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This study conducts an in-depth review of the correlation between testis tissue changes and circulating microRNAs (miRNA) in diabetes-induced male reproductive complications, drawing upon both animal and clinical studies. The original articles published in English that specifically investigate miRNAs linked to male infertility in humans or animals with either type I or ΙΙ diabetes mellitus were included. The relevant articles were gathered from the PubMed, Google Scholar, Cochrane Library, and ScienceDirect databases. The quality of study was assessed utilizing the Joanna Briggs Institute (JBI) Critical Appraisal Checklist for Prevalence Studies. We collected an overall number of 1989 citations relating to our research subject. Following the elimination of articles based on the criteria, a total of 20 papers were included in the study. Aberrant expression profiles of 25 miRNAs were identified in diabetes associated with male reproductive issues, with 15 miRNAs exhibiting increased expression and 10 miRNAs showing decreased expression. Among the chosen publications, eighteen were identified as low-risk and two were classed as moderate quality. The dysregulated miRNAs were linked to testicular injury, disrupted steroid production, decreased sperm development and quality, and erectile dysfunction. The results demonstrate that the miRNA–mRNA network is linked to the pathological progression of diabetic testicular damage or erectile dysfunction. From a therapeutic perspective, the identification of circulating miRNAs could be beneficial in the timely identification and prevention of diabetes problems, such as diabetes-induced male infertility. Among all signaling pathways influenced by modified miRNAs, the Bax-caspase-3, MAPK, PI3K-Akt, and eNOS-cGMP-PKC were the main deregulated pathways. Summary sentence: The expression of potential miRNA as diagnostic biomarkers may be evaluated in diabetes complications and might constitute a monitoring factor in the diabetes-induced male reproductive complications. [ABSTRACT FROM AUTHOR]

The article "Oncostatin M: friend or foe in PCOS pathogenesis?" delves into the complex relationship between oncostatin M (OSM) and polycystic ovary syndrome (PCOS), a common endocrine disorder in women. OSM, an adipokine, is linked to key features of PCOS such as obesity, insulin resistance, hyperandrogenism, and inflammation, but research findings on its role in PCOS are conflicting. The text underscores the necessity for further research to elucidate OSM's effects and potential as a therapeutic target in PCOS treatment, particularly in understanding its impact on granulosa cells and gene expression. [Extracted from the article]

Study aim: In this study, we evaluated the effects of acute and chronic exercise on the plasma FAs and their association with cardiac hypertrophy indices.

Combining agents with molecular targets can reduce monotherapy’s required dose and toxicity in cancer treatment. In this study, we investigated the cellular viability and the mRNA expression of vascular endothelial growth factor (VEGF) and nuclear factor kappa B (NF-κB) for the synergistic effects of imatinib and 2, 5- dimethylcelecoxib (DMC) combination in human colorectal cancer cells. The effects of imatinib and DMC on cell viability were assessed by MTT assay in HT-29 cells. The dose-effect relationships and drug interaction analyses were performed using the CompuSyn Software. NF-κB and VEGF mRNA expression after treating cells with imatinib (7 μM) and DMC (24 μM) separately and in combination (3.5 μM imatinib plus 12 μM DMC) were investigated using real-time RT-PCR. A strong synergy was observed in most of the combined dose pairs of imatinib- DMC in the growth inhibition of HT-29 cancer cells. Combined treatment with 3.5 μM imatinib and 12 μM DMC resulted in a significant (p ˂ 0.05) decrease in VEGF and NF-κB mRNA levels as compared to the vehicle-treated control group. In addition, VEGF mRNA reduction was significant at the mentioned concentrations for the imatinib-DMC combination compared to imatinib alone (p ˂ 0.05). Our results suggest VEGF as one of the cyclooxygenase2 (COX-2) independent mechanisms for the synergistic effects of imatinib-DMC. It would be beneficial to further evaluate the potential utilization of DMC for the anti-cancer application while minimizing undesired side effects related to COX-2 inhibition and reducing the side effects of imatinib therapy. [ABSTRACT FROM AUTHOR]

Mono-targeting by imatinib as a main antitumor agent does not always accomplish complete cancer suppression. 2,5-dimethyl-celecoxib (DMC) is a close structural analog of the selective cyclooxygenase-2 (COX-2) inhibitor, celecoxib, that lacks COX-2 inhibitory function. In this study, we aimed to show the apoptotic effects of imatinib in combination with DMC in human HT-29 colorectal cancer (CRC) cells. HT-29 CRC cells were treated with IC50 dose of imatinib (6.60 µM), DMC (23.45 µM), and their combination (half dose of IC50) for 24 h. The caspase-3 activity was estimated with colorimetric kit. The caspase-3 gene expression was evaluated by real-time PCR method. There was a significant up-regulation in caspase-3 enzyme activity and caspase-3 expression by imatinib and its half dose combination with DMC as compared to control. As a summary, the results of this study strongly suggest that half dose combination of imatinib with DMC induced apoptosis as potent as full dose imatinib in human HT-29 CRC cells, while minimizing undesired side effects related to imatinib mono-therapy. This study also pointed towards possible caspasedependent actions of imatinib and DMC. [ABSTRACT FROM AUTHOR]

Exercise is considered to be a "medicine" due to its modulatory roles in metabolic disorders, such as diabetes and obesity. The intensity and duration of exercise determine the mechanism of energy production by various tissues of the body, especially by muscles, in which the requirement for adenosine triphosphate (ATP) increases by as much as 100-fold. Naturally, athletes try to improve their exercise performance by dietary supplementation with, e.g., vitamins, metabolites, and amino acids. MNAM, as a vitamin B3 metabolite, reduces serum levels and liver contents of triglycerides and cholesterol, and induces lipolysis. It stimulates gluconeogenesis and prohibits liver cholesterol and fatty acid synthesis through the expression of sirtuin1 (SIRT1). It seems that MNAM is not responsible for the actions of NNMT in the adipose tissues as MNAM inhibits the activity of NNMT in the adipose tissue and acts as an inhibitor of its activity.NNMT-MNAM axis is more activated in the muscles of individuals undergoing the high-volume-low-intensity exercise and caloric restriction. Therefore, MNAM could be an important myokine during exercise and fasting where it provides the required energy for muscles through the induction of lipolysis and gluconeogenesis in the liver and adipose tissues, respectively. Increased levels of MNAM in exercise and fasting led us to propose that the consumption of MNAM during training, especially endurance training, could boost exercise capacity and improve performance. Therefore, in this review, we shed light on the potential of MNAM as a dietary supplement in sports medicine., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)