Ayman Zaky Elsamanoudy

Insulin resistance (IR) is characterized by impaired insulin signaling in skeletal muscle, liver, and adipose tissue. Increasing evidence indicates mitochondrial dysfunction as a key factor contributing to IR. Mitochondrial resilience refers to the mitochondria’s ability to adapt to metabolic stress by regulating biogenesis, dynamics, mitophagy, and redox homeostasis. Linking mitochondrial resilience with insulin signaling could be essential for maintaining metabolic health. This review aims to map and synthesize the existing literature on the relationship between mitochondrial resilience and insulin resistance, focusing on cellular and molecular mechanisms, tissue-specific roles, metabolic consequences, and translational evidence from both animal and human studies. This scoping review adhered to PRISMA-ScR guidelines and included comprehensive searches of PubMed, Scopus, Web of Science, Embase, and Google Scholar. It included experimental and observational studies, original articles, systematic reviews, and meta-analyses, while excluding non-English publications and animal studies without clinical relevance. A total of 7, 012 records were identified; after removing duplicates, screening, and assessing eligibility, 184 studies were included. The evidence shows that impaired mitochondrial biogenesis, defective mitochondrial dynamics, reduced mitophagy, and oxidative stress disturb insulin signaling and promote metabolic inflexibility. Conversely, enhancing mitochondrial resilience increases mitochondrial quantity and function. Lifestyle modification strategies and pharmacological intervention target these pathways to improve mitochondrial resilience. Importantly, understanding inter-individual differences in mitochondrial adaptive capacity may support the development of personalized therapeutic and nutritional strategies aimed at improving insulin sensitivity and metabolic outcomes. In conclusion, mitochondrial resilience provides a comprehensive framework connecting mitochondrial quality to insulin signaling and metabolic health. Focusing on mitochondrial resilience is a promising, mechanism-based strategy for preventing and managing insulin resistance and its related comorbidities.

Artificial Intelligence (AI) has emerged as a transformative tool in education, offering personalized learning, adaptive assessments, and real-time feedbac

This review aimed to investigate the relationship between endoplasmic reticulum (ER) stress, insulin resistance, and the potential mitigating effects of a low-carbohydrate, high-fat diet, Ketogenic diet (LCHF-KD). A detailed literature search using databases to achieve a comprehensive overview. The keywords of the search were “endoplasmic reticulum stress,” “insulin resistance,” “metabolic syndrome,” and “low carbohydrate-high fat diet, molecular mechanism, Biochemical effects, Metabolic effects, Signaling pathways.” Insulin resistance is a metabolic disorder characterized by decreased cell sensitivity to insulin, resulting from the interplay between genetic and environmental factors. It can act as both a result and trigger of uncontrolled endoplasmic reticulum stress. This condition is associated with several disruptions, including impaired endoplasmic reticulum-mitochondrial transport, disordered signaling pathways, macrophage dysfunction, autophagy, immune function, inflammatory responses, dysregulation of antioxidant responses, and altered expression of genes involved in the endoplasmic reticulum stress response. LCHF-KD has been shown to alleviate insulin resistance associated with endoplasmic reticulum stress. Finally, it is concluded that ER stress plays a crucial role in the development of insulin resistance and metabolic diseases, including type 2 diabetes and obesity. Therapeutic strategies, including chemical chaperones and unfolding protein response (UPR) modulators, were used to alleviate ER stress. Dietary interventions, such as the low-carbohydrate, high-fat ketogenic diet (LCHF-KD), also reduce ER stress and improve metabolic health by modulating inflammation and oxidative stress. Combining these with conventional dietary therapies and personalized medicine approaches may enhance treatment outcomes and prevent the progression of metabolic disorders.

The Asian Journal of Pharmaceutics is a peer-reviewed open-access medical journal published by Medknow Publications on behalf of the B.R. Nahata Smriti Sansthan (Memorial Trust) (Mandsaur, India). Articles address topics in pharmaceutics, biopharmaceutics, pharmaceutical chemistry, pharmacognosy, pharmacology, pharmaceutical analysis, pharmacy practice, and clinical and hospital pharmacy.

Gestational diabetes mellitus (GDM) significantly disrupts placental structure and function, leading to complications such as intrauterine growth restriction (IUGR) and preeclampsia. This study aimed to investigate the effects of GDM on placental histology, angiogenesis, and oxidative stress, as well as evaluate metformin’s protective role in mitigating these changes. A total of 60 pregnant Sprague–Dawley rats were divided into four groups: control, metformin-treated, GDM, and GDM with metformin. GDM was induced using streptozotocin (STZ) at 40 mg/kg, and metformin was administered at 200 mg/kg from gestational day (GD) 4 to GD17. Blood glucose and insulin levels were assessed, and Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) was calculated. Placentae were weighed and subjected to histological, immunohistochemical, and molecular analyses, focusing on key angiogenesis markers (VEGF, VEGFR, CD31, KLF2) and oxidative stress indicators (MDA, eNOS). GDM increased placental weight, angiogenesis (elevated VEGF, VEGFR, CD31), and oxidative stress (elevated MDA, eNOS). Histopathological changes included villous edema, membrane rupture, and hemosiderin deposition. Metformin treatment reduced placental weight; normalized VEGF, KLF2, and PlGF expression; and improved placental architecture. Additionally, oxidative stress was significantly reduced in metformin-treated GDM rats. In conclusion, GDM induces placental abnormalities, promoting excessive angiogenesis and oxidative stress, potentially leading to IUGR and other complications. Metformin showed protective effects by reducing placental overgrowth and restoring vascular and oxidative balance. These findings suggest that metformin may play a therapeutic role in improving placental health in GDM pregnancies, warranting further investigation into its long-term effects on fetal development and maternal health.

This review article studies the complex field of noncoding RNAs (ncRNAs) in cancer biology, focusing on their potential use as biomarkers and therapeutic targets. NcRNAs include circular RNAs (circRNAs), long noncoding RNAs (lncRNAs), and microRNAs (miRNAs). We discuss how ncRNAs affect gene expression in cancerous cells, the spread of cancer, and metastasis. The article illustrates the complex pathways through which ncRNAs can affect oncogenesis, tumor suppression, and therapeutic resistance. It also assesses the potential clinical uses of non-coding RNAs (ncRNAs), including their utility in cancer diagnosis, and prognosis. Besides, their potential for personalized cancer therapy is documented. Finally, it is concluded that understanding the role of ncRNA is of clinical importance regarding carcinogenesis, cancer diagnosis, and personalized therapy.

Brain insulin resistance is linked to metabolic syndrome (MetS). A low-carbohydrate, high-fat (LCHF) diet has been proposed to have a protective effect. Therefore, this study aimed to investigate the brain insulin resistance markers in a rat animal model of MetS and the protective effects of the LCHF diet. Four groups of male rats (10/group) were created. Group I (Control) was fed a regular diet. Groups II–IV were injected with dexamethasone (DEX) to induce MetS. Group II received DEX with a regular diet. Group III (DEX + LCHF) rates were fed a low-carbohydrate, high-fat diet, while Group IV (DEX + HCLF) rats were fed a high-carbohydrate, low-fat (HCLF) diet. At the end of the four-week experiment, HOMA-IR was calculated. Moreover, cerebral gene expression analysis of S-100B, BDNF, TNF-α, IGF-1, IGF-1 R, IGFBP-2, IGFBP-5, Bax, Bcl-2, and caspase-3 was carried out. In the DEX group, rats showed a significant increase in the HOMA-IR and a decrease in the gene expression of IGF-1, IGF-1 R, IGFBP-2, IGFBP-5, BDNF, and Bcl2, with a concomitant rise in S100B, TNF-α, Bax, and caspase-3. The LCHF diet group showed a significantly opposite effect on all parameters. In conclusion, MetS is associated with dysregulated cerebral gene expression of BDNF, S100B, and TNF-α and disturbed IGF-1 signaling, with increased apoptosis and neuroinflammation. Moreover, the LCHF diet showed a protective effect, as evidenced by preservation of the investigated biochemical and molecular parameters.

Factors such as aging, an unhealthy lifestyle with decreased physical activity, snacking, a standard Western diet, and smoking contribute to raising blood pressure to a dangerous level, increasing the risk of coronary artery disease and heart failure. Atherosclerosis, or aging of the blood vessels, is a physiological process that has accelerated in the last decades by the overconsumption of carbohydrates as the primary sources of caloric intake, resulting in increased triglycerides and VLDL-cholesterol and insulin spikes. Classically, medications ranging from beta blockers to angiotensin II blockers and even calcium channel blockers were used alone or in combination with lifestyle modifications as management tools in modern medicine to control arterial blood pressure. However, it is not easy to control blood pressure or the associated complications. A low-carbohydrate, high-fat (LCHF) diet can reduce glucose and insulin spikes, improve insulin sensitivity, and lessen atherosclerosis risk factors. We reviewed articles describing the etiology of insulin resistance (IR) and its impact on arterial blood pressure from databases including PubMed, PubMed Central, and Google Scholar. We discuss how the LCHF diet is beneficial to maintaining arterial blood pressure at normal levels, slowing down the progression of atherosclerosis, and reducing the use of antihypertensive medications. The mechanisms involved in IR associated with hypertension are also highlighted.

(1) Background: Type 2 diabetes (T2DM) is a chronic metabolic disease with serious health complications. T2DM is associated with many chronic illnesses, including kidney failure, cardiovascular diseases (CVD), vision loss, and other related diseases. Obesity is one of the major factors associated with insulin resistance and dyslipidemia. Recently, the development of GLP-1 Receptor agonist (GLP-1RA) showed great therapeutic potential for T2DM. Aim: To retrospectively investigate the association of the long-term use of GLP-1RA therapy in T2DM patients with HbA1c levels and dyslipidemia. (2) Methods: Retrospective data collection and analysis of demographic, clinical records, and biochemical parameters were carried out for 72 T2DM taking GLP-1RA treatments for six months. (3) Results: A total of 72 T2DM patients with a mean age = 55 (28 male and 44 female) were divided into two groups. Group 1 received statins (n = 63), and group 2 did not receive statins (n = 9). The GLP-1RA effect on BMI was significantly decreased in group 1 (p < 0.01). A significant effect was observed for HbA1c in both groups for six months of treatment duration (p < 0.05). The AST levels significantly decreased in group 2 from 25.2 to 19.4 U\L (p = 0.011). (4) Conclusions: GLP-1RA treatments were associated with weight reduction and improved glycemic control for T2DM patients. Moreover, it is suggested that it has anti-inflammatory and hepatoprotective effects. However, no direct association was found with the lipid profile in all groups of T2DM.

Assessment is fundamental to the educational process. Multiple choice questions (MCQs) and short essay questions (SEQs) are the most widely used assessment method in medical school. The current study evaluated the discriminating value of SEQs compared to MCQs as assessment tools in clinical biochemistry and correlated undergraduate students' SEQ scores with their overall scores during the academic years 2021-2022 and 2022-2023. This is a descriptive-analytical study in which MCQ and SEQ papers of clinical biochemistry were analyzed. The mean score for SEQs in males was 66.7 ± 1.2 and for females it was 64.0 ± 1.1 SEM, with a p-value of 0.09; for MCQs, the mean score for males was 68.5 ± 0.9 SEM and for females it was 72.6 ± 0.8. When analyzing the difficulty index (DI) and discrimination factor (DF) of the questions, MCQs have a mean DI of 0.70 ± 0.01,and DF of 0.05 to 0.6. SEQs have a mean DI of 0.73 ± 0.03 and DF of 0.68 ± 0.01; there was a significant difference between the DF of MCQs and SEQs (p < 0.0001). Furthermore, there was a significant difference between SEQs and MCQs when categorizing students based on their scores, except for A-scored students. According to the current study, SEQs have a higher discriminating ability than MCQs and help differentiate high-achieving students from low-achieving students.