Insulin resistance, which affects insulin-sensitive tissues, including adipose tissues, skeletal muscle, and the liver, is the central pathophysiological mechanism underlying type 2 diabetes progression. Decreased glucose uptake in insulin-sensitive tissues disrupts insulin signaling pathways, particularly the PI3K/Akt pathway. An in vitro model is appropriate for studying the cellular and molecular mechanisms underlying insulin resistance because it is easy to maintain and the results can be easily reproduced. The application of cell-based models for exploring the pathogenesis of diabetes and insulin resistance as well as for developing drugs for these conditions is well known. However, a comprehensive review of in vitro insulin resistance models is lacking. Therefore, this review was conducted to provide a comprehensive overview and summary of the latest in vitro insulin resistance models, particularly 3T3-L1 (preadipocyte), C2C12 (skeletal muscle), and HepG2 (liver) cell lines induced with palmitic acid, high glucose, or chronic exposure to insulin.

Background: Cervical cancer is one of the most prevalent gynecological cancers worldwide and contributes in highmortality of Indonesian women. The efficacy of chemotherapy as a standart therapy for cervical cancer decreases becauseit frequenly rises adverse effects. Recent studies have found that metformin has a potential anticancer effect mostlythrough reduction of cyclin expression and activation of Activated Adenosine Monophosphate Kinase (AMPK). Thisstudy aimed to investigate the effect of metfomin on expression of cyclin D1 and p53 and apoptosis in HeLa cancer cellline. Methods: HeLa cells were treated with various doses of metformin and doxorubicin as a positive control. Cytotoxiceffect of metformin was determined using the MTT assay. Immunocytochemistry was used to assess cyclin D1 and p53expression and apoptosis levels of treated HeLa cells were analyzed using flowcytometry. Data of cyclin D1 expressionwas statistically analyzed using the Kruskal-Wallis test followed by the Tamhane test, whilst ANOVA and Tukey postHoc tests were used to analyze data of p53 and apoptosis level. The significant value was p< 0.05. Results: Metforminwas able to inhibit proliferation of HeLa cells with IC50 60 mM. HeLa cells treated with 60 and 120 mM metforminhad lower cyclin D1 expression than HeLa cells treated without metformin and reached a significant difference (p=0.001). Moreover, 30 mM or higher doses of metformin increase significantly p53 expression (p< 0.001). Induction ofapoptosis was observed in HeLa cells treated with all doses of metformin and reached statistically difference (p= 0.04and p < 0.001). Conclusion: Metformin can modulate cyclin D1 and p53 expression in HeLa cancer cell line, leadingto inhibition of cell proliferation and induction of apoptosis. Other cyclin family members, CDK inhibitors and AMPKsignaling should be further investigated in order to know mechanism of metformin action.

Narra J is a multidisciplinary journal and it is published three times (April, August, December) a year. The objective is to promote articles on infection, public health, global health, tropical infection, one health and diseases in tropics. Narra J publishes original research work across all disciplines of medicine and allied sciences, related to infection, public health, global health, tropical infection, one health and diseases in tropics. The journal publishes Original articles, Short Report, Review articles, and Letters to the Editor. All articles published in Narra J are peer-reviewed and published online for immediate access and citation.

Systemic lupus erythematosus (SLE) is an inflammatory-autoimmune disease with a complex multi-organ pathogenesis, and it is known to be associated with significant morbidity and mortality. Various genetic, immunological, endocrine, and environmental factors contribute to SLE. Genomic variants have been identified as potential contributors to SLE susceptibility across multiple continents. However, the specific pathogenic variants that drive SLE remain largely undefined. In this study, we sought to identify these pathogenic variants across various continents using genomic and bioinformatic-based methodologies. We found that the variants rs35677470, rs34536443, rs17849502, and rs13306575 are likely damaging in SLE. Furthermore, these four variants appear to affect the gene expression of NCF2, TYK2, and DNASE1L3 in whole blood tissue. Our findings suggest that these genomic variants warrant further research for validation in functional studies and clinical trials involving SLE patients. We conclude that the integration of genomic and bioinformatic-based databases could enhance our understanding of disease susceptibility, including that of SLE.

Obesity has become a global health concern, and the number of individuals with obesity continues to increase significantly worldwide. Obesity increases the risk of developing chronic diseases, resulting in increases morbidity and mortality rates in humans. Zinc (chemical symbol, Zn) has been found to be associated with obesity. Zinc participates in several physiological processes, having been shown to play roles in energy balance, lipid metabolism, appetite regulation, insulin resistance, the regulation of the serum leptin concentration, as well as in inflammatory responses. However, in terms of alleviating obesity, the molecular mechanisms underlying the role of zinc in this process remain poorly understood. Therefore, the present review aimed to provide a comprehensive analysis of what is currently known regarding the molecular mechanisms of zinc supplementation in alleviating obesity, with a focus on lipid metabolism, appetite regulation, insulin signalling and the inflammatory response.

BACKGROUND: Anxiety disorder is one of the most common psychiatric problems. Prolonged stress gives rise to anxiety-like behavior in animals. Environmental interventions influence the outcome of anxiety treatment. Environmental enrichment (EE) can modulate brain’s structure and function. AIM: The objective of the study was to evaluate EE effects on anxiety-like behavior and corticosterone (CORT) level after unpredictable chronic mild stress (UCMS). METHODS: A total of 28 rats were assigned into four groups randomly: Control, UCMS, UCMS+EE, and UCMS+fluoxetine. UCMS, EE, and fluoxetine were given for 21 days. Anxiety behavior was measured on day 22nd using Elevated Plus Maze. Behavioral measurement was based on the total time spent and total entries onto open and closed arms. CORT was measured using ELISA. RESULTS: UCMS increased anxiety-like behavior as seen from reduced number of entries and time spent in open arms as well as increased number of entries and time spent in in closed arms in UCMS group than control. Rats in EE group spent more time and made more entries in the open arms than UCMS group (both p = 0.002). Anxiolytic effect of EE was stronger than fluoxetine. Plasma CORT level among groups did not differ significantly (p = 0.351). CONCLUSION: EE can ameliorate stress-induced anxiety-like behavior without affecting CORT level.