Development Of Diabetes Research Articles

Relationship between urinary tract infections and serum vitamin D level in adults and children- a literature review.

Over time, researchers have accumulated significant evidence indicating that vitamin D deficiency not only impacts skeletal health but also contributes to the development and progression of various diseases, including cancer, diabetes, and cardiovascular conditions. The risk of low serum 1, 25(OH)2D3 level ultimately directs the way to morbidity, the beginning of new diseases, and numerous infections. Infections are the first entity that affects those with vitamin D deficiency. The common infection is urinary tract infection(UTI), and its relationship with vitamin D deficiency or insufficiency remains controversial. This infection affects both men and women, but comparatively, women are more prone to this infection because of the short length of the urethra, which makes an easy entry for the bacteria. The low level of serum vitamin D increases the risk of UTIs in children. Recurrent UTIs are one of the major weaknesses in women; if left untreated, they progress to appallingly serious conditions like kidney dysfunction, liver damage, etc. Hence improving the vitamin D status may help to improve the immune system, thus making it more resistant to infections. In this review, we have focused on examining whether vitamin D deficiency and insufficiency are the causes of UTIs and the association between them in women and children. We have also described the connection between vitamin D deficiency and insufficiency with UTIs and additional nanotechnology- based treatment strategies.

Evidence of a Bi-Directional Relationship between Arterial Stiffness and Diabetes: A Systematic Review and Meta-Analysis of Cohort Studies.

There are numerous cross-sectional studies showing an association between arterial stiffness and diabetes, but the temporality of the association is unclear. To investigate the temporal relationship between arterial stiffness and diabetes. We searched MEDLINE and Embase from inception to 31 August 2023, to identify cohort studies that assessed whether arterial stiffness, as measured by pulse wave velocity (PWV), was predictive of the development of diabetes and vice versa. We summarised study data, and where possible undertook meta-analysis. We identified 19 studies that included people with type 1, type 2 and gestational diabetes. All 11 studies investigating arterial stiffness as a predictor of diabetes found a significant relationship. Six of those studies were suitable for meta-analysis. The risk of developing diabetes was greater in people with higher PWV at baseline than lower PWV (RR = 2.14, 95%CI 1.65 to 2.79, p < 0.00001) and the mean difference in baseline PWV was higher in people who developed diabetes than those who did not (mean difference: 0.77 m/s, 95%CI 0.47 to 1.06, p < 0.00001). Of 8 studies investigating diabetes as a predictor of arterial stiffness, 7 found a significant relationship. There is evidence of a bidirectional relationship between arterial stiffness and diabetes. Arterial stiffness may provide a causal link between diabetes and future cardiovascular disease.

The Impact of Light-Dark Cycle Alteration on the Acceleration of Type 1 Diabetes in NOD Mice Model.

We aimed to evaluate the effect of light-dark cycle alteration and soft drink consumption on the acceleration of type 1 diabetes mellitus (T1DM) development among non-obese diabetic (NOD) mice model. We exposed female NOD and C57BL/6 mice from the age of 5 weeks to either adlib soft drink consumption and/or T20 light-dark cycle alteration until the development of diabetes, or the mice reached the age of 30 weeks. Each group consisted of 7-15 mice. We monitored weight, length, blood glucose level, and insulin autoantibody (IAA) levels weekly. Out of 75 NOD and 22 C57BL/6 mice, 41 NOD mice developed diabetes, and 6 mice died between 7 and 8 weeks of age. The mean time to development of T1DM among NOD control mice was 20 weeks. The time to development of T1DM was accelerated by two weeks in the NOD mice exposed to light-dark cycle alteration, hazard ratio of 2.65,95th CI (0.70, 10.04) p = 0.15). The other groups developed T1DM, similar to the control group. There was a trend toward earlier development of T1DM among NOD mice exposed to light-dark cycle alteration, but this difference was not statistically significant. Further studies are needed to confirm our findings using larger sample sizes and different animal species.

The role of high mobility group box-1 on the development of diabetes complications: A plausible pharmacological target.

Diabetes mellitus has emerged as a pressing global concern, with a notable increase in recent years. Despite advancements in treatment, existing medications struggle to halt the progression of diabetes and its associated complications. Increasing evidence underscores inflammation as a significant driver in the onset of diabetes mellitus. Therefore, perspectives on new therapies must consider shifting focus from metabolic stress to inflammation. High mobility group box (HMGB-1), a nuclear protein regulating gene expression, gained attention as an endogenous danger signal capable of sparking inflammatory responses upon release into the extracellular environment in the late 1990s. Given the parallels between inflammatory responses and type 2 diabetes (T2D) development, this review paper explores HMGB-1's potential involvement in onset and progression of diabetes complications. Specifically, we will review and update the understanding of HMGB-1 and its inflammatory pathways in insulin resistance, diabetic nephropathy, diabetic neuropathy, and diabetic retinopathy. HMGB-1 and its receptors i.e. receptor for advanced glycation end-products (RAGE) and toll-like receptors (TLRs) present promising targets for antidiabetic interventions. Ongoing and future projects in this realm hold promise for innovative approaches targeting HMGB-1-mediated inflammation to ameliorate diabetes and its complications.

Exosomes and Macrophages: Bidirectional Mutual Regulation in the Treatment of Diabetic Complications.

The bidirectional regulation of macrophages and exosomes provides a meaningful research direction for the treatment of complications arising from both type 1 and type 2 diabetes mellitus. However, there is currently no comprehensive evaluation of the bidirectional regulatory role of macrophages and exosomes in diabetic complications. In this review, we aim to provide the detailed process of the bidirectional regulation mechanism of macrophages and exosomes, and how macrophage-associated exosomes use this mechanism to make it better applied to clinical practice through biotechnology. Therefore, we summarized the bidirectional regulation mechanism of macrophages and exosomes and the application based on the bidirectional regulation mechanism from two aspects of inflammation and insulin resistance. As key regulators of the immune system, macrophages are crucial in the progression of diabetic complications due to their significant impact on the regulation of cellular metabolism, inflammation, and insulin sensitivity. Furthermore, exosomes, as innovative mediators of intercellular communication, transport miRNAs, proteins, and various bioactive molecules, influencing the occurrence and progression of diabetic complications through the regulation of inflammation and insulin resistance. The bidirectional regulation between macrophages and exosomes provides a promising pathway for the treatment of diabetic complications aimed at regulating the immune response and improving insulin sensitivity. Understanding the complexity of the interaction between macrophages and exosomes can advance the treatment of diabetic complications and drug development, and bringing more innovative and effective treatment strategies for diabetic complications.

Gestational diabetes mellitus and development of intergenerational overall and subtypes of cardiovascular diseases: a systematic review and meta-analysis

ObjectiveWe aimed to summarize the association between gestational diabetes mellitus (GDM) and its intergenerational cardiovascular diseases (CVDs) impacts in both mothers and offspring post-delivery in existing literature.MethodsPubMed, Embase, Web of Science, and Scopus were utilized for searching publications between January 1980 and June 2024, with data extraction and meta-analysis continuing until 31 July 2024. Based on a predefined PROSPERO protocol, studies published as full-length, English-language journal articles that reported the presence of GDM during pregnancy and its association with any CVD development post-delivery were selected. All studies were evaluated using the Newcastle-Ottawa Scale. Maximally adjusted risk estimates were pooled using random-effects meta-analysis to assess the risk ratio (RR) of GDM, and overall and subtypes of CVDs in both mothers and offspring post-delivery.ResultsThe meta-analysis was based on 38 studies with a total of 77,678,684 participants. The results showed a 46% increased risk (RR 1.46, 95% CI 1.34–1.59) for mothers and a 23% increased risk (1.23, 1.05–1.45) for offspring of developing overall CVDs after delivery, following a GDM-complicated pregnancy. Our subgroup analysis revealed that mothers with a history of GDM faced various risks (20% to 2-fold) of developing different subtypes of CVDs, including cerebrovascular disease, coronary artery disease, heart failure, and venous thromboembolism.ConclusionsThese findings underscore the heightened risk of developing various CVDs for mothers and offspring affected by GDM, emphasizing the importance of preventive measures even right after birth to mitigate the burden of CVDs in these populations.

Deciphering the Genetic Landscape: Exploring the Relationship Between HLA-DQA1, HLA-DQB1, and HLA-DRB1 Genes in Diabetes Mellitus

Abstract: Diabetes mellitus (DM) is a complex and multifactorial metabolic disorder with a significant genetic component. The human leukocyte antigen (HLA) genes, specifically HLA-DQA1, HLA-DQB1, and HLA-DRB1, have been implicated in the susceptibility and pathogenesis of DM. This review delves into the intricate interplay of these HLA genes, seeking to unravel the genetic tapestry that contributes to the development and progression of diabetes. We begin by providing an overview of the HLA system and its critical role in immune regulation. Subsequently, we explore the current state of knowledge regarding the association between HLA-DQA1, HLA-DQB1, and HLADRB1 polymorphisms and susceptibility to both type 1 and type 2 diabetes. Emphasis is placed on recent advancements in genetic research methodologies, including genomewide association studies and next-generation sequencing, that have provided deeper insights into the genetic architecture of DM. The review also scrutinizes the functional implications of specific HLA alleles in modulating immune responses and the potential mechanisms by which they contribute to the autoimmune processes observed in type 1 diabetes. Additionally, we examine the role of HLA genes in the context of insulin resistance and beta-cell dysfunction in type 2 diabetes, shedding light on the shared and distinct genetic underpinnings of these two major forms of DM. Furthermore, we discuss the clinical implications of HLA genotyping in predicting disease risk, prognosis, and personalized treatment strategies. The integration of genetic information into clinical practice holds promise for precision medicine approaches in diabetes management.

Amelioration of Insulin Resistance after Delivery Is Associated with Reduced Risk of Postpartum Diabetes in Women with Gestational Diabetes Mellitus.

Identifying risk factors for postpartum type 2 diabetes in women with gestational diabetes mellitus (GDM) is crucial for effective interventions. We examined whether changes in insulin sensitivity after delivery affects the risk of type 2 diabetes in women with GDM. This prospective cohort study included 347 women with GDM or gestational impaired glucose tolerance, who attended the follow-up visits at 2 months postpartum and annually thereafter. Changes in insulin sensitivity were calculated using the Matsuda index at GDM diagnosis and at 2 months postpartum (ΔMatsuda index). After excluding women with pregestational diabetes or those followed up only once, we analyzed the risk of postpartum type 2 diabetes based on the ΔMatsuda index tertiles. The incidence of type 2 diabetes at the two-month postpartum visit decreased with increasing ΔMatsuda index tertiles (16.4%, 9.5%, and 1.8%, P=0.001). During a 4.1-year follow-up, 26 out of 230 women who attended more than two follow-up visits (11.3%) developed type 2 diabetes. Compared to the lowest tertile, subjects in the highest ΔMatsuda index tertile showed a significantly reduced risk of type 2 diabetes (hazard ratio, 0.33; 95% confidence interval, 0.12 to 0.93; P=0.036) after adjusting for confounders. Improvement in insulin sensitivity after delivery is associated with a reduced risk of postpartum type 2 diabetes in women with GDM. Postpartum changes in insulin sensitivity could be a useful prediction for future type 2 diabetes development in women with GDM.

Participation of the transcription factor CREB1 in the regulation of the Mdh2 gene encoding malate dehydrogenase in the liver of rats with alloxan diabetes

The aim of the study was to study the role of transcription factor CREB1 in regulating the expression of the gene encoding the mitochondrial form of malate dehydrogenase (MDH, EC 1.1.1.37) in the liver of rats with experimental diabetes. An increase in the rate of work of NAD-dependent malate dehydrogenase in rat liver cells during the development of experimental diabetes was shown, associated with the activation of the Mdh1 and Mdh2 genes encoding this enzyme. The analysis of the promoters of these genes showed that only in the Mdh2 gene there is a specific binding site with the transcription factor CREB1. It was found that in the liver of rats with pathology, there is an increase in the rate of expression of the gene encoding this transcription factor, which correlates with the expression of the Mdh2 gene. Thus, the data obtained by us confirm the possibility of positive regulation of the rate of the Mdh2 gene by the transcription factor CREB1.

Topiroxostat improves glomerulosclerosis in type 2 diabetic Nagoya Shibata Yasuda mice with early diabetic kidney disease

Reactive oxygen species production might be prevented by xanthine oxidoreductase (XOR) inhibitors, which can cause glomerulosclerosis. We aimed to investigate whether topiroxostat, an XOR inhibitor, prevents diabetic kidney disease development in mice. Six-week-old control Institute of Cancer Research (ICR) mice and type 2 diabetic Nagoya Shibata Yasuda (NSY) mice were divided into the ICR group (ICR mice which received a lard-containing high-fat diet [HFD] based on the AIN-93G diet), NSY control group (NSY mice which received the same aforementioned diet), and NSY + topiroxostat group (NSY mice which received the same aforementioned diet with addition of 0.0012% topiroxostat). After 20 weeks, plasma biomarkers, XOR activity and oxidative stress levels, which were assessed using malondialdehyde (MDA), were measured through enzyme-linked immunosorbent assay or enzymatic methods. Renal pathology was evaluated using periodic acid–Schiff staining. Redox gene and protein expression were determined using RT-qPCR and western blotting, respectively. Plasma XOR activity was lower in NSY mice treated with topiroxostat than those without. Plasma cystatin C and creatinine levels did not differ between the ICR and NSY control groups or between the NSY control and NSY + topiroxostat groups. The NSY + topiroxostat group showed a smaller mesangial area than the NSY control group. The mRNA expression of Sod3, Prdx1, Gpx2, and Gpx3 was higher in the NSY + topiroxostat group than in the NSY control group. Renal MDA levels were lower in the NSY + topiroxostat group than in the NSY control group. Topiroxostat can reduce glomerulosclerosis, and the reduction is associated with renal oxidative markers.

The Impact of Smoking and Hypertension on Cataract Development in Diabetic Patients

Background Cataracts are a leading cause of visual impairment and blindness globally, with a particularly high incidence in diabetic patients due to the complex interplay of metabolic dysregulation and hyperglycemia-induced oxidative stress. Diabetic cataract development is influenced by several modifiable risk factors including smoking and hypertension, which may exacerbate lens opacity through various biological mechanisms. This study aims to determine the effects of smoking and hypertension on cataract development in diabetic patients. Methods Conducted from December 2022 to November 2023, this cross-sectional study at a specialized diabetes and ophthalmology healthcare facility involved 60 diabetic patients. The participants were divided into two groups: those with cataracts (n=32) and those without (n=28). Data collection focused on demographics, smoking history, hypertension status, and cataract presence, using structured interviews and medical record reviews. Logistic regression was employed to analyze the association between cataracts and potential risk factors, adjusting for age, diabetes duration, and glycemic control. Results Age and genderfi were not significantly different between the two groups, with mean ages of 50.21±14.34 years in the cataract group and 49.41±12.15 years in the non-cataract group (P=0.087). The prevalence of smoking was similar between those with cataracts (14.3%) and without (15.6%), showing no significant association (P=0.885). Hypertension was more prevalent in the cataract group (71.4%) compared to the non-cataract group (53.1%), although this difference was not statistically significant (P=0.146). Logistic regression analysis indicated that smoking had a minimal effect on cataract development (OR=1.187; 95% CI=0.264-5.33; P=0.823), and while hypertension showed a stronger association (OR=2.277; 95% CI=0.749-6.92), it also lacked statistical significance (P=0.147). Conclusion Neither smoking nor hypertension showed significant associations with cataract development. These findings suggest that the influence of these factors on cataract progression may differ in diabetic individuals due to the complex interplay of metabolic and vascular changes associated with the condition.

Food Additives' Impact on Gut Microbiota and Metabolic Syndrome: A Systematic Review.

The human gut microbiota (GM) might play a significant role in the development or remission of metabolic syndrome (MetS) and associated disorders. Contributing factors include diets rich in unhealthy, processed foods that contain preservatives, emulsifiers, and stabilizers. Diet influences the GM's composition, diversity, and species richness in a time-dependent manner. Food additives can alter the GM and contribute to the pathophysiology of MetS by disrupting the intestinal barrier and inducing low-grade systemic inflammation. Our systematic review aims to clarify the relationships among food additives, GM, and MetS. We summarize current knowledge on how food additives interact with GM and the pathogenic role of the microbiota in the development of MetS, including obesity and type 2 diabetes. This review also discusses how disturbances in GM caused by stabilizers and emulsifiers may link to MetS, highlighting the impact of this condition on the development of diabetes and obesity. Furthermore, this review seeks a detailed explanation of how dietary choices related to GM dysbiosis may contribute to MetS. However,more comprehensiveand well-designed in vitro, animal, and clinical studies are needed for a better understanding, as research on the role of GM in MetS is still emerging.

RNA-binding protein GIGYF2 orchestrates hepatic insulin resistance through STAU1/PTEN-mediated disruption of the PI3K/AKT signaling cascade

BackgroundObesity is well-established as a significant contributor to the development of insulin resistance (IR) and diabetes, partially due to elevated plasma saturated free fatty acids like palmitic acid (PA). Grb10-interacting GYF Protein 2 (GIGYF2), an RNA-binding protein, is widely expressed in various tissues including the liver, and has been implicated in diabetes-induced cognitive impairment. Whereas, its role in obesity-related IR remains uninvestigated.MethodsIn this study, we employed palmitic acid (PA) exposure to establish an in vitro IR model in the human liver cancer cell line HepG2 with high-dose chronic PA treatment. The cells were stained with fluorescent dye 2-NBDG to evaluate cell glucose uptake. The mRNA expression levels of genes were determined by real-time qRT-PCR (RT-qPCR). Western blotting was employed to examine the protein expression levels. The RNA immunoprecipitation (RIP) was used to investigate the binding between protein and mRNA. Lentivirus-mediated gene knockdown and overexpression were employed for gene manipulation. In mice, an IR model induced by a high-fat diet (HFD) was established to validate the role and action mechanisms of GIGYF2 in the modulation of HFD-induced IR in vivo.ResultsIn hepatocytes, high levels of PA exposure strongly trigger the occurrence of hepatic IR evidenced by reduced glucose uptake and elevated extracellular glucose content, which is remarkably accompanied by up-regulation of GIGYF2. Silencing GIGYF2 ameliorated PA-induced IR and enhanced glucose uptake. Conversely, GIGYF2 overexpression promoted IR, PTEN upregulation, and AKT inactivation. Additionally, PA-induced hepatic IR caused a notable increase in STAU1, which was prevented by depleting GIGYF2. Notably, silencing STAU1 prevented GIGYF2-induced PTEN upregulation, PI3K/AKT pathway inactivation, and IR. STAU1 was found to stabilize PTEN mRNA by binding to its 3’UTR. In liver cells, tocopherol treatment inhibits GIGYF2 expression and mitigates PA-induced IR. In the in vivo mice model, GIGYF2 knockdown and tocopherol administration alleviate high-fat diet (HFD)-induced glucose intolerance and IR, along with the suppression of STAU1/PTEN and restoration of PI3K/AKT signaling.ConclusionsOur study discloses that GIGYF2 mediates obesity-related IR by disrupting the PI3K/AKT signaling axis through the up-regulation of STAU1/PTEN. Targeting GIGYF2 may offer a potential strategy for treating obesity-related metabolic diseases, including type 2 diabetes.Graphical

Nonlinear association between the triglyceride-glucose index and diabetes mellitus in overweight and obese individuals: a cross-sectional retrospective analysis

BackgroundThe triglyceride-glucose (TyG) index is linked to both the development and progression of diabetes, while obesity remains a significant risk factor for this disease. However, the relationship between the TyG index and overweight or obese diabetes remains unclear.MethodsThis study was a cross-sectional analysis of data from 40,633 participants with body mass index (BMI) ≥ 24 kg/m2 who were screened from January 2018 to December 2023 at Henan Provincial People’s Hospital. Participants were divided into groups of overweight or obese individuals with diabetes and those without diabetes according to the diabetes diagnostic criteria. The TyG index, the dependent variable, was determined using the equation ln [fasting triglycerides (mg/dL) × fasting glucose (mg/dL)/2]. We explored the association between TyG index and diabetes in overweight or obese individuals through multivariate logistic regression, subgroup analysis, generalized additive models, smoothed curve fitting, and analysis of threshold effects.ResultsPatients who were overweight or obese and had diabetes had higher TyG index levels than those without diabetes. After adjusting for confounders, our findings indicated a significant association between the TyG index and the risk of diabetes in overweight or obese individuals [odds ratio (OR) = 7.38, 95% confidence interval (CI): 6.98–7.81]. There was a J-shaped nonlinear association between TyG index and diabetes. When TyG index was > 4.46, the risk of diabetes increased sharply. Notably, a high baseline TyG index (Q4 group) correlated with a notably greater risk of diabetes than did the Q1 group, with an OR of 22.72 (95% CI: 20.52–25.16). Subgroup analysis revealed that the association between TyG and diabetes was stronger in females than in males (OR = 7.57, 95% CI: 6.76–8.48,), more significant in individuals with a BMI of 24–28 kg/m2 than in those with a BMI ≥ 28 kg/m2 (OR = 8.40, 95% CI: 7.83–9.02), and increased with age (OR = 8.15, 95% CI: 7.25–9.17) (all P for interaction < 0.001).ConclusionAmong overweight or obese individuals, a higher TyG index is associated with an elevated risk of diabetes, especially when TyG is > 4.46. Furthermore, factors such as sex, age, and BMI significantly influence the risk of diabetes in overweight or obese individuals. Specifically, older women with a BMI of 24–28 kg/m2 are at a greater risk of diabetes under similar TyG index conditions.

A Systematic Review of Existing Data on Statin Use and New-Onset Type 2 Diabetes: The Need for Clear Answers

Background: The relationship between statins use and the development of new-onset type 2 diabetes mellitus (NOT2DM) has been a subject of ongoing debate and investigation. In February 2012, the Food and Drug Administration (FDA) disclosed that statin use could lead to a modest rise in glycosylated hemoglobin (HbA1c) and fasting blood glucose (FBG), potentially contributing to the development of diabetes. We systematically reviewed the available evidence and summarized the impact of statin use on NOT2DM. Aim: This systematic review aims to examine and provide a comprehensive overview of existing data relating to statin use and their association with the development of new-onset type 2 diabetes (NOT2DM). The primary objectives were to assess and explore: (1) the potential association between statin use and the development of new-onset diabetes; (2) the magnitude, extent, and incidence of new-onset diabetes due to statin use. The secondary objective was to explore the underlying mechanisms. Data Sources: PubMed, Scopus, Science Direct, Wiley, and Google Scholar and databases between January 2012 and February 2021. Data Extraction: The 2 reviewers Musa Basheer Mansour and Sara Elsheikh Ahmedana [MBM and SEA] independently assessed the qualities of the extracted studies and summarized data of the selected studies in tabulated forms for outcomes of interest and performed methodological and quality assessments based on review questions, citations, country of the study, aim, population characteristics, design, setting, sample size, sample technique, data source, measures, analysis, confounder variable and key observations for systematic review. We applied search keywords such as Statins, New-onset diabetes, Diabetes mellitus, Underlying mechanism, and incidents of diabetes. Results: A total of 66 studies were identified through database searches in the initial search, and 7 studies were included in this review. Of the 2,567,888 adult patients, 861,925 were nondiabetic patients on statin use, and 1,705,963 were diabetic on statin or non-statin users. We considered Hazard Ratios (HR), Odds Ratios (OR), and Confidence Intervals (CI) of each study for further analysis. The mean OR for three studies showed that each statin therapy resulted in a 68% increased risk of NOT2DM (OR, 1.683; 95% CI: 1.273-2.237). The significant relationship between statin use and the rising risk of NOT2DM was also confirmed by an average HR of 1.53 (95% CI: 1.2-1.7) for the remaining four studies. Recent and short-term use of statins, as well as time- and dose-dependent connections, were linked to an increased risk of NOT2DM in statin users compared to non-users. These risks were more prominent among older adults, normotensive males, hypertensive females, and individuals with low physical activity. Although no proven mechanisms were found, the possible processes are discussed. Conclusion: The systematic review found a significant level of risk of NOT2DM associated with statin use. The authors argued that the short-term diabetes risk caused by statin treatment was more prevalent among patients exposed to risk factors for diabetes. Although the precise mechanisms behind this association remain unclear, this research provides clinical practice with evidence-based guidelines. Additionally, conducting future research may be appropriate based on the gaps in knowledge identified from the results of this review.

Association of race and ethnicity with the development of cystic fibrosis-related diabetes

BackgroundCF-related diabetes (CFRD) is a common, life-expectancy limiting complication of CF. While Black race and Hispanic ethnicity in youth-onset type 1 and type 2 diabetes are well-recognized risk factors for worse diabetes complications, the potential for racial/ethnic disparities in CFRD has received limited attention. MethodsWe conducted a retrospective cohort study utilizing the CF Foundation Patient Registry from 2010 to 2019 to determine the prevalence and incidence of CFRD by race/ethnicity. Three age cohorts were identified at baseline in 2010 (11–20y, 21–30y, and 31–40y). Logistic regression and Cox regression stratified by age group were used to determine the prevalence and incidence, respectively, among Hispanic, non-Hispanic Blacks (NHB), and non-Hispanic whites (NHW) after adjustment for relevant confounders, including demographics, socioeconomic status, clinical factors, and chronic medication use. ResultsAmong 14,660 registry participants, 510 were NHB and 890 Hispanic. NHB associated with higher odds of CFRD baseline prevalence in all age cohorts (11–20y: OR 2.53 (95 % CI: 1.88–3.41, P < 0.05), 21–30y: OR 1.80 (1.25–2.59, P < 0.05), and 31–40y: OR 1.93 (1.00–3.73, P < 0.05)) relative to NHW. In the 11–20y cohort, the hazard of new-onset CFRD was 40 % higher in NHB (HR 1.40 (1.09–1.8, P < 0.05)) and 19 % higher in Hispanics (HR 1.19 (1.01–1.41, P < 0.05)). ConclusionNHB had a higher prevalence of CFRD across all age groups, with NHB and Hispanics showing higher incidence of CFRD in the youngest group. Multicenter studies performed in diverse CF populations are warranted to identify modifiable factors influencing earlier CFRD development in minoritized groups and their potential contribution to diabetes complication disparities.

Association between cardiovascular health and serum vitamin D and its interaction with prediabetes and diabetes

BackgroundPrediabetes and diabetes are common and serious public health problems, and high blood glucose can lead to serious cardiovascular complications. The purpose of this article was to explore the link between CVH levels and the incidence of prediabetes and diabetes in people over 20 years old, and whether serum vitamin D status could alter this relationship. Materials and MethodsData, from six consecutive cycles of the NHANES database from 2007 to 2018 were combined, eligible participants were aged ≥20 years. After excluding missing data, a total of 19,992 subjects were enrolled in the study. Significant risk factors for prediabetes and diabetes were analyzed using univariate and multivariate logistic regression. Exploring the interaction of VD and CVH on prediabetes and diabetes based on multifactorial regression analysis. ResultsThe prevalence of prediabetes among all participants was 36.15% and the prevalence of diabetes was 16.39%. CVH and vitamin D levels are influential factors in prediabetes and diabetes, and are negatively associated with the risk of developing prediabetes and diabetes. Compared with normoglycemia, poorer CVH and vitamin D deficiency only had a synergistic multiplicative interaction on the development of diabetes, and no significant interaction was observed for the development of prediabetes. Compared with prediabetes, poorer CVH and vitamin D deficiency still had a synergistic additive interaction on the development of diabetes. ConclusionsAlthough the cross-sectional study only determine the association and do not prove causality, the current results can be used to prompt people to improve their lifestyle and risk factors to prevent prediabetes or diabetes through higher CVH and adequate Vitamin D.

Gingipain from Porphyromonas gingivalis causes insulin resistance by degrading insulin receptors through direct proteolytic effects

Periodontitis is a critical risk factor for the occurrence and development of diabetes. Porphyromonas gingivalis may participate in insulin resistance (IR) caused by periodontal inflammation, but the functional role and specific mechanisms of P. gingivalis in IR remain unclear. In the present study, clinical samples were analysed to determine the statistical correlation between P. gingivalis and IR occurrence. Through culturing of hepatocytes, myocytes, and adipocytes, and feeding mice P. gingivalis orally, the functional correlation between P. gingivalis and IR occurrence was further studied both in vitro and in vivo. Clinical data suggested that the amount of P. gingivalis isolated was correlated with the Homeostatic Model Assessment for IR score. In vitro studies suggested that coculture with P. gingivalis decreased glucose uptake and insulin receptor (INSR) protein expression in hepatocytes, myocytes, and adipocytes. Mice fed P. gingivalis tended to undergo IR. P. gingivalis was detectable in the liver, skeletal muscle, and adipose tissue of experimental mice. The distribution sites of gingipain coincided with the downregulation of INSR. Gingipain proteolysed the functional insulin-binding region of INSR. Coculture with P. gingivalis significantly decreased the INSR–insulin binding ability. Knocking out gingipain from P. gingivalis alleviated the negative effects of P. gingivalis on IR in vivo. Taken together, these findings indicate that distantly migrated P. gingivalis may directly proteolytically degrade INSR through gingipain, thereby leading to IR. The results provide a new strategy for preventing diabetes by targeting periodontal pathogens and provide new ideas for exploring novel mechanisms by which periodontal inflammation affects the systemic metabolic state.

Examining Diabetes Status by the Social Determinants of Health Among Adults in Hawai'i.

The social determinants of health (SDoH) influence health outcomes based on conditions from birth, growth, living, and age factors. Diabetes is a chronic condition, impacted by race, education, and income, which may lead to serious health consequences. In Hawai'i, approximately 11.2% of adults have been diagnosed with diabetes. The objective of this secondary cross-sectional study is to assess the relationship between the prevalence of diabetes and the social determinants of health among Hawai'i adults who participated in the Behavioral Risk Factor Surveillance System between 2018-2020. The prevalence of diabetes among adults was 11.0% (CI: 10.4-11.5%). Filipino, Japanese and Native Hawaiian adults had the highest prevalence of diabetes at 14.4% (CI: 12.7-16.2%), 14.2% (CI: 12.7-15.7%), and 13.2% (CI: 12.0-14.4%), respectively. Poverty level and education were significantly associated with diabetes status. Within employment categories, the adjusted odds ratio (AOR) for retired and unable to work adults were large at AOR: 1.51 (CI: 1.26-1.81) and AOR: 2.91 (CI: 2.28-3.72), respectively. SDoH can impact the development and management of diabetes. Understanding the role SDoH plays on diabetes status is crucial for promoting health equity, building community capacity, and improving diabetes management.

A Study of Association of Insulin Resistance with Pregnancy-induced Hypertension.

Preeclampsia is one of the important causes of maternal and fetal mortality and morbidity. One of the important risk factors for the development of diabetes is insulin resistance (IR). To evaluate the association of IR with pregnancy-induced hypertension (PIH) and its severity. Data from 70 pregnant females who had completed 20 weeks of gestation and developed PIH were analyzed and compared with 30 appropriate controls. All females underwent measurement of fasting glucose level, fasting insulin level, and blood pressure. The mean age of the women in the control group was 26.17 years, and in the study group, it was 27.09 years. All females had completed 20 weeks of gestation. Around 86.6% of women in the control group, 54.1% with a variable degree of preeclampsia, and 48.6% of women with eclampsia were at 33-38 weeks of gestation. At the time of sampling, 13.3% of women in the control group, 45.81% of women with preeclampsia, and 51.3% of women with eclampsia were at 26-32 weeks of gestation. The mean IR among the control group was 1.37, in preeclampsia, it was 2.11, and in eclampsia, it was 3.58 with a p-value of 0.000, which is very highly significant. In this study, the severity of the disease was found to be directly proportional to IR. Pregnancy complicated with preeclampsia and eclampsia showed more IR in comparison to pregnant women with normal blood pressure, and this relationship is independent of the age of pregnant women.