Type 2 Diabetes Mellitus Patients Manifest Greater Muscle Fatigability Than Healthy Individuals During Dynamic Fatigue Protocol

2021 ◽  
Author(s):  
Pooja Bhati ◽  
Deepika Singla ◽  
Sarfaraz Masood ◽  
M. Ejaz Hussain
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Healthy Individuals ◽  
Fatigue Protocol ◽  
Dynamic Fatigue

scholarly journals Dyslipidemia rather than Type 2 Diabetes Mellitus or Chronic Periodontitis Affects the Systemic Expression of Pro- and Anti-Inflammatory Genes

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Rafael Nepomuceno ◽  
Bárbara Scoralick Villela ◽  
Sâmia Cruz Tfaile Corbi ◽  
Alliny De Souza Bastos ◽  
Raquel Alves Dos Santos ◽  
...  
Keyword(s):  
Gene Expression ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Chronic Periodontitis ◽  
Healthy Individuals ◽  
Inflammatory Genes ◽  
Anti Inflammatory ◽  
Immune Related Genes

A high percentage of type 2 diabetes mellitus (T2D) patients are also affected by dyslipidemia and chronic periodontitis (CP), but no studies have determined the gene expression in patients that are simultaneously affected by all three diseases. We investigated the systemic expression of immune-related genes in T2D, dyslipidemia, and CP patients. One hundred and fifty patients were separated into five groups containing 30 individuals each: (G1) poorly controlled T2D with dyslipidemia and CP; (G2) well-controlled T2D with dyslipidemia and CP; (G3) normoglycemic individuals with dyslipidemia and CP; (G4) healthy individuals with CP; (G5) systemic and periodontally healthy individuals. Blood analyses of lipid and glycemic profiles were carried out. The expression of genes, includingIL10, JAK1, STAT3, SOCS3, IP10, ICAM1, IFNA, IFNG, STAT1,andIRF1,was investigated by RT-qPCR. Patients with dyslipidemia demonstrated statistically higher expression of theIL10andIFNAgenes, whileIFNG, IP10, IRF1, JAK1,andSTAT3were lower in comparison with nondyslipidemic patients. Anti-inflammatory genes, such asIL10, positively correlated with parameters of glucose, lipid, and periodontal profiles, while proinflammatory genes, such asIFNG, were negatively correlated with these parameters. We conclude that dyslipidemia appears to be the primary disease that is associated with gene expression of immune-related genes, while parameters of T2D and CP were correlated with the expression of these important immune genes.

scholarly journals Effects of Genetic Variants of Nuclear Receptor Y on the Risk of Type 2 Diabetes Mellitus

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Ying Wang ◽  
Shanshan Yang ◽  
Qiuyue Guan ◽  
Jinglu Chen ◽  
Xueping Zhang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Genetic Variants ◽  
Genetic Model ◽  
Genotypic Frequency ◽  
Nucleotide Polymorphisms ◽  
Healthy Individuals ◽  
Chinese Han

Nuclear factor-Y (NF-Y) consists of three evolutionary conserved subunits including NF-YA, NF-YB, and NF-YC; it is a critical transcriptional regulator of lipid and glucose metabolism and adipokine biosynthesis that are associated with type 2 diabetes mellitus (T2DM) occurrence, while the impacts of genetic variants in the NF-Y gene on the risk of T2DM remain to be investigated. In the present study, we screened five single-nucleotide polymorphisms (SNPs) with the SNaPshot method in 427 patients with T2DM and 408 healthy individuals. Subsequently, we analyzed the relationships between genotypes and haplotypes constructed from these SNPs with T2DM under diverse genetic models. Furthermore, we investigated the allele effects on the quantitative metabolic traits. Of the five tagSNPs, we found that three SNPs (rs2268188, rs6918969, and rs28869187) exhibited nominal significant differences in allelic or genotypic frequency between patients with T2DM and healthy individuals. The minor alleles G, C, and C at rs2268188, rs6918969, and rs28869187, respectively, conferred a higher T2DM risk under a dominant genetic model, and the carriers of these risk alleles (either homozygotes of the minor allele or heterozygotes) had statistically higher levels of fasting plasma glucose, cholesterol, and triglycerides. Haplotype analysis showed that SNPs rs2268188, rs6918969, rs28869187, and rs35105472 formed a haplotype block, and haplotype TTAC was protective against T2DM (OR=0.76, 95% CI=0.33-0.82, P=0.004), while haplotype GCCG was associated with an elevated susceptibility to T2DM (OR=2.33, 95% CI=1.43-3.57, P=0.001). This study is the first ever observation to our knowledge that indicates the genetic variants of NF-YA might influence a Chinese Han individual’s occurrence of T2DM.

The Variation of Disulfides in the Progression of Type 2 Diabetes Mellitus

2018 ◽  
Vol 128 (02) ◽  
pp. 77-81 ◽  
Author(s):  
Merve Ergin ◽  
Cevdet Aydin ◽  
Emine Feyza Yurt ◽  
Bekir Cakir ◽  
Ozcan Erel
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Gradual Increase ◽  
Control Group ◽  
Newly Diagnosed ◽  
Healthy Individuals ◽  
Total Thiol

Abstract Aim The purpose of this study was to examine thiol-disulfide balance in patients with type 2 diabetes mellitus. Methods This study included 32 subjects with known type 2 diabetes mellitus without complications, 30 patients with type 2 diabetes mellitus with complications, 28 newly diagnosed patients with type 2 diabetes mellitus, and 45 healthy individuals. Thiol-disulfide profile tests were quantified in all groups. Results Compared to the control group, patients in each of the diabetic groups had significantly lower native and total thiol levels, higher disulfide levels, and higher disulfide/native thiol and disulfide/total thiol ratios (p<0.05 for all). Disulfide levels were significantly lower in the newly diagnosed group than in other diabetic groups (p<0.05). There were significant associations between glycemic parameters and thiol-disulfide tests (p<0.05). Conclusions A disequilibrium between thiol-disulfide pairs occurs in patients with type 2 diabetes mellitus, and a gradual increase to disulfide levels may contribute to the disease’s severity. Deteriorated thiol-disulfide homeostasis may be relevant to the pathophysiology of type 2 diabetes mellitus.

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