Onset Of Diabetes Research Articles

Risk for progression to type 1 diabetes in first-degree relatives under 50 years of age.

The detection of pancreatic autoantibodies in first-degree relatives of patients with type 1 diabetes (T1D) is considered a risk factor for disease. Novel available immunotherapies to delay T1D progression highlight the importance of identifying individuals at risk who might benefit from emerging treatments. The objective was to assess the autoimmunity in first-degree relatives of patients with T1D, estimate the time from autoimmunity detection to the onset of clinical diabetes, and identify the associated risk factors. Retrospective multicenter study of 3,015 first-degree relatives of patients with T1D recruited between 1992 and 2018. Pancreatic autoantibodies (IAA, GADA, IA2A, and ZnT8A) were determined by radioimmunoassay, starting the analyses at diagnosis of the proband. All those with positive autoimmunity and normal fasting blood glucose without clinical symptoms of diabetes were followed up in the study. The progression rate to T1D was assessed according to sex, relationship with the proband, age at autoimmunity detection, type/number of autoantibodies, and HLA-DRB1 genotype. Cox proportional-hazard models and Kaplan-Meier survival plots were used for statistical analyses. Among the relatives, 21 progenitors [43.7 years (IQR: 38.1-47.7)] and 27 siblings [7.6 years (IQR: 5.8-16.1)] had positive autoantibodies. Of these, 54.2% (95% CI: 39.2%-68.6%) developed T1D (age at autoimmunity detection 11 months to 39 years) in a median of 5 years (IQR: 3.6-8.7; ranged from 0.9 to 22.6 years). Risk factors associated with faster progression to T1D were multiple autoimmunity and <20 years at autoimmunity detection. Younger relatives (<20 years) with multiple autoantibodies had a 5-year cumulative risk of developing diabetes of 52.9% (95% CI: 22.1%-71.6%) and a 20-year risk of 91.2% (95% CI: 50.5%-98.4%). The 20-year risk decreased to 59.9% (95% CI: 21.9%-79.5%) if only one risk factor was met and to 35.7% (95% CI: 0.0%-66.2%) if the relative was older than 20 years with one autoantibody. In first-degree relatives with autoimmunity, the time to progression to T1D is faster in children and adolescents with multiple autoantibodies. Young adults are also at risk, which supports their consideration in screening strategies for people at risk of developing T1D.

Which Social Variables Predict Diabetes Onset? Robust Findings in Two National Surveys.

The role of social factors in diabetes onset has been obscured by wide variation in their conceptualization and operationalization. We apply 3 theoretical frameworks to categorize social relationship variables along several dimensions and identify which dimension(s) are robustly associated with incident diabetes in the older adult population. The National Social Life, Health, and Aging Project (n = 2,365) and the Health and Retirement Study (n =11,824) provided longitudinal data from 57 to 90-year-old respondents over a 4- to 5-year period. Logistic regression models were used to test associations of 15 social variables measured identically in both data sets with diabetes onset measured as respondents' first report of a physician's diagnosis. In both studies, not being married, experiencing strain in a spousal relationship, and feeling lonely were associated with increased risk for diabetes onset at follow-up. Inconsistent or null findings were observed for social support, social activity, network size, number of friends and relatives, living alone, and closeness to network members. Robust findings in 2 large-scale surveys support the importance of the valence dimension (i.e., positive and negative); specifically, alleviating negative aspects of social life might more effectively reduce risk for diabetes than augmenting positive ones. Findings were not aligned with social variables differing on the subjectivity dimension (i.e., structural, functional, and qualitative aspects of social connections). Future work needs consistent conceptualization and measurement of social factors to correctly identify and categorize risk factors for diabetes onset and other health conditions in older adults.

Oxidative stress in diabetes mellitus and its complications: From pathophysiology to therapeutic strategies.

Oxidative stress due to aberrant metabolism is considered as a crucial contributor to diabetes and its complications. Hyperglycemia and hyperlipemia boost excessive reactive oxygen species generation by elevated mitochondrial respiration, increased nicotinamide adenine dinucleotide phosphate oxidase activity, and enhanced pro-oxidative processes, including protein kinase C pathways, hexosamine, polyol, and advanced glycation endproducts, which exacerbate oxidative stress. Oxidative stress plays a significant role in the onset of diabetes and its associated complications by impairing insulin production, increasing insulin resistance, maintaining hyperglycemic memory, and inducing systemic inflammation. A more profound comprehension of the molecular processes that link oxidative stress to diabetes is crucial to new preventive and therapeutic strategies. Therefore, this review discusses the mechanisms underlying how oxidative stress contributes to diabetes mellitus and its complications. We also summarize the current approaches for prevention and treatment by targeting the oxidative stress pathways in diabetes.

Regulatory T Cell Insufficiency in Autoimmune Diabetes Is Driven by Selective Loss of Neuropilin-1 on Intraislet Regulatory T Cells.

Approaches to reverse or limit regulatory T cell (Treg) insufficiency are of great interest for development of immunotherapeutic treatments for autoimmune patients, including type 1 diabetes. Treg insufficiency is heavily implicated in the progression of autoimmune diabetes in the NOD mouse model and is characterized by defects in Treg numbers, development, and/or function. Utilizing a Treg-centric screen, we show that intraislet Tregs have a uniquely dysfunctional phenotype, hallmarked by an almost complete lack of neuropilin-1 (Nrp1), a cell surface receptor required to maintain Treg stability. Intraislet Nrp1- Tregs exhibit hallmark features of fragility, including reduced suppressive capacity, decreased CD73 and Helios, and increased Rorγt and Tbet. Intraislet Nrp1- Tregs also exhibit decreased Foxp3 expression on a per cell basis, suggesting that Nrp1 may also be required for long-term Treg stability. Mechanistically, Treg-restricted augmentation of Nrp1 expression limited the onset of autoimmune diabetes in NOD mice suggesting that Nrp1 critically impacts intraislet Treg function. Transcriptional analysis showed that Nrp1 restoration led to an increase in markers and pathways of TCR signaling, survival, and suppression, and when Nrp1 protein expression is examined by cellular indexing of transcriptomes and epitopes by sequencing, significant differences were observed between Nrp1+ and Nrp1- Tregs in all tissues, particularly in markers of Treg fragility. This translated into substantive differences between Nrp1+ and Nrp1- Tregs that afforded the former with a competitive advantage in the islets. Taken together, these data suggest that maintenance of Nrp1 expression and signaling on Tregs limits diabetes onset and may serve as a strategy to combat Treg insufficiency in autoimmune disease.

Link between remnant cholesterol and the reversion to normoglycemia in Chinese adults with prediabetes: a 5-year cohort study

Despite the clear association between remnant cholesterol (RC)and diabetes risk, no study to date has examined the relationship between RC and reversal of prediabetes to normoglycemia. This retrospective cohort study included a total of 15,023 patients with prediabetes who underwent a physical examination between 2010 and 2016. The link between initial RC levels and the reversion from prediabetes to normoglycemia was analyzed using the Cox proportional-hazards regression model. Additionally, the study explored the possible relationship between RC and the probability of returning normoglycemia by applying Cox proportional hazards regression models with cubic spline functions. To address competing risks, a multivariate Cox regression analysis was undertaken, treating the onset of diabetes as a competing risk event for reversing prediabetes to normoglycemia. Additionally, the study incorporated extensive subgroup analyses alongside multiple sensitivity analyses, enhancing the reliability and robustness of the results. After adjusting for covariates, the findings indicated that RC was inversely associated with the likelihood of reverting to normoglycemia (per 5 mg/dL increase, HR = 0.918, 95% CI 0.909–0.927). The analysis also revealed a nonlinear relationship between RC and normoglycemia reversion, with an inflection point at 51.08 mg/dL. For RC values below this inflection point (RC < 50.08 mg/dL), the HR for the probability of returning to normoglycemia was 0.907 (95% CI 0.897–0.917 per 5 mg/dL). Additionally, the competing risks model demonstrated a negative relationship between RC and the reversal of prediabetes to normoglycemia (SHR = 0.92, 95% CI 0.91–0.93). Sensitivity analyses confirmed the robustness and stability of these results. This study demonstrated a negative and non-linear association between RC and the probability of reversion to normoglycemia in Chinese adults with prediabetes. By actively intervening to reduce RC levels, at least to below 51.08 mg/dL, further reduction of RC may significantly increase the probability of returning to normoglycemia from prediabetes.

Flavor and taste recognition impairments in people with type 1 diabetes

Background/objectivesAdherence to dietary recommendations is a critical component in the management of type 1 diabetes (T1D). Taste and flavor significantly influence food choices. The aim of this study was to investigate taste sensitivity and flavor recognition ability in adults with T1D compared to healthy individuals.Subjects/methodsSeventy-two people with T1D and 72 matched healthy controls participated in the study. Participants underwent the gustometry test for sweet, sour, salty, and bitter tastes and the flavor test, which consisted of oral administration of aqueous aromatic solutions identifying 21 different compounds.ResultsParticipants with T1D had significantly lower flavor scores and gustometry scores than controls (p < 0.0001 and p = 0.0063, respectively). T1D individuals showed a lower perception of sour, bitter and salty tastes than controls, while the perception of sweet taste was similar. The sex differences and age-related decline in flavor perception observed in controls were not present in the participants with T1D. Neither BMI nor disease-related parameters such as fasting blood glucose on the day of the study, glycosylated hemoglobin, age at onset of diabetes, duration of diabetes, or type of insulin treatment (insulin pump or multiple daily injections) correlated with flavor and taste perception in the T1D participants.ConclusionsFlavor and taste perception are impaired in adults with T1D, potentially affecting dietary adherence and food choices. This highlights the need for further research into the mechanisms underlying sensory changes in T1D and emphasizes the importance of targeted dietary interventions to improve health outcomes and quality of life in this population.

Potential Effects of Hyperglycemia on SARS-CoV-2 Entry Mechanisms in Pancreatic Beta Cells.

The COVID-19 pandemic has revealed a bidirectional relationship between SARS-CoV-2 infection and diabetes mellitus. Existing evidence strongly suggests hyperglycemia as an independent risk factor for severe COVID-19, resulting in increased morbidity and mortality. Conversely, recent studies have reported new-onset diabetes following SARS-CoV-2 infection, hinting at a potential direct viral attack on pancreatic beta cells. In this review, we explore how hyperglycemia, a hallmark of diabetes, might influence SARS-CoV-2 entry and accessory proteins in pancreatic β-cells. We examine how the virus may enter and manipulate such cells, focusing on the role of the spike protein and its interaction with host receptors. Additionally, we analyze potential effects on endosomal processing and accessory proteins involved in viral infection. Our analysis suggests a complex interplay between hyperglycemia and SARS-CoV-2 in pancreatic β-cells. Understanding these mechanisms may help unlock urgent therapeutic strategies to mitigate the detrimental effects of COVID-19 in diabetic patients and unveil if the virus itself can trigger diabetes onset.

Machine Learning Predicts Patients With New-onset Diabetes at Risk of Pancreatic Cancer.

New-onset diabetes represent a high-risk cohort to screen for pancreatic cancer. Develop a machine model to predict pancreatic cancer among patients with new-onset diabetes. A retrospective cohort of patients with new-onset diabetes was assembled from multiple health care networks in the United States. An XGBoost machine learning model was designed from a portion of this cohort (the training set) and tested on the remaining part of the cohort (the test set). Shapley values were used to explain the XGBoost's model features. Model performance was compared with 2 contemporary models designed to predict pancreatic cancer among patients with new-onset diabetes. In the test set, the XGBoost model had an area under the curve of 0.80 (0.76 to 0.85) compared with 0.63 and 0.68 for other models. Using cutoffs based on the Youden index, the sensitivity of the XGBoost model was 75%, the specificity was 70%, the accuracy was 70%, the positive predictive value was 1.2%, and the negative predictive value was >99%. The XGBoost model obtained a positive predictive value of at least 2.5% with a sensitivity of 38%. The XGBoost model was the only model that detected at least 50% of patients with cancer one year after the onset of diabetes. All 3 models had similar features that predicted pancreatic cancer, including older age, weight loss, and the rapid destabilization of glucose homeostasis. Machine learning models isolate a high-risk cohort from those with new-onset diabetes at risk for pancreatic cancer.

Hesperidin activates the GLP-1R/cAMP-CREB/IRS2/PDX1 pathway to promote transdifferentiation of islet α cells into β cells Across the spectrum

Background and aimsIn all age, FoShou as a Chinese medicinal herb has been active in various kinds of Traditional Chinese medicine formula to treating diabetes. Hesperidin (HES), the main monomeric component of FoShou, has been extensively investigated for interventions with pathogenic mechanism of diabetes as well as subsequent treatment of associated complications. Islet β-cells have an essential effect on dynamically regulating blood sugar. Functional abnormalities in these cells and their death are strongly associated with the onset of diabetes. Therefore, induction of islet endocrine cell lineage re-editing for damaged βcell replenishment would be a promising therapeutic tool. Previously, it has been found that HES can protect islet β-cells in vivo, But, the regenerative function of HES in islet β cells and its role in promoting differential non-β cells transdifferentiation into β cells and cell fate rewriting associated mechanisms remain unclear.This work focused on investigating whether HES can induce islet α cells transdifferentiation into β cells for achieving damaged β cell regeneration and the causes and possible mechanisms involved in the process. Materials and methodsIn brief, 60 mg/kg/d streptozotocin (STZ) was administered intraperitoneally in each male C57bL/6J mouse raised by the high-sugar and high-fat diet (HFD) to create a diabetic mouse model with severe β-cell damage. After 28 consecutive days of HES treatment (160 mg/kg; 320 mg/kg; once daily, as appropriate). Tracing the dynamics of α as well as β cell transformation, together with β cells growth and apoptosis levels during treatment by cell lineage tracing. The self-enforcing transcriptional network on which the cell lineage is based is used as a clue to explore the underlying mechanisms. Guangdong Pharmaceutical University's Animal Experiment Ethics Committee (GDPulac2019180) approved all animal experiments. ResultsLocalization by cell lineage we find that transdifferentiated newborn β-cells derived from α cells appeared in the islet endocrine cell mass of DM mice under HES'action. Compared to the model group, expressed by Tunel staining and CXCL10 levels the overall apoptosis rate of β-cells of the pancreas were reduced,the inflammatory infiltration feedback from HE staining were lower.Ki-67 positive cells showed enhanced β-cell proliferation. Decreased HbA1c and blood glucose contents, elevated C-Peptide and insulin contents which respond to ability of nascent beta cells. Also upregulated the mRNA levels of MafA, Ngn3, PDX-1, Pax4 and Arx. Moreover, increased the expression of TGR5/cAMP-CREB/GLP-1 in mouse intestinal tissues and GLP-1/GLP-1R and cAMP-CREB/IRS2/PDX-1 in pancreatic tissues. ConclusionsHES directly affects β-cells, apart from being anti-apoptotic and reducing inflammatory infiltration. HES promotes GLP-1 release by intestinal L cells by activating the TGR5 receptor in DM mouse and regulating its response element CREB signaling. GLP-1 then uses the GLP-1/GLP-1R system to act on IRS2, IRS2 as a port to influence α precursor cells to express PDX-1, with the mobilization of Pax4 strong expression than Arx so that α cell lineage is finally reversed for achieving β cell endogenous proliferation.

Single-housing-induced islet epigenomic changes are related to polymorphisms in diabetic KK mice.

A lack of social relationships is increasingly recognized as a type 2 diabetes (T2D) risk. To investigate the underlying mechanism, we used male KK mice, an inbred strain with spontaneous diabetes. Given the association between living alone and T2D risk in humans, we divided the non-diabetic mice into singly housed (KK-SH) and group-housed control mice. Around the onset of diabetes in KK-SH mice, we compared H3K27ac ChIP-Seq with RNA-Seq using pancreatic islets derived from each experimental group, revealing a positive correlation between single-housing-induced changes in H3K27ac and gene expression levels. In particular, single-housing-induced H3K27ac decreases revealed a significant association with islet cell functions and GWAS loci for T2D and related diseases, with significant enrichment of binding motifs for transcription factors representative of human diabetes. Although these H3K27ac regions were preferentially localized to a polymorphic genomic background, SNVs and indels did not cause sequence disruption of enriched transcription factor motifs in most of these elements. These results suggest alternative roles of genetic variants in environment-dependent epigenomic changes and provide insights into the complex mode of disease inheritance.

Probiotic treatment with viable α-galactosylceramide-producing Bacteroides fragilis reduces diabetes incidence in female nonobese diabetic mice.

We aimed to investigate whether alpha-galactosylceramide (α-GalCer)-producing Bacteroides fragilis could induce natural killer T (NKT) cells in nonobese diabetic (NOD)mice and reduce their diabetes incidence. Five-week-old female NOD mice were treated orally with B. fragilis, and islet pathology and diabetes onset were monitored. Immune responses were analyzed by flow cytometry and multiplex technology. Effects of ultraviolet (UV)-killed α-GalCer-producing B. fragilis and their culture medium on invariant NKT (iNKT) cells were tested ex vivo on murine splenocytes, and the immunosuppressive capacity of splenocytes from B. fragilis-treated NOD mice were tested by adoptive transfer to nonobese diabetic/severe combined immunodeficiency (NOD/SCID) mice. B. fragilis reduced the diabetes incidence from 69% to 33% and the percent of islets with insulitis from 40% to 7%, which doubled the serum insulin level compared with the vehicle-treated control mice. Furthermore, the early treatment reduced proinflammatory mediators in the serum, whereas the proportion of CD4+ NKT cell population was increased by 33%. B. fragilis growth media stimulated iNKT cells and anti-inflammatory M2 macrophages ex vivo in contrast to UV-killed bacteria, which had no effect, strongly indicating an α-GalCer-mediated effect. Adoptive transfer of splenocytes from B. fragilis-treated NOD mice induced a similar diabetes incidence as splenocytes from untreated NOD mice. B. fragilis induced iNKT cells and M2 macrophages and reduced type 1 diabetes in NOD mice. The protective effect seemed to be more centered on gut-pancreas interactions rather than a systemic immunosuppression. B. fragilis should be considered for probiotic use in individuals at risk of developing type 1 diabetes.

Risk Factors for Orbital Complication in Odontogenic Rhinosinusitis

Background: Orbital involvement is the most common complication in rhinosinusitis presenting about 60-75%. The manifestation of orbital complications such as eyelid edema, proptosis, eye movement disorder and loss of vision. The potential risk factors for developing complications are described in several studies. Purpose: To examine the risk factors for orbital complication in odontogenic rhinosinusitis. Methods: A retrospective case control study of 34 patients from July 2022 to July 2023 based on medical records. The subjects were classified into two groups, the case group involving odontogenic rhinosinusitis patients with orbital complication and the control group involving patients without orbital complications. Risk factors were sex, onset of odontogenic sinusitis, sinonasal symptoms, diabetes, histopathological findings, laboratory findings and CT scan images of sinus. The characteristics of orbital complications and the types of pathogenic bacteria cultivated were recorded. Results: There number of patients in each group were 17, with the female to male ratio of 2,4:1, aged 8 to 81 years were enrolled in this study. The most common orbital complication was sub periosteal abscess (41%). We found 64% positive bacterial growth from tissue culture dominated by Staphylococcus sp. (54.5%). Histopathological examination showed the main inflammatory cell of the sinus mucosal epithelium was neutrophil in both groups. The logistic regression test showed that the risk factors for orbital complication were absolute neutrophil count p 0.008, OR 81.062, mucopurulent discharge p 0.009, OR 0.006 and sinus involvement p 0.027, OR 0.152. Conclusion: Orbital complications were associated with sinus involvement with main symptom involving mucopurulent discharge and higher absolute neutrophil count.

An Interesting Case of Cushing Syndrome

An Interesting Case of Cushing Syndrome A 36 year old female presented to dermatology department with Multiple ulcers present in B/L axilla, B/L inframammary fold and B/L gluteal fold (Left &gt; Right) since 3 months. Patient was referred from dermatology department to General Medicine for opinion on puffiness of face and swelling of legs . Patient had history of topical steroid use for itchy lesions in B/L axilla and inframammary folds 4 months back . H/o weight gain present. (6 kg). H/o puffiness of face and striae present over the abdomen. Patient had no known comorbidities previously. On physical examination patient had moon face ,facial plethora + ,Buffalo hump ,Loss of axillary hair, centripetal obesity , Abdominal striae , Sparse pubic hair , Pallor +. Systemic examination was normal. Investigations revealed new onset diabetes , serum cortisol was low (&lt;0.5 mcg/ml) , serum acth was low (1pg/ml) , HB was low (7.9gm/dl) , total count was elevated (15,600) . Patient was diagnosed to have Iatrogenic (Topical steroid induced) Cushing Syndrome with Steroid induced atrophy and ulceration of skin &amp; subcutaneous tissue leading to secondary fungal and bacterial infection , tinea incognito with secondary bacterial infection , iron deficiency anemia and newly detected Type 2 Diabetes mellitus. Patient was appropiately treated with iv antibiotics (Inj Piperacillin Tazobactum 4.5 g iv thrice daily), daily dressing on other supportive measures along with discontinuation of steroids. Patient improved symptomatically after discontinuing topical steroids, the cushingoid features started decreasing. The ulcers also started to heal. The patient was started on Tab. Hydrocortisone 10mg - 0 – 5mg and was referred for Endocrinologist opinion

Exploring Multitargets Treatment for Diabetes

Diabetes Mellitus (DM) is a degenerative disease that modifies the body’s glucose metabolism. Although glucose is a vital energy source for body cells, individuals with diabetes can either not use insulin efficiently or do not create enough of this hormone, which controls blood sugar. This review aimed to explore the multi-target treatment for diabetes. This study investigates explicitly recent reports published in peer-reviewed journals indexed in various databases, including Web of Science, Scopus, PubMed, Google Scholar, and Science Direct. Individuals with diabetes are more likely to experience other health issues, such as elevated blood pressure and cholesterol. Environmental factors that can influence the onset of diabetes include air pollution, temperature and weather, and stress. With the shortage of diabetes specialists and healthcare experts coupled with an inefficient healthcare service in low- and middle-income nations, there is a need to introduce more creative approaches to treat diabetes. Although literature reveals that no one-size-fits-all method is available for managing diabetes because each person's reaction to the disease varies depending on several factors, such as the diabetes stage and the person’s susceptibility to complications, this study posits that there could be a headway in diabetes management by exploring multi-targets treatment. Introducing lifestyle change, diet modification and physical activity could reduce the risk of death due to diabetes. This study also highlights how diabetes can be managed in the rural and urban settings. Adopting telemedicine and web-based initiatives could impact diabetes treatment positively.

Longitudinal metabolite and protein trajectories prior to diabetes mellitus diagnosis in Danish blood donors: a nested case–control study

Aims/hypothesisMetabolic risk factors and plasma biomarkers for diabetes have previously been shown to change prior to a clinical diabetes diagnosis. However, these markers only cover a small subset of molecular biomarkers linked to the disease. In this study, we aimed to profile a more comprehensive set of molecular biomarkers and explore their temporal association with incident diabetes.MethodsWe performed a targeted analysis of 54 proteins and 171 metabolites and lipoprotein particles measured in three sequential samples spanning up to 11 years of follow-up in 324 individuals with incident diabetes and 359 individuals without diabetes in the Danish Blood Donor Study (DBDS) matched for sex and birth year distribution. We used linear mixed-effects models to identify temporal changes before a diabetes diagnosis, either for any incident diabetes diagnosis or for type 1 and type 2 diabetes mellitus diagnoses specifically. We further performed linear and non-linear feature selection, adding 28 polygenic risk scores to the biomarker pool. We tested the time-to-event prediction gain of the biomarkers with the highest variable importance, compared with selected clinical covariates and plasma glucose.ResultsWe identified two proteins and 16 metabolites and lipoprotein particles whose levels changed temporally before diabetes diagnosis and for which the estimated marginal means were significant after FDR adjustment. Sixteen of these have not previously been described. Additionally, 75 biomarkers were consistently higher or lower in the years before a diabetes diagnosis. We identified a single temporal biomarker for type 1 diabetes, IL-17A/F, a cytokine that is associated with multiple other autoimmune diseases. Inclusion of 12 biomarkers improved the 10-year prediction of a diabetes diagnosis (i.e. the area under the receiver operating curve increased from 0.79 to 0.84), compared with clinical information and plasma glucose alone.Conclusions/interpretationSystemic molecular changes manifest in plasma several years before a diabetes diagnosis. A particular subset of biomarkers shows distinct, time-dependent patterns, offering potential as predictive markers for diabetes onset. Notably, these biomarkers show shared and distinct patterns between type 1 diabetes and type 2 diabetes. After independent replication, our findings may be used to develop new clinical prediction models.Graphical

Prevalence, Characteristics and Risk Factors Analysis of Prediabetes: A Cross-Sectional Study

Background Prediabetes, a reversible condition before the onset of diabetes, is a significant concern in healthcare globally. The global prediabetes epidemic has emerged and has considerably impacted health expenditures. Various risk factors play important roles in the progression of prediabetes to diabetes. Intensive lifestyle and pharmacological interventions can significantly reduce the risk of diabetes progression. Objective This study aimed to determine the prevalence, characteristics, and risk factors of prediabetes state of Medan in August 2023. Methods The sample consisted of 89 participants. This was an analytical cross-sectional study in the community that met the inclusion and exclusion criteria. The determination of prediabetes is based on the results of blood tests, namely, the examination of fasting blood sugar levels (FBGL), 2-hour postprandial oral glucose tolerance test (OGTT), and hemoglobin A1c (HbA1C). Other examinations included lipid profiling (total cholesterol, HDL-C, LDL-C, and triglycerides). Data processing was performed using SPSS via univariate and bivariate analyses (chi-square test). Results Of the 89 participants, the prevalence of prediabetes based on HbA1c, FBGL and 2-hours OGTT levels was 28.1%, 50.6%, and 28.1%, respectively. 82% of the participants were female, and 53.9% were overweight or obese based on body mass index (BMI). The risk factors related to the prevalence of prediabetes were HbA1c level, impaired FBGL, and impaired 2-hours OGTT. Other risk factors such as age, sex, daily exercise, diet, BMI, waist-hip ratio, acanthosis nigricans, lipid profile, and blood pressure did not correlate significantly with the risk factors (p&gt;0.05). Conclusion This study found that the prevalence of prediabetes was 67.4% in Medan, 82% of the participants were female, and more than 50% of participants were overweight or obese. HbA1c, FBGL, and 2-hour postprandial OGTT were the most important risk factors for prediabetes.

Reg2 treatment is protective but the induced Reg2 autoantibody is destructive to the islets in NOD mice

Regenerating family protein 2 (Reg2) is a trophic factor which stimulates β-cell replication and resists islet destruction. However, Reg2 also serves as an islet autoantigen, which makes it complicated to judge the effectiveness in treating diabetes. How Reg2 treatment behaves in non-obese diabetic (NOD) mice is to be investigated. NOD mice were treated with recombinant Reg2 protein, Complete Freund’s adjuvant (CFA) + PBS and CFA+Reg2 vaccinations, CFA+PBS- and CFA+Reg2-immunized antisera, and single chain variable fragment (scFv)-Reg2 and mIgG2a-Reg2 antibodies. Glycemic level, bodyweight, serum Reg2 antibody titer, glucose tolerance, and insulin secretion were determined. Islet morphological characteristics, insulitis, cell apoptosis, islet cell components, and T cell infiltration were analyzed by histological examinations. The autoantigenicity of constructed Reg2C and Reg2X fragments was determined in healthy BALB/c mice, and the bioactivity in stimulating cell proliferation and survival was assessed in insulinoma MIN6 cells. Reg2 administration alleviated diabetes in NOD mice with improved glucose tolerance and insulin secretion but elevated serum Reg2 autoantibodies. Histomorphometry showed reduced inflammatory area, TUNEL signal and CD8 + T cell infiltration, and increased β-cell proportion in support of the islet-protective effect of Reg2 treatment. CFA+PBS and CFA+Reg2 immunizations prevented diabetic onset and alleviated insulitis while injections of the antisera offered mild protections. Antibody treatments accelerated diabetic onset without increasing the overall incidence. Reg2C fragment depletes antigenicity, but reserves protective activity in streptozotocin (STZ)-treated MIN6 cells. In conclusion, Reg2 treatment alleviates type 1 diabetes (T1D) by preserving islet β-cells, but induces Reg2 autoantibody production which poses a potential risk of accelerating diabetic progression.

Formulation and Evaluation of Polyherbal Antidiabetic Tablet

About 60% of people use traditional medicines that are made from medicinal plants. This article focuses on Indian herbal medicines and plants that are utilized, particularly in India, to treat diabetes. Diabetes is a serious illness that affects many people worldwide from all areas of life. It is proven to be a serious health issue in India, particularly in the cities. Although there are many ways to lessen diabetes' negative effects and its secondary complications, herbal formulations are preferred because they have fewer side effects and are less expensive. A list of medicinal plants having established antidiabetic properties, as well as herbal medications used to treat diabetes, is compiled. These includes, Tinospora cordifolia, Azadirachta indica, Enicostemma axillare, Momordica Charantia, Phyllanthus emblica, Centratherum anthelminticum. Damage caused by free radicals is one of the etiologic factors linked to the onset of diabetes and its complications, so an anti-diabetic drug having antioxidant qualities would be more advantageous. Historically, substances and extracts obtained from various natural resources, particularly plants, have been a valuable tool for managing and treating diabetes-related issues and complications. Therefore, this review aids the reader in understanding the significance of various herbal and polyherbal formulations that have been used traditionally to treat diabetes mellitus.

Positive parental history of diabetes is associated with early diagnosis, better dietary compliance, and glycemic control among type 2 diabetes patients in southern Sri Lanka

BackgroundParental history of diabetes is an established risk factor for type 2 diabetes mellitus (T2DM). There is limited data on the association of parental history with the prevalence of T2DM in Sri Lanka. The study aims to examine the prevalence and correlation of parental history and factors such as the onset age, glycaemic control, and self-reported dietary compliance among T2DM patients. With a rising incidence of T2DM in Sri Lanka, understanding the impact of parental history on age at diagnosis and glycemic control can aid in targeted screening and interventions.MethodsA cross-sectional study was carried out on 500 T2DM patients attending a diabetes clinic in Galle, the capital of Southern Sri Lanka with a multiethnic population. Convenient sampling strategy was followed in the recruitment process and a questionnaire-based method was used to collect the data. All the collected data was analysed using SPSS V 25.0.Results51.2% had a parental history of T2DM, and those with a positive parental history were diagnosed six years earlier than those with a negative parental history (p < 0.001). A significant correlation between parental history and gestational diabetes mellitus (GDM) was observed (p < 0.001). Patients with a parental history reported better dietary adherence (p < 0.001). Binary logistic regression analysis revealed patients with positive parental history had significantly lower HbA1C (p = 0.003, OR = 0.748).ConclusionT2DM patients with a parental history showed significant association with early diabetes onset, GDM, better glycemic control, and dietary adherence.

Associations of insulin sensitivity and immune inflammatory responses with child blood lead (Pb) and PM2.5 exposure at an e-waste recycling area during the COVID-19 lockdown.

Fine particular matter (PM2.5) and lead (Pb) exposure can induce insulin resistance, elevating the likelihood of diabetes onset. Nonetheless, the underlying mechanism remains ambiguous. Consequently, we assessed the association of PM2.5 and Pb exposure with insulin resistance and inflammation biomarkers in children. A total of 235 children aged 3-7years in a kindergarten in e-waste recycling areas were enrolled before and during the Corona Virus Disease 2019 (COVID-19) lockdown. Daily PM2.5 data was collected and used to calculate the individual PM2.5 daily exposure dose (DED-PM2.5). Concentrations of whole blood Pb, fasting blood glucose, serum insulin, and high mobility group box 1 (HMGB1) in serum were measured. Compared with that before COVID-19, the COVID-19 lockdown group had lower DED-PM2.5 and blood Pb, higher serum HMGB1, and lower blood glucose and homeostasis model assessment of insulin resistance (HOMA-IR) index. Decreased DED-PM2.5 and blood Pb levels were linked to decreased levels of fasting blood glucose and increased serum HMGB1 in all children. Increased serum HMGB1 levels were linked to reduced levels of blood glucose and HOMA-IR. Due to the implementation of COVID-19 prevention and control measures, e-waste dismantling activities and exposure levels of PM2.5 and Pb declined, which probably reduced the association of PM2.5 and Pb on insulin sensitivity and diabetes risk, but a high level of risk of chronic low-grade inflammation remained. Our findings add new evidence for the associations among PM2.5 and Pb exposure, systemic inflammation and insulin resistance, which could be a possible explanation for diabetes related to environmental exposure.