Pathogenesis Of Diabetes Mellitus Research Articles

Serum microcystin-LR levels and risk of gestational diabetes mellitus: A Chinese nested case-control study.

Previous experimental studies have reported an association between microcystin-LR (MC-LR) and glucose homeostasis, but whether exposure to MC-LR is a risk factor for the pathogenesis of gestational diabetes mellitus (GDM) requires further epidemiological study. This study aims to explore the effects of MC-LR on GDM. A prospective nested case-control study was performed in the Hunan Provincial Maternal and Child Health Hospital (HPMCHH) in South China. A total of 119 patients with GDM and 238 controls were enrolled in the study. The two independent samples t-test, or chi-square test was used to compare the difference between the GDM group and the non-GDM group. Binary logistic regression was used to obtain odds ratios (ORs) by controlling for confounders. The cumulative incidence of GDM in our sample was 13.7%. The detection rate of MC-LR in the GDM group were significantly higher than those in the control group (44.2% vs. 29.4%; p=0.007). Our results show that an elevated serum MC-LR level in the first trimester of pregnancy was related to an increased risk of GDM (OR: 1.924; 95% CI: 1.092-3.391; p<0.05). When stratified by age, educational level, parity, and passive smoking, significantly relationships were observed among those aged >30 years, lower income, higher education, none passive smoking, and more likely to be multiparous. Our data reveals that serum MC-LR level in the first trimester is independently associated with GDM.

The Relationship between Diabetes Mellitus and Pancreatic Cancer-Diabetes Mellitus as a Red Flag for Pancreatic Cancer.

The relationship between diabetes mellitus (DM) and pancreatic cancer is complex-DM is both a risk factor and early sign of pancreatic cancer. DM is a risk factor for pancreatic cancer because it increases insulin resistance, intrapancreatic concentrations of insulin, and the bioavailability of IGF, subsequently promoting ductal cell proliferation. Accordingly, treatment targeting the insulin/IGF pathway is the focus of many researchers. Antidiabetic drugs modify the risk for pancreatic cancer-metformin's antineoplastic effect being most notable and indicating potential clinical use in pancreatic cancer. New-onset DM can also be the first manifestation of pancreatic cancer. There are several theories for the pathogenesis of DM in pancreatic cancer, the most important being that DM is a paraneoplastic syndrome caused by diabetogenic factors. As a consequence of this intricate relationship, new-onset DM after the age of 50 is considered a red flag for pancreatic cancer, prompting the need for screening in this patient population. Multiple clinical studies are currently underway exploring this matter. A better understanding of the relationship between DM and pancreatic cancer could aid in developing novel screening and treatment strategies for pancreatic cancer. This could ultimately improve the prognosis and quality of life of patients with pancreatic cancer.

Endocrine System Related to Diabetes Mellitus

Diabetes mellitus has a complicated and poorly understood pathogenesis. However, it turns out to be an abnormal metabolic state linked to systemic vascular bed injury. Additionally, the endocrine system is not functioning normally in people with diabetes mellitus, according to the body of data. Uncertainty surrounds the relationship between the alterations in the endocrine system and the hormonal environment caused by aberrant glucose and fat metabolism, decreased insulin action, or both. A review of the literature shows that the entire endocrine system, including the hormones produced by the hypothalamus, pituitary, adrenal, thyroid, and parathyroid glands as well as the vitamin D system, the gonads, and the adipose tissue, is dysfunctional. Some of these abnormalities may be corrected with proper metabolic management and insulin therapy. It is still unknown how much these endocrine system changes contribute to the vascular pathologies seen in people with diabetes mellitus and whether some of the abnormalities seen in the endocrine system are due to a fundamental cellular defect in the diabetic syndrome. A complex, long-term metabolic condition called diabetes mellitus causes increased blood glucose levels as a result of insufficient insulin synthesis or uptake. The goal of this review article is to give a thorough overview of the complex interactions between the endocrine system and diabetes mellitus pathogenesis. It is still unknown how much these endocrine system changes contribute to the vascular pathologies seen in people with diabetes mellitus and whether some of the abnormalities seen in the endocrine system is due to a fundamental cellular defect in the diabetic syndrome. A complex, long-term metabolic condition called diabetes mellitus causes increased blood glucose levels as a result of insufficient insulin synthesis or uptake. The goal of this review article is to give a thorough overview of the complex interactions between the endocrine system and diabetes mellitus pathogenesis. It results from dysregulation of the endocrine system, primarily involving the pancreas, and its hormones, particularly insulin and glucagon. This review article provides an in-depth analysis of recent advances in our understanding of the endocrine system’s; role in diabetes mellitus, encompassing both type 1 and type 2 diabetes. The review begins by elucidating the pivotal roles of the endocrine system in maintaining glucose homeostasis, highlighting the pancreas; contribution through the secretion of insulin and glucagon. It explores the etiological factors that underlie diabetes, including genetics, lifestyle, and environmental influences. The article then delves into the pathophysiological mechanisms responsible for the onset and progression of diabetes mellitus, encompassing insulin resistance, β-cell dysfunction, and the involvement of various hormones, cytokines, and adipocytes. A large worldwide health burden is posed by diabetes mellitus, a set of metabolic illnesses characterized by increased blood glucose levels. The endocrine system, which is made up of numerous glands and hormones, is intricately related to the aetiology of diabetes and plays a crucial role in regulating glucose metabolism. The goal of this in-depth review article is to give a complete analysis of the state of knowledge at the moment about how the endocrine system and diabetes mellitus interact. Beginning with a discussion of the physiological part played by the endocrine system in maintaining glucose homeostasis, the overview highlights the important hormones insulin, glucagon, and others as well as the major participants in this process. After that, it explores the complex aetiology of diabetes mellitus, including type 1, type 2, and gestational diabetes, highlighting the role that genetic, environmental, and lifestyle variables have in the progression of the disease. Advancements in the understanding of the endocrine system’s; intricate signalling pathways, including insulin secretion, insulin resistance, and hormonal regulation, are explored in detail.

Evaluation of interleukin-33 & sST2 levels in type-2 diabetic mellitus patients with or without metabolic syndrome.

Diabetes mellitus (DM) is characterized by increase in blood glucose levels due to defective insulin secretion or insulin sensitivity. Interleukins (ILs) are known to play an important role in the pathogenesis of DM. The aim of this study was to investigate the serum concentration of IL-33 and its receptor soluble ST2 (sST2) in patients with diabetes and draw a correlation between their serum levels and different standard glycaemic indices of patients affected with type-2 diabetes with or without metabolic syndrome. Thirty type-2 diabetic individuals and 30 healthy controls were recruited for this study. Serum and plasma were separated by centrifugation of blood for quantitative measurement of IL-33, sST2 and other biochemical parameters. It was observed that serum IL-33 levels were significantly less and sST2 levels were significantly high in type-2 diabetic individuals as compared to healthy controls. A significant correlation between the serum IL-33 concentration and fasting plasma glucose (FPG) and postprandial plasma glucose (PPG) levels were also found. Additionally, data also elucidated that serum levels of high-density lipoprotein, low-density lipoprotein or triglyceride in type-2 diabetics did not influence the serum levels of IL-33 and sST2, thereby excluding these factors as the major drivers of changes in serum IL-33 and sST2 concentration. This study demonstrated alteration in serum levels of IL-33 and sST2 in type-2 diabetic individuals. Further mechanistic studies, focusing on the progression of type-2 diabetes could elucidate the involvement of IL-33 in the cellular acquisition of insulin resistance as observed in type-2 diabetics.

Salidroside protects pancreatic β-cells against pyroptosis by regulating the NLRP3/GSDMD pathway in diabetic conditions.

The NACHT, LRP, and PYD domains-containing protein 3 (NLRP3) inflammasome-evoked chronic inflammation is involved in the pathogenesis of diabetes mellitus (DM), and the NLRP3/gasdermin D (GSDMD)-mediated canonical pathway of pyroptosis leads to the loss of pancreatic β-cells and failure of pancreatic function in DM. A previous study demonstrated that salidroside (SAL) alleviates the pathological hyperplasia of pancreatic β-cells in db/db mice. However, it is not clear whether the NLRP3/GSDMD pathway-mediated pyroptosis can be regulated by SAL. In addition, the action of SAL on pancreatic β-cells in DM remains poorly understood. Thus, this study aimed to investigate the effects and underlying mechanisms of SAL on pancreatic β-cell pyroptosis. Rat insulinoma (INS-1) cells were cultured in a medium containing either high glucose (HG) or HG plus high insulin (HG-HI), and the effects of SAL on cell viability, AMP-activated protein kinase (AMPK) activity, reactive oxygen species (ROS) generation, NLRP3/GSDMD activation, and pyroptotic body formation were assessed. Streptozocin-induced DM mice were used to further investigate the effects of SAL on pancreatic pyroptosis. The results revealed aberrances on cell viability, AMPK activity, ROS generation, NLRP3/GSDMD activation, and pyroptotic body formation in HG- and HG-HI-exposed INS-1 cells; these abnormal effects were corrected by SAL in both a concentration- and AMPK-dependent manner. Moreover, SAL administration activated AMPK, suppressed NLRP3/GSDMD signaling, and protected pancreatic β-cells against pyroptosis in DM mice. These findings suggest that SAL promotes AMPK activation to suppress NLRP3/GSDMD-related pyroptosis in pancreatic β-cells under DM conditions.

ROLE OF BIOLOGICAL CLOCK MALFUNCTION IN THE PATHOGENESIS OF DIABETES MELLITUS

Purpose. This paper provides a review of biological clock (BC) malfunction as a possible pathophysiological mechanism underlying the development of type 1 and 2 diabetes mellitus (DM). Objective of the review. A total of 69 scientific papers were found using the Cochrane Library, PubMed, eLibrary.ru and Medscape, and analyzed. The search covered the period from 2012 to 2023 and used the combination of the following keywords: “diabetes mellitus”, “biological clock”, “melatonin”. Results. It covers the main physiological aspects of BC operation and their contribution to the maintenance of the body’s homeostasis. Also discussed are issues related to BC-mediated regulation of glucose and insulin levels. Arguments are provided to corroborate the involvement of BC malfunction in the development of DM through biological rhythm desynchronization, activation of mitochondrial dysfunction, and oxidative stress. Another point of discussion is disrupted melatonin synthesis as a marker of BC malfunction and as a possible trigger of the development of DM. Conclusion. The theory of the involvement of BC malfunction in DM pathogenesis is up-to-date and supported by scientific evidence and therefore needs to be researched and developed further.

DIABETIC RETINOPATHY AND CLINICALLY SIGNIFICANT MACULAR EDEMA IN TYPE- 1 DIABETES MELLITUS: A CLINICAL STUDY

Type-1 diabetes mellitus is a metabolic disease resulting from autoimmune disorder involving the pancreas which causes selective destruction of beta cells responsible for insulin production. Multiple genetic and environmental factors contribute to the pathogenesis of type-1 diabetes mellitus. Management involves insulin administration and strict glycemic control. In this study 100 patients of type-1 diabetes were studied for retinopathy changes during a period of 2 years from December 2019 to December 2021. The age of onset of disease was noted and fundus examination was done with indirect ophthalmoscope or by using 90D lens. Laboratory workup including fasting and post-prondial blood sugars and HbA1C levels. The incidence and severity of diabetic retinopathy and clinically signicant macular edema (CSME) was noted and found to be associated with increased duration of diabetes and poor glycemic control.

Gestational Diabetes Mellitus and Antenatal Corticosteroid Therapy-A Narrative Review of Fetal and Neonatal Outcomes.

There, we review the pathogenesis of gestational diabetes mellitus (GDM), its influence on fetal physiology, and neonatal outcomes, as well as the usage of antenatal corticosteroid therapy (ACST) in pregnancies complicated by GDM. MEDLINE and PubMed search was performed for the years 1990-2022, using a combination of keywords on such topics. According to the aim of the investigation, appropriate articles were identified and included in this narrative review. GDM is a multifactorial disease related to unwanted pregnancy course and outcomes. Although GDM has an influence on the fetal cardiovascular and nervous system, especially in preterm neonates, the usage of ACST in pregnancy must be considered taking into account maternal and fetal characteristics. GDM has no influence on neonatal outcomes after ACST introduction. The ACST usage must be personalized and considered according to its gestational age-specific effects on the developing fetus.

Elajik Asit, Diyabetik Böbrek Hasarında TGFβ1/Smad Kaynaklı Böbrek Fibrozisini İnhibe Eder

Aim: Free radical formation increases due to hyperglycemia occurring in the pathogenesis of diabetes mellitus (DM), and as a result, oxidative stress occurs. Hyperglycemia-mediated oxidative stress plays an important role in the pathogenesis of diabetic nephropathy. The antihyperglycemic, antioxidative, anti-apoptotic, and anti-inflammatory effects of ellagic acid (EA) have been demonstrated by many studies. In this study, it was aimed to demonstrate the antifibrotic effect of EA on TGFβ1/Smad signaling in rats with streptozotocin induced diabetic nephropathy. Material and Methods: A total of 24 male Sprague Dawley rats, weighing 200-250 g, were used in this study. The animals were divided into four groups as control, EA, DM, and DM+EA. The kidney tissues were used for histological and immunohistochemical procedures. While the collagen density in kidney tissues was revealed by Masson's trichrome staining, the expression levels of fibrotic markers TGFβ1, p-Smad3, and αSMA were determined by the immunocytochemical method. Results: It was shown that the collagen density in the renal tissue of the DM group increased significantly in the intertubular area, while the collagen density in the EA-treated DM group was statistically significantly decreased. When TGFβ1, p-Smad3, and αSMA immunopositivity in kidney tissue sections of all groups were evaluated, the highest staining intensity was in the DM group, while the intensity of staining was close to the control group in the treatment group. It was observed that αSMA, TGFβ1, and p-Smad3 protein expression were down-regulated with EA treatment. Conclusion: EA reduced fibrosis in diabetic nephropathy by returning profibrotic parameters to normal levels.

MicroRNA‑143‑3p levels are reduced in the peripheral blood of patients with gestational diabetes mellitus and influences pancreatic β‑cell function and viability.

Pancreatic β-cell dysfunction has been demonstrated to mediate key roles in the pathogenesis of gestational diabetes mellitus (GDM). Accumulating evidence has supported the functional involvement of microRNAs (miRNAs) in various types of diabetes, including GDM. However, the detailed biological effect of miRNAs in pancreatic β-cell dysfunction remains poorly understood. In the present study, microarray data of miRNAs in the blood plasma of patients with GDM were retrieved from the Gene Expression Omnibus dataset under the accession number GSE98043. Reverse transcription-quantitative PCR (RT-qPCR) was performed to measure the expression levels of miR-143-3p in the blood plasma isolated from 30 female patients with GDM women and 30 healthy female individuals. Subsequently, murine pancreatic β-cell line, MIN6 cells were treated with high glucose (HG) to construct in vitro cell models of GDM. miR-143-3p in HG-treated MIN6 cells was overexpressed or knocked down using miR-143-3p mimics and miR-143-3p inhibitor. Cell viability, insulin secretion and proinflammatory cytokine production were examined using CCK-8 and ELISA, respectively Cell apoptosis was measured by flow cytometry assay. The protein expression levels of proteins involved in the TAK1/NF-κB pathway were also assessed using western blot. The levels of miR-143-3p were found to be markedly lower in samples from patients with GDM, which were in turn negatively correlated with blood glucose levels. Overexpression of miR-143-3p in MIN6 cells significantly reversed HG-induced cell apoptosis and impairments in cell viability and insulin secretion. In addition, miR-143-3p overexpression attenuated HG-induced proinflammatory cytokine production by MIN6 cells. Subsequently, TGFβ-activated kinase 1 (TAK1), an upstream regulator of the NF-κB pathway, was found to be a direct target of miR-143-3p in pancreatic β cells through luciferase assays and western blot. Overexpression of TAK1 was revealed to abolish the curative effects of miR-143-3p on insulin secretion, cell viability and inflammatory response in HG-treated MIN6 cells. In addition, miR-143-3p could inactivate the NF-κB pathway by inhibiting TAK1 expression. Collectively, these results suggest that miR-143-3p levels are downregulated in the peripheral blood of patients with GDM. Therefore, miR-143-3p overexpression may serve as a method for preventing pancreatic β cell dysfunction by inhibiting the TAK1/NF-κB pathway.

Role of microelements in the development of endocrine pathology

Due to the continual increase in the incidence of endocrine diseases in the world, their prevention and treatment have become topical. Diseases of the endocrine system are often accompanied by the development of comorbidities and complications, which negatively affect the quality of life and survival of patients. Currently, research is focused on the status of trace elements in patients with various diseases. Numerous current studies are devoted to investigating the influence of the balance of trace elements on the etiology and pathogenesis of diabetes mellitus, obesity, and some thyroid diseases, including autoimmune ones. The role of iodine, selenium, iron, zinc, and copper in the development and progression of these diseases has been established, but the findings of these studies are sometimes contradictory.&#x0D; This review focuses on national and foreign studies on the role of trace elements in the development of endocrine pathology, and gives a brief description of the most significant mineral substances, as well as the effect of their imbalance on the structure and function of the organs of the endocrine system. This review recommends further studies on this issue incorporating concomitant diseases, as well as the mutual influences of mineral substances on each other, which can lead to a change in the concentration of trace elements in the body.

Regeneration of Pancreatic β-Cells for Diabetes Therapeutics by Natural DYRK1A Inhibitors.

The pathogenesis of diabetes mellitus is characterized by insulin resistance and islet β-cell dysfunction. Up to now, the focus of diabetes treatment has been to control blood glucose to prevent diabetic complications. There is an urgent need to develop a therapeutic approach to restore the mass and function of β-cells. Although exogenous islet cell transplantation has been used to help patients control blood glucose, it is costly and has very narrow application scenario. So far, small molecules have been reported to stimulate β-cell proliferation and expand β-cell mass, increasing insulin secretion. Dual-specificity tyrosine-regulated kinase 1A (DYRK1A) inhibitors can induce human β-cell proliferation in vitro and in vivo, and show great potential in the field of diabetes therapeutics. From this perspective, we elaborated on the mechanism by which DYRK1A inhibitors regulate the proliferation of pancreatic β-cells, and summarized several effective natural DYRK1A inhibitors, hoping to provide clues for subsequent structural optimization and drug development in the future.

Особенности патогенеза и лечения сахарного диабета в период пандемии COVID-19

Особенности патогенеза и лечения сахарного диабета в период пандемии COVID-19

Maternal and Placental DNA Methylation Changes Associated with the Pathogenesis of Gestational Diabetes Mellitus.

Gestational diabetes mellitus (GDM) is an important metabolic complication of pregnancy, which affects the future health of both the mother and the newborn. The pathogenesis of GDM is not completely clear, but what is clear is that with the development and growth of the placenta, GDM onset and blood glucose is difficult to control, while gestational diabetes patients' blood glucose drops and reaches normal after placenta delivery. This may be associated with placental secretion of insulin-like growth factor, adipokines, tumor necrosis factor-α, cytokines and insulin resistance. Therefore, endocrine secretion of placenta plays a key role in the pathogenesis of GDM. The influence of DNA methylation of these molecules and pathway-related genes on gene expression is also closely related to the pathogenesis of GDM. Here, this review attempts to clarify the pathogenesis of GDM and the related maternal and placental DNA methylation changes and how they affect metabolic pathways.

Encouraging Tactics with Genetically Modified Probiotics to Improve Immunity for the Prevention of Immune-Related Diseases including Cardio-Metabolic Disorders

The PI3K/AKT/mTOR signaling pathway may play crucial roles in the pathogenesis of obesity and diabetes mellitus, as well as metabolic syndromes, which could also be risk factors for cardio-metabolic disorders. Consistently, it has been shown that beneficial effects may be convoyed by the modulation of the PI3K/AKT/mTOR pathway against the development of these diseases. Importantly, the PI3K/AKT/mTOR signaling pathway can be modulated by probiotics. Probiotics have a variety of beneficial properties, with the potential of treating specific diseases such as immune-related diseases, which are valuable to human health. In addition, an increasing body of work in the literature emphasized the contribution of genetically modified probiotics. There now seems to be a turning point in the research of probiotics. A better understanding of the interactions between microbiota, lifestyle, and host factors such as genetics and/or epigenetics might lead to a novel therapeutic approach with probiotics for these diseases. This study might provide a theoretical reference for the development of genetically modified probiotics in health products and/or in functional foods for the treatment of cardio-metabolic disorders.

DIFFERENTIAL NUMBER OF LEUCOCYTES IN PATIENTS WITH TYPE 2 DIABETES MELLITUS TREATED WITH DIABETIC VASCULAR FOOT EXERCISE

Background : Disturbance Wound healing is one of the complications of type 2 diabetes mellitus (DM). Disorders of leukocyte profile have been associated with DM pathogenesis and complications. Objective : To investigate the differential leukocyte count in patients with type 2 diabetes treated with diabetic vascular leg exercises. Methods : A re-experimental study design P with a one-group pre-test-post-test design was used in the study, which was conducted on people with DM in Bengkulu Tengah. Blood plasma specimen collection before (30 samples) and after (30 samples) diabetic vascular leg exercise. The leukocyte diffcount was analyzed microscopically. Results : There were significant differences in segmented neutrophils (p = 0.013), lymphocytes (p = 0.029), monocytes (0.043) in people with diabetes before and after diabetes exercise intervention. There was no significant difference in basophils (p = 1,000), eosinophils (p = 0.594), stem neutrophils (p = 0.236) in people with diabetes before and after the diabetes exercise intervention. Conclusion : diabetes physical exercise modulates leukocyte count differential in people with type 2 DM in Central Bengkulu. The results of the study support the development of diabetes physical exercise as a therapeutic modality for DM patients to prevent complications from a young age.&#x0D; &#x0D; &#x0D;

Mushroom polysaccharides with potential in anti-diabetes: Biological mechanisms, extraction, and future perspectives: A review.

Diabetes mellitus (DM) is a global health threat. Searching for anti-diabetic components from natural resources is of intense interest to scientists. Mushroom polysaccharides have received growing attention in anti-diabetes fields due to their advantages in broad resources, structure diversity, and multiple bioactivities, which are considered an unlimited source of healthy active components potentially applied in functional foods and nutraceuticals. In this review, the current knowledge about the roles of oxidative stress in the pathogenesis of DM, the extraction method of mushroom polysaccharides, and their potential biological mechanisms associated with anti-diabetes, including antioxidant, hypolipidemic, anti-inflammatory, and gut microbiota modulatory actions, were summarized based on a variety of in vitro and in vivo studies, with aiming at better understanding the roles of mushroom polysaccharides in the prevention and management of DM and its complications. Finally, future perspectives including bridging the gap between the intervention of mushroom polysaccharides and the modulation of insulin signaling pathway, revealing structure-bioactivity of mushroom polysaccharides, developing synergistic foods, conducting well-controlled clinical trials that may be very helpful in discovering valuable mushroom polysaccharides and better applications of mushroom polysaccharides in diabetic control were proposed.

Evaluation of Lipid Peroxidation in the Saliva of Diabetes Mellitus Type 2 Patients with Periodontal Disease.

As oxidative stress has been implicated in the pathogenesis of diabetes mellitus and periodontitis, it may serve as a link between these conditions. Therefore, as a part of the present study, salivary lipid peroxidation (LP) in periodontitis patients with and without diabetes mellitus type 2 (DM2) was evaluated, along with the periodontal therapy effectiveness. The study sample comprised of 71 DM2 patients with periodontitis and 31 systemically healthy controls suffering from periodontitis of comparable severity. In all participants, periodontal indices-plaque index (PI), gingival index (GI), papilla bleeding index (PBI), probing pocket depth (PPD), and clinical attachment level (CAL)-were recorded, and salivary LP was measured using a spectrophotometric method prior to treatment initiation and three months post-treatment. At baseline, mean salivary LP in DM2 patients was higher than that measured for the control group, but the difference did not reach statistical significance (p &gt; 0.05), whereas a positive significant correlation was found between PPD and LP in both groups. Three months after nonsurgical periodontal therapy, clinical periodontal parameters and salivary LP levels were significantly reduced in both groups (p &lt; 0.05). These findings indicate that the improvement in clinical periodontal status following nonsurgical periodontal therapy is accompanied by a significant decrease in salivary LP in DM2 patients, suggesting that periodontitis, rather than diabetes, is the primary driver of the elevated salivary LP in this group.

Maternal serum preptin levels in the pathogenesis and diagnosis of Gestational diabetes mellitus.

Gestational diabetes mellitus (GDM) is a metabolic disorder that occurs during pregnancy that increases both maternal and fetal mortality and morbidity. It was investigated whether there is a change in circulating levels of preptin, a new peptide secreted from pancreatic beta cells, due to GDM in pregnant women. The relationship between serum preptin levels with insulin and other metabolic parameters was also evaluated in these subjects. Eighty-five patients diagnosed as GDM and 89 healthy pregnant women with 75 mg oral glucose tolerance test (OGTT) was assessed in terms of serum preptin levels. The serum preptin levels of the GDM group were significantly higher than those of the control group (p=0.001; p < 0.01). For the cutoff value of preptin measurement of 335.3 ng/L, the sensitivity was 97.65%, specificity was 87.64%, positive predictive value was 88.3% and negative predictive value was 97.5%. The risk of developing the disease is 294.273 times higher in patients with preptin level of 335.3 and above. We think that the reason for the increase in serum preptin levels in GDM is probably the response to glucose. The current results indicate that preptin plays an important role in elucidating the pathology of GDM. In addition, the search for a practical marker for the diagnosis of GDM suggests that the measurement of preptin level is promising.

The role of pathogens in diabetes pathogenesis and the potential of immunoproteomics as a diagnostic and prognostic tool.

Diabetes mellitus (DM) is a group of metabolic diseases marked by hyperglycemia, which increases the risk of systemic infections. DM patients are at greater risk of hospitalization and mortality from bacterial, viral, and fungal infections. Poor glycemic control can result in skin, blood, bone, urinary, gastrointestinal, and respiratory tract infections and recurrent infections. Therefore, the evidence that infections play a critical role in DM progression and the hazard ratio for a person with DM dying from any infection is higher. Early diagnosis and better glycemic control can help prevent infections and improve treatment outcomes. Perhaps, half (49.7%) of the people living with DM are undiagnosed, resulting in a higher frequency of infections induced by the hyperglycemic milieu that favors immune dysfunction. Novel diagnostic and therapeutic markers for glycemic control and infection prevention are desirable. High-throughput blood-based immunoassays that screen infections and hyperglycemia are required to guide timely interventions and efficiently monitor treatment responses. The present review aims to collect information on the most common infections associated with DM, their origin, pathogenesis, and the potential of immunoproteomics assays in the early diagnosis of the infections. While infections are common in DM, their role in glycemic control and disease pathogenesis is poorly described. Nevertheless, more research is required to identify novel diagnostic and prognostic markers to understand DM pathogenesis and management of infections. Precise monitoring of diabetic infections by immunoproteomics may provide novel insights into disease pathogenesis and healthy prognosis.