Insulin-dependent Diabetes Research Articles

'Sick day ketones in childhood diabetes' an audit reviewing and comparing inpatient management of children presenting unwell to oxford university hospital 2022-2023, with ISPAD guidelines

'Sick day ketones in childhood diabetes' an audit reviewing and comparing inpatient management of children presenting unwell to oxford university hospital 2022-2023, with ISPAD guidelines

Does real time continuous glucose monitoring improve glycaemic control in patients with Wolfram syndrome and insulin dependent diabetes mellitus?

Does real time continuous glucose monitoring improve glycaemic control in patients with Wolfram syndrome and insulin dependent diabetes mellitus?

Factors Associated with Insulin Self-Administration Knowledge and Practices Among Hospitalized Diabetes Mellitus Patients in Peshawar, Pakistan

Background: Diabetes Mellitus (DM) is a rapidly growing chronic condition requiring effective management, including insulin self-administration (ISA). Proper ISA knowledge and practices are crucial for optimal glycemic control, yet gaps remain, particularly in low-resource settings.Objective: To assess ISA knowledge and practices among insulin-dependent DM patients and identify associated sociodemographic and clinical factors.Methods: This cross-sectional study was conducted among 116 DM patients at a public hospital in Peshawar, Pakistan. Data were collected through face-to-face interviews and medical records review. Knowledge was assessed using a validated questionnaire based on ADA guidelines, while practices were observed using a structured checklist. Data were analyzed using SPSS version 25, applying descriptive and inferential statistics, including Chi-square tests for associations.Results: Of the participants, 50% had average ISA knowledge, 34.5% had poor knowledge, and 15.5% had good knowledge. Regarding practices, 37.1% exhibited poor, 29.3% fair, and 33.6% good practices. Significant associations were found between ISA knowledge and age (p = 0.004), education (p < 0.001), and previous training (p = 0.002).Conclusion: Knowledge and practices regarding ISA were suboptimal, influenced by age, education, and training. Tailored educational programs are needed to improve DM management.

Basic principles of treatment and follow-up of children with acute odontogenic infection and insulin-dependent diabetes mellitus

The purpose of the study is to substantiate the basic principles of treatment and clinical dental observation of children with acute odontogenic inflammatory disease and insulin-dependent diabetes mellitus as an accompanying disease. Material and methods. A medical examination was conducted for 213 children who were treated at the St. Petersburg city children’s hospital of K.A. Raukhus of. The dental status of children with insulin-dependent diabetes mellitus and children of the control group without concomitant diseases was assessed using the Fedorov-Volodkina index, the KPU index and analysis of the caries intensity according to the T.F. Vinogradova table, periodontal conditions according to the PMA index (papillary-marginal-alveolar). The state of microhemocirculation of periodontal tissues was also assessed using Doppler ultrasound and the use of a reflex cold test. In children diagnosed with “Acute odontogenic osteomyelitis of the jaws,” laboratory blood parameters, the composition of the microbial flora of wound discharge, and the length of hospitalization were studied. Results. Based on the data obtained, an algorithm for treatment and dispensary dental observation of children with diabetes was presented. The detection of diabetes mellitus in children of any age should be accompanied by increased attention to the dental health of these patients. If teeth affected by caries are identified during a preventive examination, immediate treatment is required. It is necessary to ensure constant follow-up of the child by an endocrinologist. Doppler examination of the microhemocirculatory bed vessels of the mucosa of the alveolar process of the jaw revealed that an adequate response to a reflex cold test was detected only in the control group patients, those who do not have insulin-dependent diabetes mellitus. With the development of acute odontogenic osteomyelitis of the jaw in children suffering from insulin-dependent diabetes mellitus, hospitalization is necessary when the first clinical symptoms of the inflammatory process appear. Immediately after hospitalization and immediate surgical sanitation of a purulent focus of infection in the oral cavity, drug therapy should be started: antibacterial, infusion, symptomatic, as well as insulin therapy. The results of this study are especially relevant in the treatment of children with a duration of insulin-dependent diabetes mellitus of more than 5 years and a decompensated course of endocrine disease. Conclusions. The results of the study allowed us to expand our understanding of the impact of diabetes on the oral health of children, to establish risk factors for the development of acute odontogenic osteomyelitis of the jaws in children of different age categories with insulin-dependent diabetes mellitus, as well as the characteristics of the course of odontogenic osteomyelitis of the jaws in each of the cases. Based on the identified features, the principles of diagnosis and treatment of acute odontogenic osteomyelitis of the jaws in children with insulin-dependent diabetes mellitus have been formulated.

Regulatory CD4+ T cells redirected against pathogenic CD8+ T cells protect NOD mice from development of autoimmune diabetes.

In this study, we report a novel therapeutic approach redirecting antigen-specific CD4+ T cells recognizing a hybrid insulin peptide (BDC2.5 T cell receptor (TCR) transgenic CD4+ T cells) to attract and suppress islet-specific CD8+ T cells T cells in the non-obese diabetic (NOD) mouse model, and prevent the development of autoimmune diabetes. Purified BDC2.5 CD4+ T cells were induced to differentiate into regulatory T cells (Tregs). The Tregs were then electroporated with mRNA encoding chimeric human β2 microglobulin (hβ2m) covalently linked to insulin B chain amino acids 15-23 (designated INS-eTreg) or islet-specific glucose-6-phosphatase related protein (IGRP) peptide 206-214 (designated IGRP-eTreg). Immunoregulatory functions of these engineered regulatory T cells (eTregs) were tested by in vitro assays and in vivo co-transfer experiments with β-cell-antigen-specific CD8+ T cells in NOD.Scid mice or by adoptive transfer into young, pre-diabetic NOD mice. These eTregs were phenotyped by flow cytometry, and shown to have high expression of FoxP3, as well as other markers of Treg function, including IL-10. They suppressed polyclonal CD4+ T cells and antigen-specific CD8+ T cells (recognizing insulin or IGRP), decreasing proliferation and increasing exhaustion and regulatory markers in vitro. In vivo, eTregs reduced diabetes development in co-transfer experiments with pathogenic antigen-specific CD8+ T cells (INS-CD8+ or IGRP-CD8+ cells) into NOD.Scid mice. Finally, when the eTreg were injected into young NOD mice, they reduced insulitis and prevented spontaneous diabetes in the recipient mice. Our results suggest a novel therapeutic strategy to protect NOD mice by targeting antigen-specific cytotoxic CD8+ T cells, using redirected antigen-specific CD4+ Treg cells, to suppress autoimmune diabetes. This may suggest an innovative therapy for protection of people at risk of development of type 1 diabetes.

Detection Diabetes Glucose Mathematically by Taylor’s Function

Diabetes is a syndrome of metabolic disorders caused by hereditary and environmental factors. Our bodies contain a variety of hormones. Blood sugar levels are controlled by insulin, growth hormone, and glucagon, as well as adrenaline. glucose and thyroid hormone Diabetes is divided into three types. Type 1 diabetes is often known as juvenile diabetes, whereas type 2 diabetes is commonly referred to as adult-onset diabetes, whereas type 3 diabetes is a temporary condition that affect pregnant women, we ignore the type1, type 3 and We focus on the second type because of its importance in all societies, with the following glycemic control mechanisms (##).

Rheumatological manifestations of H syndrome.

H syndrome (HS) is a rare autosomal recessive genodermatosis characterised by cutaneous hyperpigmentation, hypertrichosis, sclerodermatous thickening, and multisystemic involvement. It results from mutations in the SLC29A3 gene encoding the human equilibrative nucleoside transporter 3, leading to impaired histiocyte apoptosis and unchecked proliferation. We report the case of a 24-year-old Moroccan male who had a history of insulin-dependent diabetes mellitus. He developed hyperpigmented skin patches with hypertrichosis and induration. Musculoskeletal findings included bilateral hallux valgus, pes planus, reducible flexion contractures of the proximal interphalangeal joints, and restricted ankle dorsiflexion. Additional findings consist of lymphadenopathy, hepatomegaly, hypogonadism, and ophthalmic manifestations. Investigations showed elevated sedimentation rate, anaemia, and osteopaenia. Ankle ultrasound revealed calcaneal enthesopathy and subcutaneous infiltration. In reporting this case, we aim to highlight the significant rheumatological involvement that can arise in patients with H syndrome and explore potential treatment options to improve the musculoskeletal findings.

Emerging Diabetes Therapies: Regenerating Pancreatic β Cells.

The incidence of diabetes mellitus (DM) is steadily increasing annually, with 537 million diabetic patients as of 2021. Restoring diminished β cell mass or impaired islet function is crucial in treating DM, particularly type 1 DM. However, the regenerative capacity of islet β cells, which primarily produce insulin, is severely limited, and natural regeneration is only observed in young rodents or children. Hence, there is an urgent need to develop advanced therapeutic approaches that can regenerate endogenous β cells or replace them with stem cell (SC)-derived or engineered β-like cells. Current strategies for treating insulin-dependent DM mainly include promoting the self-replication of endogenous β cells, inducing SC differentiation, reprogramming non-β cells into β-like cells, and generating pancreatic-like organoids through cell-based intervention. In this Review, we discuss the current state of the art in these approaches, describe associated challenges, propose potential solutions, and highlight ongoing efforts to optimize β cell or islet transplantation and related clinical trials. These effective cell-based therapies will generate a sustainable source of functional β cells for transplantation and lay strong foundations for future curative treatments for DM.

Mycobacterium paratuberculosis: A HERV Turn-On for Autoimmunity, Neurodegeneration, and Cancer?

Human endogenous retroviruses (HERVs) are remnants of ancient retroviral infections that, over millions of years, became integrated into the human genome. While normally inactive, environmental stimuli such as infections have contributed to the transcriptional reactivation of HERV-promoting pathological conditions, including the development of autoimmunity, neurodegenerative disease and cancer. What infections trigger HERV activation? Mycobacterium avium subspecies paratuberculosis (MAP) is a pluripotent driver of human disease. Aside from granulomatous diseases, Crohn's disease, sarcoidosis and Blau syndrome, MAP is associated with autoimmune disease: type one diabetes (T1D), multiple sclerosis (MS), rheumatoid arthritis (RA) and autoimmune thyroiditis. MAP is also associated with Alzheimer's disease (AD) and Parkinson's disease (PD). Autoimmune diabetes, MS and RA are the diseases with the strongest MAP/HERV association. There are several other diseases associated with HERV activation, including diseases whose epidemiology and/or pathology would prompt speculation for a causal role of MAP. These include non-solar uveal melanoma, colon cancer, glioblastoma and amyotrophic lateral sclerosis (ALS). This article further points to MAP infection as a contributor to autoimmunity, neurodegenerative disease and cancer via the un-silencing of HERV. We examine the link between the ever-increasing number of MAP-associated diseases and the MAP/HERV intersection with these diverse medical conditions, and propose treatment opportunities based upon this association.

Gut-Brain Nexus: Mapping Multi-Modal Links to Neurodegeneration at Biobank Scale.

Alzheimer's disease (AD) and Parkinson's disease (PD) are influenced by genetic and environmental factors. Using data from UK Biobank, SAIL Biobank, and FinnGen, we conducted an unbiased, population-scale study to: 1) Investigate how 155 endocrine, nutritional, metabolic, and digestive system disorders are associated with AD and PD risk prior to their diagnosis, considering known genetic influences; 2) Assess plasma biomarkers' specificity for AD or PD in individuals with these conditions; 3) Develop a multi-modal classification model integrating genetics, proteomics, and clinical data relevant to conditions affecting the gut-brain axis. Our findings show that certain disorders elevate AD and PD risk before AD and PD diagnosis including: insulin and non-insulin dependent diabetes mellitus, noninfective gastro-enteritis and colitis, functional intestinal disorders, and bacterial intestinal infections, among others. Polygenic risk scores revealed lower genetic predisposition to AD and PD in individuals with co-occurring disorders in the study categories, underscoring the importance of regulating the gut-brain axis to potentially prevent or delay the onset of neurodegenerative diseases. The proteomic profile of AD/PD cases was influenced by comorbid endocrine, nutritional, metabolic, and digestive systems conditions. Importantly, we developed multi-modal prediction models integrating clinical, genetic, proteomic and demographic data, the combination of which performs better than any single paradigm approach in disease classification. This work aims to illuminate the intricate interplay between various physiological factors involved in the gut-brain axis and the development of AD and PD, providing a multifactorial systemic understanding that goes beyond traditional approaches.

Prenatal and Postnatal Exposure to Antibiotics and the Risk of Type 1 Diabetes in Finnish Children: A Registry-based Study

ObjectiveTo study whether prenatal and postnatal exposure to antibiotics is associated with the risk of type 1 diabetes in childhood. Study designA case-cohort study including 2,869 children diagnosed with type 1 diabetes by the end of 2009, born January 1, 1996, to December 31, 2008, in Finland and a reference cohort (n =74,263) representing 10% of each birth cohort. Exposure to antibiotics was assessed in different time periods. The data were derived from Special Reimbursement Register, Drug Prescription Register, and Population Register and analyzed with weighted Cox proportional hazards regression models. ResultsExposure to any antibiotics before or during pregnancy, in the neonatal ward, during the first year of life, or during the two first years of life, was not associated with the risk of type 1 diabetes in the offspring. Exposure to macrolides in the year preceding pregnancy (adjusted HR 1.17 [95% CI 1.02, 1.33]) and to sulfonamides and trimethoprim during pregnancy (adjusted HR 1.91 [1.07, 3.41]) was associated with an increased risk of type 1 diabetes in the offspring. Exposure to sulfonamides and trimethoprim during first two years of life was associated with decreased risk of type 1 diabetes (adjusted HR 0.84 [0.73, 0.97]). Number of antibiotic purchases among mothers or children was not associated with type 1 diabetes risk. ConclusionsPrenatal and postnatal exposure to antibiotics in general did not increase the risk of type 1 diabetes in the offspring. However, type of antibiotic and timing of exposure may play a role in type 1 diabetes risk.

Discovery of a TRMT10A mutation in a case of atypical diabetes: Case report

It is notable that monogenic forms of diabetes are exceedingly uncommon, with only 28 genes thus far identified. Such conditions frequently result in the dysfunction of pancreatic cells responsible for insulin production. Mutation in the TRMT10A gene leads to a rare genetic disease that is associated with endocrine and metabolic disorders, including diabetes and short stature. This article presents a review of the existing literature on the subject, describing the association between TRMT10A gene mutation and diabetes. It also presents the clinical case of a young girl with type 1 diabetes and facial dysmorphia. TRMT10A gene mutation has been linked to syndromic juvenile diabetes in a manner analogous to Wolfram's syndrome. This form of diabetes, which manifests in early childhood and is associated with microcephaly, epilepsy and intellectual disability, is caused by mutations in the gene for homolog A of tRNA methyltransferase 10 (TRMT10A). This emphasizes the importance of using a targeted panel to recognize previously unidentified monogenic diabetes among early-onset non-insulin-dependent diabetes in the absence of obesity and autoimmunity. In view of the aforementioned data, it is recommended that TRMT10A sequencing be considered in children or adults with early-onset diabetes and a history of intellectual disability, microcephaly and epilepsy.

Breakdown and Repair of Peripheral Immune Tolerance in Type 1 Diabetes.

Failures in peripheral immune tolerance mechanisms create a permissive environment for autoimmune diabetes initiation and disease progression. Biomarker analyses provide tools that allow recognition of this loss of tolerance, reflecting a serial acquisition of pathogenic characteristics causally linked to islet β-cell dysfunction and death. Autoimmune effector cell activation and expansion, ineffective immune regulation, and tissue response to injury during active disease each represent challenges to homeostasis; however, they also represent targets for therapeutic intervention, with the potential for restoration of tolerance. Limited success in recent clinical trials demonstrates that tolerance in type 1 diabetes (T1D) is achievable, but currently occurs in few subjects and is not durable in most. Combining therapeutic agents to rebuild multiple immune components to restore tolerance, particularly addressing both effector and regulatory T-cell dysfunction, is needed.

Four Decades of Research Productivity and Hot Spots in Pancreas Transplantation.

Background: The field of pancreas transplantation has undergone transformative phases, progressing from its promising inception in 1966 to becoming a standard treatment for patients with insulin-dependent diabetes. This bibliometric analysis explores the progression of pancreas transplantation research over a period of four decades, mapping milestones, contributors, and emerging trends. Methods: Our bibliometric analysis utilizes the comprehensive Scopus database, which includes publication titles, author information, affiliations, abstracts, keywords, and journal details. The search strategy was centered on research related to pancreas and pancreas-kidney transplantation. The analysis encompasses the time frame spanning from 1983 to 2023, with the data extraction taking place on October 7th, 2023. Results: The analysis of 4,897 articles uncovered unique trends in the field of pancreas transplantation research. The years 1989, 1996, and 2021 saw significant increases in the number of publications, which corresponded to the responses to clinical challenges and advancements. Contributions by authors from the United States of America were the most numerous, with 1,905 publications and 49,949 citations. The research topics were highlighted by keywords such as "graft survival," "graft rejection," and" Immunosuppressive treatment." Conclusion: The fluctuations in publication trends that have been identified indicate dynamic reactions to changing priorities and challenges. Although it has limitations, this analysis provides valuable insights for researchers, clinicians, and policymakers who are dealing with the complex field of pancreas transplantation literature. Further bibliometric research may advance our knowledge and direct future initiatives in this developing field.

Management of insulin-dependent diabetes in low-resource countries: results from the chronic noncommunicable disease project in Iringa rural district of Tanzania

INTRODUZIONE Le malattie croniche non trasmissibili stanno vivendo una importante crescita del carico di malattia, soprattutto nei paesi a basso e medio-basso reddito. Tra di esse il diabete rappresenta un’importante sfida: la prevalenza è in crescita esponenziale in Africa, dove scarsità di accessibilità alle cure e di risorse rendono la problematica ancor più gravosa. La terapia insulinica in particolare è molto costosa e poco maneggevole. L’obiettivo dello studio è quello di trovare risposte ai bisogni emergenti della popolazione diabetica in questi contesti. MATERIALI E METODI È stato effettuato uno studio osservazionale retrospettivo e prospettico della popolazione diabetica in trattamento con insulina umana mista regolare/intermedia 30/70, nell’ambito del progetto chronic non-communicable diseases del CUAMM nell’ospedale di Tosamaganga in un’area rurale della Tanzania, paese a medio-basso reddito dell’Africa subsahariana. I dati sono stati estrapolati dal database del progetto e da interviste ai pazienti in trattamento insulinico attivo da marzo a agosto 2023. RISULTATI Sono stati riscontrati un miglioramento dei valori di glicemia, emoglobina glicata e peso nel tempo; una riduzione del numero di ricoveri, un netto miglioramento del performance status e un basso tasso di ipoglicemie maggiori. L’83.1% dei pazienti non possiede una assicurazione sanitaria, la maggior parte ha difficoltà economiche a supportare i costi del trasporto per recarsi a visita; il counseling ricevuto su terapia e stile di vita è ritenuto molto utile ed efficace. CONCLUSIONE L’insulina umana mista regolare/ intermedia 30/70 è efficace e sicura. Il basso costo e la maggiore maneggevolezza ne rende auspicabile l’utilizzo nei paesi a basse risorse per questioni di compliance e disponibilità economiche. Incrementare l’accesso alle cure e favorire personale qualificato è importante per migliorare la cura del diabete in paesi a basse risorse. PAROLE CHIAVE paesi a risorse limitate; malattie croniche non trasmissibili; diabete mellito; insulina umana mista regolare/intermedia 30/70.

Latent Autoimmune Diabetes in Adults (LADA) Occurring in a Patient with Primary Biliary Cholangitis

Latent Autoimmune Diabetes in Adults (LADA) Occurring in a Patient with Primary Biliary Cholangitis

Decoding the Mysteries of Auto-Immune Disorders

An autoimmune disease (AI) happens when the immune system doesn’t recognise its cells. This leads to a problem with how it reacts to these cells. Some of these diseases can be due to your genes, the environment, or even certain infections. They can affect specific organs or the whole body. Examples of autoimmune diseases are insulin-dependent diabetes mellitus, rheumatoid arthritis, systemic lupus erythematosus, scleroderma, thyroiditis, and multiple sclerosis. But wait—there's more! Other conditions like arteriosclerosis, inflammatory bowel disease, schizophrenia, & some types of infertility also fall into this category. Around 3% of people in North America & Europe have autoimmune disorders. About three out of four people affected are women. How our immune system works and maintains tolerance is a wonder. The present paper aims to explore autoimmune diseases and what causes the immune system to react in a specific way

Embryonic, Fetal, and Neonatal Complications in Infants of Diabetic Mothers: Insights from the Cincinnati Diabetes in Pregnancy Program Project Grant.

This study aimed to review how the Cincinnati Diabetes in Pregnancy Program Project Grant (PPG) contributed to the understanding and treatment of neonatal complications in infants of diabetic mothers (IDMs). This is a retrospective review of all PPG work on glycemic control at different pregnancy time points and its association with embryonic, fetal, and neonatal complications, such as congenital malformations (CMs), intrauterine growth restriction, macrosomia, hypoglycemia, respiratory distress syndrome (RDS), asphyxia, and polycythemia. We found that maternal vasculopathy and poor glycemic control during embryogenesis, but not frequency of maternal hypoglycemic episodes or insulin therapy, are independent risk factors for major CMs. A suggestive association of major CMs with maternal Magnesium deficiency was also observed. Poor glycemic control during late embryogenesis and early fetal development was associated with an increased risk of minor CMs. We described a biphasic pattern of fetal growth whereby early growth delay was followed by enhanced fetal growth associated with neonatal macrosomia. Macrosomia was associated with poorer glycemic control in the third trimester and an increased risk of birth trauma. Macrosomia was also correlated with animal-origin insulin concentrations in cord blood, demonstrating that insulin bound to antibodies can cross the placenta and may affect the fetus. We also showed that neonatal hypoglycemia was significantly associated with third-trimester glycemic control, in addition to hyperglycemia occurring during labor. With modern management and adequate prenatal care, IDMs are no longer at increased risk for RDS. Perinatal asphyxia was associated with increased proteinuria appearing in pregnancy, maternal hyperglycemia before delivery, and prematurity. Polycythemia in IDMs is prevalent and correlates with proxy measurements of fetal hypoxemia (nucleated red blood cells at delivery) and poorer glycemic control in late pregnancy. The PPG in its various phases revealed the important role of glycemic control at nearly every stage of pregnancy including labor. KEY POINTS: · Poor glycemic control during embryogenesis is a major risk factor for CMs.. · Magnesium deficiency might contribute to major malformations.. · Macrosomia is associated with poor glycemic control in the third trimester.. · Strict glycemic control reduces fetal and neonatal morbidity in pregnancies with insulin-dependent diabetes mellitus..

CD4+ T cells reactive to a hybrid peptide from insulin-chromogranin A adopt a distinct effector fate and are pathogenic in autoimmune diabetes

T cell-mediated islet destruction is a hallmark of autoimmune diabetes. Here, we examined the dynamics and pathogenicity of CD4+ Tcell responses to four different insulin-derived epitopes during diabetes initiation in non-obese diabetic (NOD) mice. Single-cell RNA sequencing of tetramer-sorted CD4+ Tcells from the pancreas revealed that islet-antigen-specific Tcells adopted a wide variety of fates and required XCR1+ dendritic cells for their activation. Hybrid-insulin C-chromogranin A (InsC-ChgA)-specific CD4+ Tcells skewed toward a distinct T helper type 1 (Th1) effector phenotype, whereas the majority of insulin B chain and hybrid-insulin C-islet amyloid polypeptide-specific CD4+ T cells exhibited a regulatory phenotype and early or weak Th1 phenotype, respectively. InsC-ChgA-specific CD4+ Tcells were uniquely pathogenic upon transfer, and an anti-InsC-ChgA:IAg7 antibody prevented spontaneous diabetes. Our findings highlight the heterogeneity of Tcell responses to insulin-derived epitopes in diabetes and argue for the feasibility of antigen-specific therapies that blunts the response of pathogenic CD4+ Tcells causing autoimmunity.

Prevalence of latent autoimmune diabetes in adults and insulin resistance: a systematic review and meta-analysis.

Latent autoimmune diabetes in adults is a form of diabetes that progresses slowly and is controlled by diet and oral glucose-lowering medications before insulin is required. The aim of the present study was to evaluate the prevalence of latent autoimmune diabetes in adults. The present study was conducted based on PRISMA 2020-27-item checklist. To find the studies conducted in line with the purpose of the study, PubMed, Web of Science, Scopus, Science Direct, Web of Knowledge, EBSCO, Wiley, ISI, Elsevier, Embase databases and Google Scholar search engine were reviewed from 2013 to August 2023. Meta-analysis was performed using effect size with 95% confidence interval. Data analysis was done using STATA/MP. v17 software. The present study was carried out based on the PRISMA 2020 27-point checklist. To find out which studies were carried out in accordance with the purpose of the study, from 2013 to August, the databases PubMed, Web of Science, Scopus, Science Direct, Web of Knowledge, EBSCO, Wiley, ISI, Elsevier, Embase and the search engine Google Scholar reviewed 2023. Meta-analysis was performed using effect size with 95% confidence interval. Data analysis was carried out using STATA/MP. v17 software. The overall prevalence of Latent autoimmune diabetes of adults was found to be 7% (95%CI 0-20). Subgroup analysis of Latent autoimmune diabetes of adults in the context of geographic regions showed a higher prevalence in North America (15%) and South East Asia (5%). Since the identification of Latent autoimmune diabetes of adult patients with other forms of diabetes is misdiagnosed due to the combination of phenotypic features with T1D and T2D, studying its prevalence is of great importance.