Background Insulin resistance (IR) and fat accumulation in visceral adipose tissue are key players in developing type 2 diabetes (T2D). Several adipose tissue derived-gene polymorphisms are related to higher body mass index (BMI), insulin resistance and T2D. The association of omentin rs2274907 (Val109Asp) and fat-mass and obesity-associated (FTO) rs9939609 gene polymorphisms with overweight/obesity and T2D is controversial. The aim of this study was to determine the association between omentin Val109Asp and FTO rs9939609 polymorphisms and insulin resistance in newly-diagnosed T2D patients. Methods The case-control study included 83 newly-diagnosed T2D patients and 85 healthy matched controls, aged 20–80 years. Fasting blood glucose and insulin levels were measured by the enzymatic method and enzyme-linked-immunosorbent assay, respectively. Insulin resistance was calculated using the homeostasis model assessment (HOMA) index. Genotyping was examined using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Results There are significant differences between both omentin Val109Asp and FTO rs9939609 polymorphisms and studied individuals ( P = 0.011 and P = 0.0001, respectively). Both genetic polymorphisms of omentin Val109Asp and FTO rs9939609 (T/A) are significantly related to higher HOMA index ( P = 0.030 and P = 0.046, respectively). However, omentin Val109Asp polymorphism was only related to individuals who were overweight/obese. Additionally, both omentin Val109Asp and FTO rs9939609 polymorphisms were significantly positively correlated to familial history of diabetes ( P = 0.046 and P = 0.024, respectively). Conclusions Omentin V109D and FTO rs9939609 genetic variations may change insulin metabolism and have key roles in developing T2D through insulin resistance. Thus, the evaluation of these polymorphic regions may be helpful for predicting type 2 diabetes.

The sperm mitochondrial cysteine-rich protein (SMCP) is a rapidly evolving cysteine- and proline-rich protein that is localized in the mitochondrial capsule and enhances sperm motility. The sequences of the SMCP protein, gene, and mRNA in a variety of mammals have been compared to understand their evolution and regulation. SMCP can now be reliably identified by its tripartite structure including a short amino-terminal segment; a central segment containing short tandem repeats rich in cysteine, proline, glutamine, and lysine; and a C-terminal segment containing no repeats, few cysteines, and a C-terminal lysine. The SMCP gene is located in the epidermal differentiation complex (EDC), a large gene cluster that functions in forming epithelial barriers. Similarities in chromosomal location, molecular function, intron-exon structure, and protein organization argue that SMCP originated from an EDC gene and acquired spermatogenic cell-specific transcriptional and translational regulation and a novel cellular function in sperm motility. The SMCP 5' UTR and 3' UTR contain conserved elements and uORFs that may function in cytoplasmic regulation of gene expression, and the levels of SMCP mRNA in human are much lower than in other mammals, a feature of male-biased expression. The evolution of SMCP has been accompanied by changes in the sequence, number, and length of repeat units, including three alleles in dogs. The major proteins associated with the mitochondrial capsule, SMCP and phospholipid hydroperoxide glutathione peroxidase, provide outstanding examples of changes in cellular function driven by selective pressures on sperm motility, an important determinant of male reproductive success.

Different factors influence the development and control of ageing. It is well known that progressive telomere shorting is one of the molecular mechanisms underlying ageing. The shelterin complex consists of six telomere-specific proteins which are involved in the protection of chromosome ends. More particularly, this vital complex protects the telomeres from degradation, prevents from activation of unwanted repair systems, regulates the activity of telomerase, and has a crucial role in cellular senescent and ageing-related pathologies. This review explores the organization and function of telomeric DNA along with the mechanism of telomeres during ageing, followed by a discussion of the critical role of shelterin components and their changes during ageing.

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MicroRNAs (miRNAs) are small protected molecules with a length of 18 to 25 nucleotides. Many studies have recently been conducted on miRNAs, illustrating their role in regulating many biological, physiological, and pathological activities, such as maintaining cellular signalling and regulating cellular pathways. The main role of miRNAs is to regulate the expression of genes after translation, which can lead to the destruction or suppression of translation by binding to mRNAs. As any change in the regulation of miRNAs is associated with several physiological abnormalities, such as type 2 diabetes and its complications, these molecules can be used for therapeutic purposes or as biomarkers for the diagnosis of diseases such as diabetes and its complications. In this review article, we will discuss important findings about the miRNAs and the role of these molecules in different phases of the wound‐healing process of chronic wounds, especially diabetic ulcer.

Background Omentin, releasing by adipose-tissue may be related to glucose metabolism. The omentin circulating levels and the related mRNA expression in visceral adipose-tissue are different in types of diabetes and the exact function of this molecule is still unknown. The aim of this study was to examine omentin gene expression in adipose-tissues of type-1 and type-2 diabetic mice for the investigation of the effects of fat-mass and insulin–glucose metabolism. Methods In this study, 36 C57BL/6 mice were divided into four experimental groups, including control, type-1 diabetes (inducted by streptozotocin), type-2 diabetes with obesity (high-fat diet + low-dose-streptozotocin [HFD + STZ]), and type-2 with normal weight (normal-pellet diet + low-dose-streptozotocin [NPD + STZ]). The present study involved the measurements of oral-glucose-tolerance-test and the levels of biochemical parameters, including blood glucose, omentin, insulin, lipid-profile, as well as aminotransferases. In addition, the omentin mRNA expression was evaluated by real-time polymerase-chain-reaction. Results The results of omentin gene expression analysis showed a significant difference between mRNA expressions in the experimental groups. The plasma omentin levels were significantly higher in type-1 diabetes group and lower in type-2 diabetes with NPD + STZ; however, the plasma omentin levels were not changed in the HFD + STZ group. In addition, the findings of serum-biochemical analysis revealed significant differences, compared to the control-group. Conclusions The omentin expression may be affected by insulin and glucose levels in different types of diabetes more than fat-mass, and due to the local activity, the serum omentin may not comply with its gene expression.

Background: Granulocyte colony-stimulating factor (G-CSF) expressed in engineered Escherichia coli (E. coli) as a recombinant protein is utilized as an adjunct to chemotherapy for improving neutropenia. Recombinant proteins overexpression may lead to creation of inclusion bodies whose recovery is a tedious and costly process. To overcome the problem of inclusion bodies, secretory production might be a used. To achieve a mature secretory protein product, suitable signal peptide (SP) selection is a vital step Objective: In the present study we aimed in silico evaluation of proper SPs for secretory production of recombinant G-CSF in E. coli Methods: Signal peptide website and UniProt were used to collect the SPs and G-CSF sequences. Then, SignalP were utilized in order to predict the SPs and location of their cleavage site. Physicochemical features and solubility were investigated by ProtParam and Protein-sol tools. Fusion proteins sub-cellular localization were predicted by ProtCompB Results: LPP, ELBP, TSH, HST3, ELBH, AIDA and PET were excluded according to SignalP. The highest aliphatic index belonged to OMPC, TORT and THIB and PPA. Also, the highest GRAVY belonged to OMPC, ELAP, TORT, BLAT, THIB, and PSPE. Furthermore, G-CSF fused with all SPs were predicted as soluble fusion proteins except three SPs. Finally, we found OMPT, OMPF, PHOE, LAMB, SAT, and OMPP can translocate G-CSF into extracellular space Conclusion: Six SPs were suitable for translocating G-CSF into the extracellular media. Although growing data indicated that the bioinformatics approaches can improve the precision and accuracy of studies, further experimental investigations are required for final validation

Breast cancer (BC) is the most prevalent malignancy and the second leading cause of death among women worldwide that is caused by numerous genetic and environmental factors. Hence, effective treatment for this type of cancer requires new therapeutic approaches. The traditional methods for treating this cancer have side effects, therefore so much research have been performed in last decade to find new methods to alleviate these problems. The study of the molecular basis of breast cancer has led to the introduction of gene therapy as an effective therapeutic approach for this cancer. Gene therapy involves sending genetic material through a vector into target cells, which is followed by a correction, addition, or suppression of the gene. In this technique, it is necessary to target tumour cells without affecting normal cells. In addition, clinical trial studies have shown that this approach is less toxic than traditional therapies. This study will review various aspects of breast cancer, gene therapy strategies, limitations, challenges and recent studies in this area.