladefoged ◽  
Karsten Buschard ◽  
Ann Maria Kruse Hansen
Inflammation ◽  
2012 ◽  
Vol 36 (1) ◽  
pp. 251-257 ◽  
Author(s):  
Zhao-Shun Jiang ◽  
Su-Xia Wang ◽  
Hong-Xia Jia ◽  
Jing Wang ◽  
Yuan-Tao Liu

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Yuze Li ◽  
Dianzhong Li ◽  
Jinfeng Zhang ◽  
Shurui Liu ◽  
Haijun Chen ◽  
...  

The purpose of this study is to explore why type 2 diabetes mellitus (T2DM) patients are susceptible to pulmonary tuberculosis through detection of serum Toll-like receptor 4 (TLR4), an important immune-related receptor, especially in terms of content and TLR4gene polymorphism. Patients with T2DM complicated by pulmonary tuberculosis (T2DMTB) were selected as the case group and T2DM patients without tuberculosis were selected as the control group. Forty patients in each group were randomly selected and their serum TLR4levels were detected and compared. Determination of six sites of TLR4gene polymorphism was carried out in 238 T2DMTB patients and 310 patients with T2DM, and results showed that the serum TLR4content of the T2DMTB group was significantly lower than that of the T2DM group (p<0.05). The six sites of TLR4gene polymorphism did not show significant associations with T2DMTB risk. No statistically significant differences in genotype distributions were observed between T2DMTB patients and patients with T2DM when studied using the recessive and dominant genetic models. How two diseases with contradictory nutritional statuses can occur in the same person is difficult to explain from environmental factors perspective alone. Future research should study the causes of T2DMTB from the perspective of genetics.


2021 ◽  
Author(s):  
Nezaket COBAN ◽  
Aysegul Bayramoglu ◽  
Zeynep TEMIZ

Abstract Type 2 diabetes mellitus (T2DM) is very common worldwide and genetically heterogeneous. One of the microvascular complications is diabetic nephropathy (DN). In recent years, T2DM has been described as a disease caused by chronic inflammation. The imbalance between pro- and anti-inflammatory cytokines causes inflammation. One of the candidate genes associated with T2DM and DN is the Interleukin-6 (IL-6) gene, one of the pro-inflammatory cytokines. This study was conducted to determine the polymorphism frequencies of the IL-6 gene rs1800796 and investigate the role of this polymorphism in the development of T2DM and DN. Genomic DNA that was obtained from 261 people was used in the study. IL-6 gene rs1800796 polymorphism was determined using the PCR, restriction fragment length polymorphism (RFLP) and electrophoresis. IL-6 gene PCR products were discontinued by treatment with restriction enzyme BsrBI and were analyzed in 2% agarose gel electrophoresis. IL-6 (Bioassay technology laboratory, Shangai, China) level was examined by enzyme-linked immunosorbent assay (ELISA) using a commercial kit. The results were statistically analyzed. The frequencies of rs1800796 genotypes were found to be GG 70.7%, GC 28.5%, CC 0.8% in the control group and GG 87.8%, GC 9.9 %, CC 2.3% in T2DM patients. Although there was a statistically significant difference between the control group and the T2DM patient group in genotype and allele frequencies, there was no significant difference in DN. The G allele frequency was also significantly higher in the T2DM group (p=0.000). IL-6 levels were determinated increased in patients with Type-2 diabetes compared to the control group. However; there was no significant statistically. We can say that IL-6 rs1800796 polymorphism is related to T2DM and G allele can be used as a useful genetic marker; this polymorphism is not related to DN, though.


2018 ◽  
Vol 09 (07) ◽  
Author(s):  
Taís Silveira Assmann ◽  
Natalia Emerim Lemos ◽  
Letícia de Almeida Brondani ◽  
Rodrigo Carlessi ◽  
Carmen Maldonado Bernal ◽  
...  

2018 ◽  
Vol 64 (13) ◽  
pp. 15 ◽  
Author(s):  
Inass Mohamed Taha ◽  
Azza M Abdu Allah ◽  
Eman Masoud Abd El Gayed

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