Vol 20, No 1 (2024)

Insulin is an endocrine hormone produced by the beta cells of islets of Langerhans in the pancreas. It regulates blood sugar levels and various anabolic activities such as glycogenesis and lipid synthesis. Despite the fact that insulin therapy has been around for 100 years, insulin formulations are continually being improved to lower the risk of hypoglycaemia and other adverse effects, including weight gain. The development of insulin pens has significantly reduced the consequences of hypoglycaemia instead of vials and syringes. Both injectable devices were well-received by the patients. In the population under study, the efficacy and safety profiles of the pen appeared to be comparable to those of the vial/syringe. However, more patients reported that they would like to keep using pen devices. This article aimed to summarize the background of insulin, its mechanism, types, needle size, injection technique, adverse drug reactions and various studies related to insulin. It has been recommended intensive treatment of type-1 and type-2 diabetes patients to achieve good metabolic control and avoid chronic complications caused by poor glycaemic control. Healthcare professionals should address concerns about safe and effective implementation of inpatient hypoglycaemic control and insulin usage and they should empower patients to self-manage their diabetes, so they may improve their quality of life as well as avoid potential complications. Much more progress is expected in the future, at a faster pace, based on the implementation of well-organized recovery efforts, advancing technologies, and scientific collaboration.

Background:Over the past two decades, insulin glargine 100 U/mL (Gla-100) has emerged as the "standard of care" basal insulin for the management of type 1 diabetes mellitus (T1DM). Both formulations, insulin glargine 100 U/mL (Gla-100) and glargine 300 U/mL (Gla- 300) have been extensively studied against various comparator basal insulins across various clinical and real-world studies. In this comprehensive article, we reviewed the evidence on both insulin glargine formulations in T1DM across clinical trials and real-world studies.

Methods:Evidence in T1DM for Gla-100 and Gla-300 since their approvals in 2000 and 2015, respectively, were reviewed.

Results:Gla-100 when compared to the second-generation basal insulins, Gla-300 and IDeg-100, demonstrated a comparable risk of overall hypoglycemia, but the risk of nocturnal hypoglycemia was higher with Gla-100. Additional benefits of Gla-300 over Gla-100 include a prolonged (>24- hours) duration of action, a more stable glucose-lowering profile, improved treatment satisfaction, and greater flexibility in the dose administration timing.

Conclusion:Both glargine formulations are largely comparable to other basal insulins in terms of glucose-lowering properties in T1DM. Further, risk of hypoglycemia is lower with Gla-100 than Neutral Protamine Hagedorn but comparable to insulin detemir.

About 50.8 million people were diagnosed with diabetes in 2011; the count has increased by 10 million in the last five years. Type-1 diabetes could occur at any age, but predominantly in children and young adults. The risk of developing type II diabetes mellitus in the offspring of parents with DM II is 40% if one parent has DM II and approaches 70% if both parents have DM II. The process of developing diabetes from normal glucose tolerance is continuous, with insulin resistance being the first stage. As prediabetes progresses slowly to DM II, it may take approximately 15-20 years for an individual to become diabetic. This progression can be prevented or delayed by taking some precautions and making some lifestyle amendments, e.g., reducing weight by 5-7% of total body weight if obese, etc. Retinoblastoma protein is one of the pocket proteins that act as crucial gatekeepers during the G1/S transition in the cell cycle. A loss or defect in single- cell cycle activators (especially CDK4 and CDK6) leads to cell failure. In diabetic or stress conditions, p53 becomes a transcription factor, resulting in the transactivation of CKIs, which leads to cell cycle arrest, cell senescence, or cell apoptosis. Vitamin D affects insulin sensitivity by increasing insulin receptors or the sensitivity of insulin receptors to insulin. It also affects peroxisome proliferator-activated receptors (PPAR) and extracellular calcium. These influence both insulin resistance and secretion mechanisms, undertaking the pathogenesis of type II diabetes. The study confines a marked decrement in the levels of random and fasting blood glucose levels upon regular vitamin D intake, along with a significant elevation of retinoblastoma protein levels in the circulatory system. The most critical risk factor for the occurrence of the condition came out to be family history, showing that patients with first-degree relatives with diabetes are more susceptible. Factors such as physical inactivity or comorbid conditions further aggravate the risk of developing the disease. The increase in pRB levels caused by vitamin D therapy in prediabetic patients directly influences blood glucose levels. pRB is supposed to play a role in maintaining blood sugar levels. The results of this study could be used for further studies to evaluate the role of vitamin D and pRB in regeneration therapy for beta cells in prediabetics.

Diabetic Nephropathy (DN), with an increasing rate of mortality and morbidity, is considered the main cause of End-Stage Renal Disease (ESRD). A wide spectrum of biomarkers exist for early detection of DN, but they suffer from low specificity and sensitivity, indicating the urgent demand for finding more effective biomarkers. Also, the pathophysiology of tubular damage and its relation to DN are not yet completely understood. Kidney Injury Molecule-1 (KIM-1) is a protein that is expressed at substantially low contents in the kidney under physiological conditions. A number of reports have demonstrated the close relationship between urine and tissue KIM-1 levels and kidney disorders. KIM-1 is known as a biomarker for diabetic nephropathy and renal injury. In this study, we aim to review the potential clinical and pathological roles of KIM-1 in diabetic nephropathy.

Diabetes mellitus is a type of metabolic disorders. Various pharmaceutical interventions and animal models have been used to investigate the genetic, environmental, and etiological aspects of diabetes and its effects. In recent years for the development of ant-diabetic remedies, numerous novel genetically modified animals, pharmaceutical substances, medical techniques, viruses, and hormones have been developed to screen diabetic complications. A unique disease-treating drug with new properties is still being sought after. The current review tried to include all published models and cutting-edge techniques. Experimental induction of diabetes mellitus in animal models and in vitro methods are essential for advancing our knowledge, a thorough grasp of pathophysiology, and the creation of novel therapeutics. Animal models and in vitro techniques are necessary to develop innovative diabetic medications. New approaches and additional animal models are required for diabetes research to advance. This is particularly true for models produced via dietary modifications, which have various macronutrient compositions. In this article, we review the rodent models of diet-induced diabetic peripheral neuropathy, diabetic retinopathy, and diabetic nephropathy and critically compare the key characteristics of these micro-vascular complications in humans and the diagnostic criteria with the parameters used in preclinical research using rodent models, taking into consideration the potential need for factors that can accelerate or aggravate these conditions.

Diabetes is a severe chronic disease that arises when insulin generation is insufficient, or the generated insulin cannot be used in the body, resulting a long-term metabolic disorder. Diabetes affects an estimated 537 million adults worldwide between the age of 20 to 79 (10.5% of all adults in this age range). By 2030, 643 million people will have diabetes globally, increasing to 783 million by 2045. According to the IDF 10th edition, the incidence of diabetes has been rising in South-East Asia (SEA) nations for at least 20 years, and current estimates have outperformed all previous forecasts. This review aims to provide updated estimates and future projections of diabetes prevalence at the national and global levels by using data from the 10th edition of the IDF Diabetes Atlas 2021. For this review, we studied more than 60 previously published related articles from various sources, such as PubMed and Google Scholar, and we extracted 35 studies out of 60. however, we used only 34 studies directly related to diabetes and its prevalence at the global, SEA, and Indian levels. This review article concludes that in 2021 more than 1 in 10 adults worldwide developed diabetes. The estimated prevalence of diabetes in adults (20 to 79 years) has more than tripled since the first edition in 2000, rising from an estimated 151 million (4.6% of the world’s population at the time) to 537.5 million (10.5%) of the world’s population today. The prevalence rate will be higher than 12.8% by 2045. In addition, this study indicates that the incidence of diabetes in the world, Southeast Asia, and India was 10.5%, 8.8%, and 9.6%, respectively, throughout 2021 and will rise to 12.5%, 11.5%, and 10.9%, respectively by 2045.

Background:The existence of aberrant myocardial activity and function in the exclusion of those other cardiovascular events, such as atherosclerosis, hypertension, and severe valve disease, is known as diabetic cardiomyopathy. Diabetes patients are much more prone to death from cardiovascular illnesses than from any other cause, and they also have a 2–5 fold higher likelihood of acquiring cardiac failure and other complications.

Objective:In this review, the pathophysiology of diabetic cardiomyopathy is discussed, with an emphasis on the molecular and cellular irregularities that arise as the condition progresses, as well as existing and prospective future treatments.

Method:The literature for this topic was researched utilizing Google Scholar as a search engine. Before compiling the review article, several research and review publications from various publishers, including Bentham Science, Nature, Frontiers, and Elsevier, were investigated.

Result:The abnormal cardiac remodelling, marked by left ventricular concentric thickening and interstitial fibrosis contributing to diastolic impairment, is mediated by hyperglycemia, and insulin sensitivity. The pathophysiology of diabetic cardiomyopathy has been linked to altered biochemical parameters, decreased calcium regulation and energy production, enhanced oxidative damage and inflammation, and a build-up of advanced glycation end products.

Conclusion:Antihyperglycemic medications are essential for managing diabetes because they successfully lower microvascular problems. GLP-1 receptor agonists and sodium-glucose cotransporter 2 inhibitors have now been proven to benefit heart health by having a direct impact on the cardiomyocyte. To cure and avoid diabetic cardiomyopathy new medicines are being researched, including miRNA and stem cell therapies.