ABSTRACT
Objective: All the aforementioned data have stimulated interest in studying other potential therapies for T1DM including noninsulin pharmacological therapies. The present study attempts to investigate the effect of adjunctive therapy with metformin and acarbose in patients with Type-1 diabetes mellitus
Method: In a single-center, placebo-controlled study [IRCT201102165844N1] we compared the results of two clinical trials conducted in two different time periods on 40 patients with Type-1 diabetes mellitus. In the first section, metformin was given to the subjects. After six months, metformin was replaced with acarbose in the therapeutic regimen. In both studies, subjects were checked for their BMI, FBS, HbA1C, TGs, Cholesterol, LDL, HDL, 2hpp, unit of NPH and regular insulin variations
Results: Placebo-controlled evaluation of selected factors has shown a significant decrease in FBS and TG levels in the metformin group during follow up but acarbose group has shown substantial influence on two hour post prandial [2hpp] and regular insulin intake decline. Moreover, Comparison differences after intervention between two test groups has shown that metformin has had superior impact on FBS and HbA1C decline in patients. Nonetheless, acarbose treatment had noteworthy influence on 2hpp, TGs, Cholesterol, LDL, and regular insulin intake control
Conclusion: The results of this experiment demonstrate that the addition of acarbose or metformin to patients with Type-1 diabetes mellitus who are controlled with insulin is commonly well tolerated and help to improve metabolic control in patients
ABSTRACT
Objective: micro-RNAs [miRNAs] are a class of posttranscriptional regulators that play crucial roles in various biological processes. Emerging evidence suggests a direct link between miRNAs and development of several diseases including type 2 diabetes [T2D]. In this study, we aimed to investigate the effect of predicted miRNA and target genes on insulin resistance
Materials and Methods: this experimental study was conducted on the C2C12 cell line. Using bioinformatics tools miRNA-135 and two respective target genes-insulin receptor [Insr] and vesicle associated membrane protein 2 [Vamp2]- were selected as potential factors involved in insulin resistance process. Levels of glucose uptake miRNA expression and respective gene targets were determined after cell transfaction by miR-135
Results: it was determined that Insr gene expression was significantly down-regulated in miR-135 transfected C2C12 cell line [P
Conclusion: our data indicated no change on the Vamp2 expression level after miRNA transfection, while expression level of Insr was reduced and miR-135 expression was contrarily increased leading to poor stimulation of glucose uptake through insulin, and development of insulin resistance phenotype in C2C12 cell line
ABSTRACT
Objective: MicroRNAs [miRNAs] are a class of small non-coding RNAs that play pivotal roles in many biological processes such as regulating skeletal muscle development where alterations in miRNA expression are reported during myogenesis. In this study, we aimed to investigate the impact of predicted miRNAs and their target genes on the myoblast to myocyte differentiation process
Materials and Methods: This experimental study was conducted on the C2C12 cell line. Using a bioinformatics approach, miR-214 and miR-135 were selected according to their targets as potential factors in myoblast to myocyte differentiation induced by 3% horse serum. Immunocytochemistry [ICC] was undertaken to confirm the differentiation process and quantitative real-time polymerase chain reaction [PCR] to determine the expression level of miRNAs and their targets
Results: During myoblast to myocyte differentiation, miR-214 was significantly down-regulated while miRNA-135, Irs2, Akt2 and Insr were overexpressed during the process
Conclusion: miR-214 and miR-135 are potential regulators of myogenesis and are involved in skeletal muscle development through regulating the IRS/PI3K pathway
ABSTRACT
Hepatitis C virus [HCV] envelope glycoprotein-2 [E2] inhibits the interferon [IFN]induced, double stranded RNA activated protein kinase [PKR] via PKR eukaryotic initiation factor-2a phosphorylation homology domain [PePHD]. Present study examined the genetic variability of the PePHD in patients receiving interferon therapy. The PePHD region from HCV genotype 1a/1b infected patients receiving IFN was amplified by reverse transcriptase polymerase chain reaction [RT-PCR] and analyzed using bidirectionaly sequencing. The PePHD sequence was different in pretreatment isolates from three months treated patients. It was shown that the major PePHD quasispecies could change after three months IFN therapy and in one patient; the major PePHD quasispecies could change after six months IFN therapy. These mutations were occurred at codons 665, 666 and 667 of followed-up samples and at codons 660, 661, 666 and 670 of randomly treated patients. Some of these mutations were similar to those reported in previous studies. Other mutations were also detected in upstream and downstream regions of PePHD which may have influenced the structure, conformation and configuration of this region and thereby suppressing PePHD inhibitory properties. In conclusion our data suggested that HCV E2 PePHD may play an important role in determining the interferon response among Iranian HCV infected patients