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Background: Diabetes is a leading cause of mortality and morbidity globally. Hypoglycemia is a rate-limiting issue in achieving rigorous glycemic control in diabetic patients. Many diabetic patients on insulin therapy are not aware of hypoglycemic symptoms. This study aimed to determine the prevalence of hypoglycemic symptoms in diabetic patients on Insulin. Materials & Methods: A cross-sectional study was conducted from July to October 2023 at Khyber Teaching Hospital Peshawar. A convenient sampling technique was used for data collection, and data was collected using socio-demographic characteristics, Clark's questionnaire, and questions related to hypoglycemic symptoms. The sample size was determined using the WHO formula. Data were analyzed using SPSS 24. A p-value of <0.05 demonstrated statistically significant findings. Results: The study included 345 diabetic patients. Among them, 156 (43.2%) were males and 189 (52.4%) were females. The majority of participants were uneducated, 250 (69.3%). About 18% of patients were aware of hypoglycemic symptoms. There was no association between the duration of diabetes and gender and awareness of hypoglycemic symptoms, while an association was found between education and awareness of hypoglycemic symptoms (p<0.001). Most participants said that they consume sugar when they experience hypoglycemic symptoms. Conclusion: The majority of participants were unaware of hypoglycemic symptoms. These patients experience symptoms such as perspiration and trembling with hypoglycemia. The study also found an association between patients' awareness of their symptoms and educational attainment. Most participants admitted to consuming sugar in response to hypoglycemic symptoms. [ABSTRACT FROM AUTHOR]

Accumulating studies have demonstrated the protective roles of mesenchymal stem cells against several disorders. However, one of their crucial limitations is reduced viability under stress conditions, including the hyperglycemia induced by diabetes. The molecular mechanisms involved in diabetes-induced kidney injuries are not fully elucidated. In this study, we found that high glucose (HG) reduced human proximal tubular epithelial cell viability. Further, hyperglycemia induced oxidative stress-mediated apoptosis and fibrosis in HK-2 cells via activation of the mitogen-activated protein kinases (MAPKs) including c-Jun N-terminal kinase JNK and p38 kinase. Carboxyl terminus of HSP70 interacting protein (CHIP) overactivation considerably rescued cell viability under HG stress. Moreover, Western blot analysis, flow cytometry, and MitoSOX staining revealed that hyperglycemia-induced mitochondrial oxidative stress production and apoptosis were attenuated in CHIP-overexpressing Wharton's jelly-derived mesenchymal stem cells (WJMSCs). Co-culture with CHIP-expressing WJMSCs maintained HK-2 cell viability, and inhibited apoptosis and fibrosis by attenuating HG-induced ROS-mediated MAPK activation. CHIP-overexpressing WJMSCs also rescued the decreased kidney weight and hyperglycemia-induced kidney damage observed in streptozotocin-induced diabetic rats. Cumulatively, the current research findings demonstrate that CHIP suppresses hyperglycemia-induced oxidative stress and confers resistance to MAPK-induced apoptosis and fibrosis, and suggests that CHIP protects WJMSCs and the high quality WJMSCs have therapeutic effects against diabetes-induced kidney injuries. [Display omitted] The hyperglycemia induced by diabetes can lead to kidney damage, and therapeutic interventions are limited. Mesenchymal stem cells are promising therapies; however, they suffer from limited viability in stress conditions, including hyperglycemia. CHIP overexpression in WJMSCs rescues hyperglycemia-induced kidney injuries in high glucose and STZ-induced diabetic rats. CHIP-overexpressing WJMSCs are a promising therapeutic option for the prevention of diabetes-induced kidney damage. [ABSTRACT FROM AUTHOR]

Recent studies indicate that umbilical cord stem cells are cytoprotective against several disorders. One critical limitation in using stem cells is reduction in their viability under stressful conditions, such as diabetes. However, the molecular intricacies responsible for diabetic conditions are not fully elucidated. In this study, we found that high glucose (HG) conditions induced loss of chaperone homeostasis, stabilized PTEN, triggered the downstream signaling cascade, and induced apoptosis and oxidative stress in Wharton's jelly derived mesenchymal stem cells (WJMSCs). Increased Carboxyl terminus of Hsc70 interacting protein (CHIP) expression promoted phosphatase and tensin homolog (PTEN) degradation via the ubiquitin‐proteasome system and shortened its half‐life during HG stress. Docking studies confirmed the interaction of CHIP with PTEN and FOXO3a with the Bim promoter region. Further, it was found that the chaperone system is involved in CHIP‐mediated PTEN proteasomal degradation. CHIP depletion stabilizes PTEN whereas PTEN inhibition showed an inverse effect. CHIP overactivation suppressed the binding of FOXO3a with bim. Coculturing CHIP overexpressed WJMSCs suppressed HG‐induced apoptosis and oxidative stress in embryo derived cardiac cell lines. CHIP overexpressing and PTEN silenced WJMSCs ameliorated diabetic effects in streptozotocin (STZ) induced diabetic rats and further improved their body weight and heart weight, and rescued from hyperglycemia‐induced cardiac injury. Considering these, the current study suggests that CHIP confers resistance to apoptosis and acts as a potentiation factor in WJMSCs to provide protection from degenerative effects of diabetes. [ABSTRACT FROM AUTHOR]