Gestational diabetes mellitus (GDM) affects 9-25% of pregnancies. Undiagnosed or poorly managed GDM is associated with both short- and long-term complications in the fetus and mother. The pathogenesis of GDM is complex and has not yet been fully elucidated. Several biomarkers found in maternal serum have the potential for the early diagnosis of GDM. The aim of this narrative review was to explore novel biomarkers that have not been comprehensively described in previous reviews. We believe these biomarkers may allow for the detection of GDM in the early stages of pregnancy, enabling timely proper treatment and potentially preventing complications for both the mother and the fetus.

In recent years, the increase of the post-transplantation diabetes mellitus (PTDM) after renal transplantation encourages people to do a lot of research on the disease. This paper conducted a bibliometric study on PTDM related literature to explore the risk factors of diabetes after kidney transplantation, as well as the current status, hotspots and development trends of PTDM research, so as to provide reference for researchers in related fields.

We searched the Web of Science Core Collection (WoSCC) database for PTDM literature from January 1, 1990, to August 20, 2023, and used VOSviewer, CiteSpace, and the R package 'bibliometrix' to do bibliometric analysis.

Obesity, 3 months after transplantation tacrolimus concentration >10 ng/mL, temporary hyperglycemia, delayed graft function, acute rejection is specific risk factors related to PTDM in renal transplant recipients. In addition, 74 countries led by China and the United States published 1546 papers, and the number of PTDM-related publications is increasing every year. Primary institutions included the University of California, Los Angeles, Mayo Clinic, University of Oslo, and University of Toronto. The Journal of Transplantation is the most widely read journal in the subject. The authors with the most published literature are Trond Jenssen and Adnan Sharif, and the most cited author is Kasiske BL. Expectations for continued growth in global PTDM research are increasingly high. Future studies will mainly focus on exploring the risk factors of PTDM and identifying new therapeutic approaches and targets.

Data on the association between the degree of platelet and coagulative-fibrinolytic variables abnormalities and the risk of in-hospital mortality in acute aortic dissection (AAD) are limited.

This multicentre retrospective cohort study included patients diagnosed with AAD by aortic computed tomographic angiography between 2010 and 2021 in five tertiary hospitals in China. The primary outcome was defined as all-cause mortality during hospitalization. Associations between platelet counts, coagulation-fibrinolytic parameters and all-cause in-hospital mortality were assessed using Cox proportional hazards regression models.

Among the 2567 participants, the median age was 54 years (interquartile range, IQR: 47-63); 531 (20.7%) were female, and the in-hospital mortality rate was 589 (23.0%). The Cox proportional hazards regression model indicated that lower platelet count, prothrombin activity (PTA), and fibrinogen levels and longer prothrombin time (PT) and thrombin time (TT) were linearly positively associated with an increased risk of in-hospital mortality (p < 0.05). A non-linear and positive association was confirmed between D-dimer levels and in-hospital mortality risk (p < 0.05). Additionally, a significant interaction between platelet counts and D-dimer levels was observed (p = 0.029). According to the subgroup analysis, compared to those in the reference group, those with thrombocytopenia (<140 × 109/L) and high D-dimer levels (>14.6 µg/mL) had a 3.59-fold increased risk of in-hospital mortality (HR, 3.59; 95% CI, 2.00-6.42).

Our analysis revealed associations between changes in platelet count, PT, PTA, TT, fibrinogen and D-dimer levels and outcomes in patients with AAD. Furthermore, the combined effect of thrombocytopenia and high D-dimer levels significantly increased the risk of in-hospital mortality.

Obesity is a complicated, multifactorial, and highly avoidable disease. There is a complicated relationship between type 2 diabetes mellitus (T2DM) and obesity. Surgical intervention is regarded as one of the greatest efficacious treatments for morbid obesity, where T2DM exhibits remarkable amelioration and remission. The objective of this work is to evaluate endogenous insulin by measuring postprandial C-peptide before and 6 months after LSG. We will also assess metabolic improvement, including remission of T2DM and prediabetes, 6 months after LSG. A total of 60 Egyptian patients, aged 18-60 years, with a body mass index (BMI) > 35, prediabetes, or type 2 diabetes, were recruited from bariatric outpatient clinics at Cairo University Hospitals. The study assessed the postprandial C-peptide, fasting blood sugar, HbA1C, and lipid profile before and 6 months following LSG. A significant improvement was observed in the metabolic profile in the form of reduction of BMI, HbA1c, lipid profile, and control of hypertension 6 months postoperatively. There was a significant reduction of postprandial C-peptide 6 months postoperatively. Fifty-five patients (91.7%) achieved complete remission of prediabetes and diabetes 6 months postoperatively, while 4 patients showed only improvement of diabetes and 1 patient in the prediabetic group did not achieve remission. In conclusion, LSG demonstrates encouraging outcomes in terms of metabolic profile enhancement, insulin resistance improvement as indicated by significant reduction in C-peptide level, remission of prediabetes and T2DM, and effective weight loss.

Previous evidence suggests that infectious diseases may contribute to the development of neurodegenerative diseases (NDDs) while individuals with hyperglycemia may be at increased risk for both infection and NDDs due to dysregulated inflammation levels. This study aimed to examine the association between hospital-treated infectious diseases and the risk of NDDs among patients with prediabetes and diabetes and whether the associations differed by the number of infections and potential effect modifiers.

Using data from the UK Biobank, we conducted a prospective study involving 69,731 individuals, consisting of 48,149 participants with prediabetes and 21,582 participants with diabetes. Hospital-treated infectious diseases and NDDs were identified through record linkage to Health Episode Statistics and the Scottish Morbidity Records. Cox regression models were applied to assess the association between hospital-treated infectious diseases and the risk of developing NDDs, and to evaluate the trend of this association in relation to the number of infections. The modification effects by age, sex, smoking status, alcohol consumption, sleep duration, body mass index (BMI), glycated hemoglobin (HbA1c) levels, comorbidities, and diabetes medication use were investigated.

Over a median follow-up of 10.75 years, 1,867 participants (2.57 per 1,000 person-years) were diagnosed with NDDs. We found hospital-treated infectious diseases were significantly associated with an increased risk of NDDs among both individuals with prediabetes or diabetes (adjusted HR [aHR] 3.11, 95 % CI 2.83-3.42). Specifically, hospital-treated infectious diseases were associated with a higher risk of developing Alzheimer's disease, vascular dementia, all-cause dementia, Parkinson's disease, and multiple sclerosis. Moreover, a greater number of infection diagnoses was associated with a higher risk of NDDs. Consistent associations between infection and an increased risk of NDDs were observed, regardless of factors representing age, sex, lifestyle, and diabetes severity.

Hospital-treated infectious diseases were significantly associated with the risk of NDDs in individuals with diabetes and prediabetes, with similar associations observed for bacterial and viral infections. These findings emphasize the importance of implementing infection prevention strategies and monitoring of infectious comorbidities in the management of NDDs among patients with prediabetes and diabetes.

This study aimed to investigate the relationship between age at diabetes diagnosis (ADD) and the development and progression of diabetic retinopathy (DR). This study combined analysis of the National Health and Nutrition Examination Survey (NHANES) data with Mendelian randomization (MR). We employed regression models, propensity score matching, generalized additive model smoothing splines (GAM), random forest algorithms, and other analytical techniques. Cross-sectional analysis of NHANES data (n = 877) showed that the DR group had a significantly younger ADD compared to the DR-free group (P < 0.001). Regression analysis revealed a significant inverse association between ADD and DR prevalence (OR = 0.96, P < 0.001). MR analysis further supported this inverse relationship (OR = 0.42, P = 0.003). Two non-linear analytical approaches identified peak DR occurrence probability at ages 24.45 (GAM) and 24.2 (Shapley additive explanations dependence plots). Additionally, younger ADD was associated with increased DR severity across all categories (P < 0.05). In conclusion, older ADD was associated with a protective effect against the development and progression of DR, as supported by both analysis of NHANES data and MR. These findings underscore the importance of increased vigilance and more frequent screening for DR in patients diagnosed with diabetes at a young age.

Background: Diabetic peripheral neuropathy is associated with morbidity and mortality in people with diabetes mellitus. Aims: In this study, we determined relationships of the body-mass index (BMI), systolic blood pressure, diastolic blood pressure, fasting blood glucose, HbA1c, and ankle-brachial index (ABI) with diabetic peripheral neuropathy risk. Methods: A cross-sectional study was conducted with 1088 Indonesians and data collected using self-reported questionnaires, laboratory examinations, and physical examinations. Instruments included a digital scale, height measurement device, digital sphygmomanometer, Doppler ultrasound, 10-g monofilament, and a 128-Hz tuning fork. Data analysis used the Chi-square test, Fisher Exact, and multiple logistic regression test with significance p < .05. Results: The BMI (p < .001), blood pressure (p < .001), ABI (p < .001), fasting blood glucose (p = .016), and HbA1c (p < .001) were significantly related to peripheral neuropathy risk. The conditions of obesity, hypertension, high ABI, high fasting blood glucose, and high HbA1c significantly increased the risk of peripheral neuropathy. Moreover, participants with ≥4 co-occurring abnormal levels of the BMI, systolic blood pressure, diastolic blood pressure, fasting blood glucose, HbA1c, and ABI had significantly synergistically increased risks of peripheral neuropathy, and the more abnormal conditions there were, the higher the risk of peripheral neuropathy. Conclusions: Abnormalities of the BMI, blood pressure, fasting blood glucose, HbA1c, and ABI significantly and synergistically increased the risk of peripheral neuropathy and can be considered predictors of peripheral neuropathy. Nurses are expected to be aware of these predictors so that they can immediately take appropriate steps if they encounter abnormal conditions by optimizing their role as educators.

To explore the associations of central obesity indicators including waist circumference (WC), waist-to-height ratio (WHtR), and weight-adjusted waist index (WWI) with the impairment of basic activities of daily living (BADL) and instrumental activities of daily living (IADL) among middle-aged and elderly population in China. This prospective study used baseline data from 2011 and follow-up data, involving 6440 and 9646 participants, respectively. Binary logistic regression analysis was used to assess the relationships. Restricted cubic spline (RCS) curve was also used to analyze the correlation trends. Stratified analyses were performed to identify potential differences. Receiver operating characteristic curves were plotted to evaluate the predictive value of each indicator. WC (OR = 1.01, 95% CI:1.01-1.02), WHtR (OR = 1.21, 95% CI = 1.09-1.33), and WWI (OR = 1.10, 95% CI:1.02-1.19) were significantly associated with BADL impairment. Only WWI (OR = 1.16, 95%CI:1.09-1.23) was associated with IADL impairment. WC, WHtR and WWI were linearly associated with BADL impairment while WWI was linearly associated with IADL impairment. The risk association between WWI and BADL was stronger in drinking individuals and males. In the participants with a BMI less than 24 kg/m² and who had received a high school education or above, the increase in WWI was accompanied by a more significant risk of IADL impairment. The predictive ability of WWI is higher than that of WC and WHtR, with AUC values of 0.597 and 0.615. WWI, as a comprehensive indicator of central obesity, may be useful in comprehensively identifying the risk of early daily living activity impairment among middle-aged and elderly population.

Insulin resistance (IR) is an important pathologic component in the occurrence and development of cardiovascular disease (CVD). The estimated glucose disposal rate (eGDR) is a measure of glucose handling capacity, that has demonstrated utility as a reliable marker of IR. The study aimed to determine the predictive utility of IR assessed by eGDR for CVD risk.

This nationwide prospective cohort study utilized data of 6416 participants from the China Health and Retirement Longitudinal Study (CHARLS) who were free of CVD but had complete data on eGDR at baseline. The Boruta algorithm was performed for feature selection. Multivariate Cox proportional hazards regression models and restricted cubic spline (RCS) analysis were conducted to examine the associations between eGDR and CVD, and the results were expressed with hazard ratio (HR) and 95% confidence interval (CI) values. The area under the receiver operating characteristic (ROC) curve (AUC), calibration curve, Hosmer-Lemeshow test, net reclassification improvement (NRI), and decision curve analysis (DCA) were employed to evaluate the clinical efficacy of eGDR in identifying CVD. Subgroup analysis was performed to explore the potential association of with CVD in different populations.

During a median follow-up of 106.5 months, 1339 (20.87%) incident CVD cases, including 1025 (15.96%) heart disease and 439 (6.84%) stroke, were recorded from CHARLS. The RCS curves demonstrated a significant and linear relationship between eGDR and all endpoints (all P for nonlinear > 0.05). After multivariate adjustment, the lower eGDR levels were found to be significantly associated with a greater prevalence of CVD. Compared to the lowest quartile, the highest eGDR quartile was associated with a decreased risk of CVD (HR 0.686, 95% CI 0.545-0.862). When assessed as a continuous variable, individuals with a unit increasement in eGDR was related to a 21.2% (HR 0.788, 95% CI 0.669-0.929) lower risk of CVD, a 18.3% (HR 0.817, 95% CI 0.678-0.985) decreased risk of heart disease, and 39.5% (HR 0.705, 95% CI 0.539-0.923) lower risk of stroke. The eGDR had an excellent predictive performance according to the results of ROC (AUC = 0.712) and χ2 likelihood ratio test (χ2 = 4.876, P = 0.771). NRI and DCA analysis also suggested the improvement from eGDR to identify prevalent CVD and the favorable clinical efficacy of the multivariate model. Subgroup analysis revealed that the trend in incident CVD risk were broadly consistent with the main results across subgroups.

A lower level of eGDR was found to be associated with increased risk of incident CVD, suggesting that eGDR may serve as a promising and preferable predictor for CVD.

Background: Although prediabetes increases the risk of developing diabetes, its role in neuropathy remains unclear. We aim to assess alterations in the corneal nerve structure and function in prediabetes and risk factors for corneal nerve loss. Methods: An examination of IVCM and corneal sensitivity was conducted on a cohort of 75 participants, comprising 23 controls, 32 prediabetes, and 20 Type 2 diabetes. Semiautomatic analysis was employed to quantify the corneal nerve fiber length (CNFL), corneal nerve fiber density (CNFD), and dendritic cell (DC) density. Results: CNFL and CNFD were lower in prediabetes and Type 2 diabetes than in the controls, and they were associated with DC density. CNFL and CNFD were lower in Type 2 diabetes than in prediabetes. DC density was higher in prediabetes and Type 2 diabetes than in controls. However, there were no differences in corneal sensitivity between controls and prediabetes. Multivariable regression analysis demonstrated an association between reduced CNFL and age, BMI, fasting plasma glucose (FPG), and uric acid (UA) levels in prediabetes. In Type 2 diabetes, age, HbA1c, blood urea nitrogen (BUN), creatinine (Cr), and triglyceride levels exhibited associations with reduced CNFL. Conclusions: Corneal nerve damage was detected in prediabetes using IVCM. The patients with prediabetes showed signs of nerve structure damage, and the corneal nerve structure damage occurred before the nerve function changes. Immune cells also participate in the occurrence and development of DCN and are related to the corneal neuropathy. Understanding the corneal nerve fiber condition through IVCM may prove crucial in monitoring prediabetic neuropathy.

The relationship between objectively measured hearing ability and the risk of incident heart failure (HF) remains unclear. This study aimed to assess this association, explore potential modifying factors, and examine whether psychological factors mediate this relationship.

We included 164 431 participants from the UK Biobank without HF at baseline. Speech-in-noise hearing ability was measured using the Digit Triplets Test and quantified by the speech-reception-threshold (SRT). Incident HF was identified through hospital admission and death records. Mediation analyses assessed the role of social isolation, psychological distress, and neuroticism.

Over a median follow-up of 11.7 years, 4449 (2.7%) participants developed incident HF. Higher SRT levels were associated with an increased risk of HF (adjusted HR per SD increment 1.05, 95% CI 1.02 to 1.08). Compared with those with normal hearing, participants with insufficient hearing, poor hearing, or hearing aid use had higher HF risks (adjusted HRs 1.15, 1.28, and 1.26, respectively). Psychological distress mediated 16.9% of the association between SRT levels and HF, while social isolation and neuroticism mediated 3.0% and 3.1%, respectively. The association was stronger in participants without coronary heart disease or stroke at baseline.

Poor hearing ability is associated with an increased risk of incident HF, with psychological distress playing a notable mediating role. These findings suggest that hearing health and psychological well-being should be considered in cardiovascular risk assessment and prevention strategies.

To assess the association between physical activity (PA), sedentary time (ST), and sleep with body composition, and to explore the effects of reallocating ST to PA or sleep on body composition in individuals with prediabetes and overweight/obesity.

Baseline data from the PREDIPHONE trial, including 159 participants (mean age 59.6 years) with prediabetes (Fasting Plasma Glucose 100-125 mg/dl) and overweight/obesity (Body Mass Index 27-40 kg/m²), were analyzed. Body composition was assessed via bioelectrical impedance, while PA, ST, and sleep were measured with accelerometry. Linear regression and isotemporal substitution models evaluated associations. Increased ST was positively associated with body fat mass (kg) (β = 0.016; CI 95%: 0.003-0.030), body fat mass (%) (β = 0.009; 0.001-0.018), and visceral adipose tissue (β = 0.005; 0.001-0.010). Moderate-to-vigorous PA (MVPA) was negatively associated with body fat mass (kg) [β = -0.031; 0.055- (-0.008)], body fat mass (%) [β = -0.017; -0.032-(-0.003)], and Visceral adipose tissue [β = -0.009; -0.02-(-0.002)]. Replacing ST with MVPA was linked to lower Visceral adipose tissue [β = -0.012; -0.024-(-0.001)] and body fat mass (kg) [β = -0.039; -0.074-(-0.006)], but not with lean mass. No significant associations were found when substituting ST with light PA or sleep.

In individuals with prediabetes and overweight/obesity, replacing ST with MVPA could reduce body fat and VAT but not increases lean mass.

Data regarding the relationship between acromegaly and oxidative stress (OS) remain limited. Dynamic thiol-disulfide homeostasis (TDH) is vital for antioxidant protection, and ischemia-modified albumin (IMA) serves as a marker of OS. This study aimed to measure serum TDH parameters and IMA levels in acromegaly patients, comparing them with healthy controls.

This cross-sectional study consecutively included 81 patients and 55 controls, matched for age, gender, and body mass index. Serum levels of native thiol, total thiol, and disulfide (TDH parameters) were measured using the automated spectrophotometric method developed by Erel and Neselioglu, along with serum IMA levels.

In patients, serum native and total thiol levels were significantly lower (p = 0.005 and p = 0.007), while serum IMA levels were significantly higher (p = 0.001). Disulfide levels were similar. Patients with active disease (N = 32), patients in remission (N = 49), and controls (N = 55) were compared. In post-hoc analyses; serum TDH parameters and IMA levels were similar in remission and active disease patients. Native and total thiol levels were significantly lower in patients in remission compared to controls (p = 0.01 and p = 0.04). IMA levels were significantly higher in patients in remission compared to controls (p = 0.04). Serum thiol levels positively correlated with serum insulin-like growth factor-1 levels and negatively with age and disease duration, while age independently exerted a negative impact on serum thiol levels.

Our findings may indicate increased OS in the acromegalic process, which may contribute to the development of acromegaly and its related complications and comorbidities.

People with diabetes mellitus (DM) have a significantly increased risk of sarcopenia. A cross-sectional analysis was performed using nationally representative data to evaluate possible sarcopenia in middle-aged and older adults with diabetes mellitus, and to develop and validate a prediction model suitable for possible sarcopenia in middle-aged and older adults with diabetes mellitus in the Chinese community.

Data from the China Health and Retirement Longitudinal Study (CHARLS), which focuses on people 45 years of age or older, served as the basis for the prediction model. CHARLS 2015 participants were used in the study, which examined 53 factors. In order to guarantee model reliability, the study participants were split into two groups at random: 70% for training and 30% for validation. Ten-fold cross-validation and Least Absolute Shrinkage and Selection Operator (LASSO) regression analyses were used to determine the best predictors for the model. The factors associated with sarcopenia in DM were researched using logistic regression models. Nomogram were constructed to develop the predictive model. The performance of the model was assessed using area under the curve (AUC), calibration curves and decision curve analysis (DCA).

A total of 2,131 participants from the CHARLS database collected in 2015 passed the final analysis, and the prevalence of sarcopenia was 28.9% (616/2131). Eight factors were subsequently chosen as predictive models by LASSO logistic regression: age, residence, body mass index, diastolic blood pressure, cognitive function, activities of daily living, peak expiratory flow and hemoglobin. These factors were used in the nomogram predictive model, which showed good accuracy and agreement. The AUC values for the training and validation sets were 0.867 (95%CI: 0.847~0.887) and 0.849 (95%CI: 0.816~0.883). Calibration curves and DCA indicated that the nomogram model exhibited good predictive performance.

The nomogram predictive model constructed in this study can be used to evaluate the probability of sarcopenia in middle-aged and older adult DM, which is helpful for early identification and intervention of high-risk groups.

To develop a clinically applicable and promotable prediction model for assessing the risk of gestational diabetes mellitus (GDM) within the context of primary healthcare institutions.

The construction and the internal validation of the prediction model involved a cohort of 6,216 pregnant women observed from January 2019 to June 2019 in a Class A tertiary hospital in western China. External validation was subsequently conducted with 443 pregnant women from October 2020 to June 2021. Core characteristics were identified and the model was established using the least absolute shrinkage and selection operator (LASSO) regression. Internal validation was performed using the Bootstrap method. Model evaluation included discrimination and calibration tests, decision curve analysis (DCA), and the clinical impact curve. Visualization of the model was achieved through a static nomogram and a risk-scoring model.

The simplified prediction model possessed seven variables, including age, prepregnancy body mass index (BMI), polycystic ovary syndrome (PCOS), history of GDM, family history of diabetes, fasting plasma glucose (FPG), and urine glucose. This model exhibited a predictive accuracy, as reflected by a C-index of 0.736 (95% CI: 0.720 ~ 0.753) in the training set. The C-indexes were 0.735 and 0.694 in the internal and external testing set. Well-fitted calibration curves, the DCA curve, and the clinical impact curve demonstrated the feasibility of the simplified prediction model. For enhanced clinical application, the static nomogram and the risk-scoring model were employed to visualize the model.

This study developed a prediction model for assessing the risk of GDM among women from 8 to 14 weeks of gestation in western China. The model demonstrated moderate discriminatory ability, well-fitted calibration, and convenient visualization, suggesting its suitability for implementation and widespread adoption, particularly within the context of primary healthcare institutions.

To compare the prevalence of GDM and pregnancy outcomes between the one-step and two-step methods of universal screening among Thai pregnant women.

A randomized controlled trial was conducted on singleton Thai pregnant women at a gestational age of 24-28 weeks. They were randomly assigned to either the one-step method group (a universal 75-gm 2-h oral glucose tolerance test: OGTT) or the two-step method group (a universal 50-gm oral glucose challenge test followed by a 100-gm 3-h OGTT). The women received standard antenatal care. The prevalence of GDM and obstetric outcomes were compared.

A total of 143 women meeting the inclusion criteria were randomly allocated into the one-step group (72 cases) and the two-step group (71 cases). The prevalence of GDM was significantly higher in the one-step group than in the two-step group, with rates of 24/73 (33.3%) vs 8/70 (11.3%); P value 0.002; relative risk of 2.96, 95% CI: 1.43-6.14, respectively. Demographic data and maternal and neonatal outcomes were comparable between the two groups.

The one-step method can markedly increase the prevalence of GDM to nearly three times that of the two-step method, leading to a substantial increase in care costs and burdens without clear benefits. Convincingly, the one-step method as a new approach may not be suitable for universal screening in a busy antenatal care setting, especially in low-resource health centers in developing countries or among populations with a high prevalence of GDM.

The objective of this cross-sectional study was to clarify the relationship between the type of first-degree family history of diabetes (FHD) and the presence and age at onset of diabetes (AOD) in the Japanese general population.

Using anonymized processed data collected from community-based health checkups, we classified 10,691 subjects into 5 groups according to the type of FHD as follows: (1) no FHD; (2) diabetes only in a sibling (sFHD); (3) diabetes only in the mother (mFHD); (4) diabetes only in the father (pFHD); and (5) diabetes in ≥ 2 family members, e.g., one parent plus a sibling or both parents (FHD in ≥ 2 family members).

Results of multivariate logistic regression analysis performed using the no FHD group as reference revealed a significant association between a positive FHD and the presence of diabetes (odds ratio: sFHD, 3.67; mFHD, 3.70; pFHD, 2.88; FHD in ≥ 2 family members, 6.35; P < 0.0001 for all). Moreover, the AOD was significantly younger in all the four groups with FHD than in the group without FHD (P < 0.01), being the youngest in the group of FHD in ≥ 2 family members.

Our results revealed that the degree of associations between a positive FHD and the presence of diabetes and AOD differ according to the type of FHD. In particular, FHD in ≥ 2 family members appears to be especially strongly associated with a high risk of diabetes and a younger AOD.

Clonal hematopoiesis of indeterminate potential (CHIP) is an age-related disorder that is associated with macrovascular diseases, such as coronary artery disease and stroke. However, the effects of CHIP on microvascular complication have not been explored in individuals with type 2 diabetes. We wanted to determine whether CHIP is associated with diabetic microvascular complications (DMCs). CHIP was associated with a high risk of DMCs, specifically, diabetic retinopathy and diabetic kidney disease, but not diabetic neuropathy. Gene-specific analyses suggested that some driver genes were associated with risk of developing DMCs. These findings indicated that CHIP may represent a novel risk factor for DMCs among individuals with type 2 diabetes, distinct from traditional risk factors, which may have implications for prevention and management of DMCs.

Clinical studies involving observation have uncovered a mutual relationship between allergic disorders and diabetes, yet the precise causal link remains undetermined.

We conducted two-sample bidirectional Mendelian randomization analyses using single nucleotide polymorphisms (SNPs) associated with allergic conditions (asthma, allergic rhinitis, atopic dermatitis) from genome-wide studies and SNPs related to type 2 diabetes from FinnGen. Initially, we evaluated the causal link between allergic disorders and type 2 diabetes through a univariate Mendelian randomization study, incorporating inverse variance weighting, MR-Egger, and the weighted median estimator. To address potential confounding, we employed multivariate Mendelian randomization. Finally, we validated mediators influencing the correlation between asthma and type 2 diabetes.

The Inverse variance weighted method showed that asthma genetically increased the risk of type 2 diabetes [Asthma-type 2 diabetes: β(95%CI)＝0.892 (0.152-1.632), p = 0.018]. Allergic rhinitis and type 2 diabetes exhibit a mutual protective effect: β(95% CI)＝-1.333 (-2.617 to -0.049), p = 0.042; type 2 diabetes-Allergic rhinitis: β(95%CI)＝-0.002 (-0.004 to -0.000), p = 0.018. The Multivariable Mendelian randomization study results showed that after excluding confounding factors, asthma still demonstrates statistical significance in relation to type 2 diabetes. Through mediation analysis, it was discovered that lung function and the percentage of monocytes in leukocytes exert an inhibitory effect on the mediation between asthma and type 2 diabetes.

The Multivariable Mendelian randomization study indicates asthma as a risk factor for type 2 diabetes. Lung function, and the percentage of monocytes in leukocytes, play an inhibitory role in asthma and type 2 diabetes mediating effects.

The ocular surface (OS), like other mucosal sites, hosts a diverse microbiome. However, the impact of hyperglycemia associated with diabetes on OS microbial composition remains poorly understood. In this study, we established type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) models in C57BL/6J mice by administering high-dose streptozotocin (STZ) for T1DM and low-dose STZ combined with a high-fat diet for T2DM. The OS microbiome was characterized and analyzed using 16S rRNA sequencing. The results showed that neither T1DM nor T2DM significantly affected microbial richness compared to normal mice; however, T2DM led to a significant reduction in microbial diversity. This reduction in microbial diversity in T2DM is consistent with known microbial dysbiosis in diabetes, which may contribute to the pathogenesis of ocular complications such as dry eye disease and diabetic retinopathy. Community composition analysis identified Proteobacteria, Pelagibacterium, and Aliihoeflea as the core OS bacteria in normal mice. Diabetes significantly altered the OS microbial composition at various taxonomic levels. Specifically, T1DM was associated with 9 signature bacterial species, including Oceanospirillales, Bacillales, Halomonas, unclassified_f_Lachnospiraceae, and Anoxybacillus. T2DM exhibited 17 bacterial markers, including Firmicutes, Staphylococcus, Corynebacterium, and Parasutterella. Functional prediction of the microbiota using PICRUSt2 indicated potential impairments in carbohydrate metabolism due to diabetes. In conclusion, diabetic mice exhibit severe dysregulation of their OS microbiota, and restoring microbial balance in diabetic patients may represent a promising strategy for preventing and treating diabetic OS pathologies.

Accurately estimating biological age is beneficial for measuring aging and predicting risk. It is widely accepted that the prevalence of spine compression increases significantly with age. However, biological age based on vertebral morphological data is rarely reported. In this study, a total of 2,364 participants from the National Health and Nutrition Examination Survey were enrolled, and morphological parameters of the spine were collected from lateral radiographs scanned by dual energy X-ray absorptiometry. The biological age of the spine, called SpineAge, was calculated with the parameters by machine learning models. The SHapley Additive exPlanation was used for better interpreting each parameter's contribution. Besides, an Accelerated Aging Index (AAI) was defined as SpineAge minus chronological age and was used to quantify the accelerating aging degree of the spine. The results indicated that the SpineAge performed better than chronological age did in predicting 2-year and 5-year all-cause mortality. After adjusting all covariates, there was a significant association between AAI and all-cause mortality risk. Specifically, each 1-year increase in AAI was associated with a 25.9% increase in all-cause mortality risk (Hazards ratio, 1.259; 95% CI, 1.087-1.457; P < 0.001). Considering the first quartile of AAI as a reference, the mortality risks for the second, third, and fourth quartiles were 2.389 (95% CI, 1.064-5.364; P = 0.035), 5.911 (95% CI, 2.241-15.590; P < 0.001) and 22.925 (95% CI, 4.744-110.769; P < 0.001) times higher, respectively. Our study developed a novel and highly applicable biological-age predictor for predicting individualized long-term prognosis and facilitating personalized care.

  We aimed to examine both the expression levels of high mobility group box 1 (HMGB1) and vascular cell adhesion molecule-1 (VCAM-1) proteins in the placentas of pregnant women with gestational diabetes mellitus (GDM) and control groups by immunohistochemical (IHC) method.

  An experimental case-control study was conducted, including 40 pregnant women complicated with GDM and 40 healthy pregnant women. Placental tissues obtained following cesarean delivery were subjected to routine tissue monitoring. The placental sections were stained with VCAM-1 and HMGB1 immunostains and subjected to IHC examination under a light microscope. H-score (HS) was used to evaluate the results of IHC staining by semi-quantitative analysis. Pathway analysis in Cytoscape software identified GDM-associated proteins within HMGB1 and VCAM-1 interaction networks, followed by GO analysis to explore associated biological processes.

  Placental HGMB1 expression was significantly increased in the GDM group compared to the control group (p<0.001). However, placental VCAM-1 expression was found to be statistically similar in GDM and control groups (p=0.584). The shared 19 proteins were identified between HMGB1 and GDM, and 13 between VCAM-1 and GDM, with notable GO biological process terms such as immune system activation for HMGB1 and interleukin-6 regulation for VCAM-1 associated with GDM.

  We consider that GDM-related inflammation and oxidative stress may contribute to tissue damage and inflammation by increasing placental HMGB1 expression. The blockade of HMGB1 and its receptors might represent a promising therapeutic approach to control inflammation in GDM. Understanding the distinct roles of HMGB1 and VCAM-1 may provide valuable insights for the development of targeted therapies aimed at mitigating the inflammatory processes associated with GDM and improving maternal and fetal outcomes.

Non-functional adrenal incidentaloma (NFAI) is associated with an increased risk of adverse cardiometabolic outcome. Identifying predictors of atherosclerotic cardiovascular disease (ASCVD) may enable more appropriate management strategies in patients with NFAI. We aimed to investigate the body composition parameters and ASCVD risk in patients with NFAI.

Eighty patients with NFAI and 80 controls matched for age, gender and body mass index (BMI) were included. ASCVD risk was assessed on Framingham Risk Score (FRS) and American Heart Association/American College of Cardiology (AHA/ACC) score. Body composition was evaluated using a segmental body composition analyzer.

There were no significant differences in age, gender, blood pressure or body composition parameters between the two groups. Patients with NFAI had higher FRS and AHA/ACC scores than controls (P=0.017, P=0.024, respectively). In patients with NFAI, independent predictors for FRS were serum cortisol level after 1mg dexamethasone suppression test (DST) and waist/hip ratio (WHR), while independent predictors for AHA/ACC score were serum cortisol level after 1mg DST, WHR and fasting plasma glucose (FPG), in various multivariate linear regression models.

FRS and AHA/ACC scores may be useful in determining ASCVD risk in patients with NFAI, and serum cortisol level after 1mg DST is an independent predictor of ASCVD in these patients, even in the absence of hypercortisolism.

Sodium-Glucose Co-Transporter 2 (SGLT2) inhibitors, known as Gliflozins, have demonstrated efficacy in managing type 2 diabetes mellitus (T2DM) and providing cardiovascular and renal benefits. Given the prevalence of diabetes, heart failure (HF), and chronic kidney disease (CKD) in the UAE, there is a need to evaluate the prescribing patterns of Gliflozins in these population. The objective of this study was to explore the relationship between Gliflozins use for patients who were admitted to the hospital at least once from 2021 to 2023 and different clinical factors.

A retrospective medication review was conducted from 2021 to 2023 at tertiary-level care hospital in Ajman, UAE. Data were collected on prescribed Gliflozins, patient demographic information, BMI, HbA1c levels, and comorbidities (HF, CKD). Chi-square tests and binary logistic regression were used to explore associations between Gliflozin use and clinical factors.

Out of the 255 patients' data collected, Gliflozin use was significantly associated with obesity (p = 0.002), higher HbA1c levels (p < 0.001), and comorbidities, particularly HF (61.5% of HF patients) and CKD. The use of Gliflozins increased each year. Patients with HF were 8.03 times more likely to use Gliflozins, and those with diabetes were 6.86 times more likely, underscoring the multidimensional role of these medications.

Gliflozin prescribing patterns in the UAE reflect global trends, with increased use among patients with diabetes, HF, and CKD. Further research is recommended to explore factors influencing prescription practices and optimize Gliflozin therapy if gliflozins use considerably increase in new diagnosis of diabetes and CKD even in mild conditions.

The prevalence and incidence of diabetes in pediatrics have dramatically increased over the last three decades. Comparatively, pediatric diabetes has faster pancreatic β-cells decline and early progression to complications compared with adult diabetes. Therefore, diabetic complications are a major concern in children and adolescents with diabetes. Diabetes has detrimental effects on the macro- and microvascular systems, resulting in cardiovascular diseases, leading causes of morbidity and mortality in youth with diabetes. Oxidative stress plays a critical role in developing cardiovascular complications in the context of pediatric diabetes. In pediatric patients with diabetes, several factors can contribute to the development of excess reactive oxygen species and oxidative stress, including nutritional deficiencies, puberty, environmental exposures, and metabolic disorders such as obesity and high blood pressure. The present study aims to raise awareness of diabetic cardiovascular complications in children and adolescents with diabetes and the role of oxidative stress and their molecular mechanisms in the pathogenesis of cardiovascular complications. In addition, some novel therapeutic strategies for the treatment and prevention of diabetic cardiovascular complications in the pediatric populations are highlighted. In summary, children and adolescents with diabetes no matter type 1 diabetes (T1D) or type 1 diabetes (T2D), have many features similar to those in adults with same kinds of diabetes, but also have many their own features distinct from adults. By developing targeted therapies and preventive measures, healthcare providers can better address the rising incidence of diabetes-related complications in children and adolescents.

Antigen-specific immunotherapy shows potential for inducing long-term immune tolerance in type 1 diabetes (T1D), yet its clinical application is hampered by uncertainty regarding dominant epitopes. Conversely, non-antigen-specific treatments such as anti-CD3 monoclonal antibodies (mAbs) present a more straightforward approach but struggle to maintain tolerance after treatment. Addressing these issues is critical for advancing T1D therapies.

The phenotypic and metabolic properties of two subsets of exhausted CD8+ T cells were analyzed in both humans and NOD mice. T-cell receptor (TCR) diversity and Bulk RNA sequencing provided insights into the transcriptomic profiles and TCR reactivity of these cells. Mechanistic studies were conducted using the HEK-293 T cell line and primary cells. Single-cell RNA sequencing (scRNA-seq) was applied to evaluate the characteristics of different CD8+ T cell subsets following two types of immunotherapies. In NY8.3 mice, the effect of mitochondrial fission inhibitors on immunotherapy results was evaluated. Final validation was carried out with peripheral blood mononuclear cells (PBMCs) from T1D patients.

Our study reveals the diversity of two distinct exhausted CD8+ T cell subsets in T1D through flow cytometry, highlighting unique clinical features, phenotypes, and functions. Notable differences in TCR reactivity and metabolic pathways between these subsets were identified through TCR sequencing and transcriptomic analyses in NOD mice. Both antigen-specific and non-antigen-specific stimuli produced unique exhausted CD8+ T cell subsets. Our research identified leucine-rich repeat kinase 2 (Lrrk2) as a key regulator of mitochondrial fission, influencing the interconversion of exhausted CD8+ T cell subsets by phosphorylating dynamin-related protein 1 (DRP1) at serine 637 (Ser637) and serine 616 (Ser616). scRNA-seq confirmed that antigen-specific immunotherapy effectively suppresses T cell signaling, induces exhaustion, and promotes the development of terminally exhausted T (TEX) cells. Mitochondrial division inhibitor 1 (Mdivi-1) enhanced the therapeutic effect of anti-CD3 mAb treatment by promoting the development of more TEX cells.

Our results point to a new immunotherapeutic approach that targets exhausted CD8+ T cells' energy metabolism, offering valuable insights for advancing clinical strategies in T1D therapy.

Diabetes mellitus (DM) is an emerging comorbidity among people living with HIV receiving antiretroviral therapy (ART), potentially impacting treatment outcomes, including virologic failure. Identifying key determinants of DM in this population is crucial for improving patient care. A hospital-based cross-sectional study was conducted from January 01 to May 30, 2024 at Woldia Comprehensive Specialized Hospital, Ethiopia. A total of 253 HIV patients on ART for at least six months were randomly selected. Data were collected via structured questionnaires, clinical measurements, and medical record reviews. DM was diagnosed on the basis of a fasting blood glucose level ≥ 126 mg/dl or random plasma glucose level ≥ 200 mg/dl. Logistic regression models were employed to identify factors associated with DM, reporting adjusted odds ratios (AORs) with 95% confidence intervals (CIs). Statistical significance was set at p < 0.05. The prevalence of DM among the study participants was 9.9%. Compared with female patients, male patients had a significantly greater risk of developing DM (AOR = 4.29, 95% CI = 1.079-17.04). A family history of DM was associated with a nearly 11-fold increased risk (AOR = 10.65, 95% CI = 2.82-40.20). Overweight individuals (BMI > 25 kg/m²) had a nearly sixfold-fold greater risk of DM (AOR = 5.95, 95% CI = 1.56-22.65). Additionally, ART interruption and restarting of ART were significantly associated with increased DM risk (AOR = 6.11, 95% CI = 1.88-19.84). Approximately one in ten HIV patients on ART had DM. The significant factors included male sex, family history of DM, overweight status, and ART interruption. These findings highlight the need for routine metabolic screening, targeted interventions and continuous monitoring to mitigate DM risk and optimize HIV care.

Diabetes mellitus is characterized by a state of hyperglycemia, which can lead to severe complications if left untreated or poorly managed. Diabetic peripheral neuropathy (DPN) is one common complication. This condition is characterized by damage to the nerves that supply the legs and feet as well as problems with blood vessels, the heart, or urinary tract. To alleviate pain for patients, clinicians resort to long-term treatment regimens of nerve pain medications, which are usually either anticonvulsants or antidepressants. However, little is understood about the underlying mechanisms of DPN. Many pathogenic pathways have been proposed, one of which is mitochondrial dysfunction. Mitochondrial dysfunction includes a range of possible deficiencies given the number of functions controlled by or located in mitochondria, including their core function of bioenergetics. This review focuses on mitochondrial bioenergetics, including respiration/ATP synthesis and reactive oxygen species (ROS) production, as well as calcium homeostasis and apoptosis, and their potential as targets for the effective treatment of diabetic peripheral neuropathy.

Personal care products frequently contain endocrine disrupting chemicals (EDCs) including parabens and phthalates, which can alter glucose metabolism. The postpartum period is a time of rapid metabolic change, but whether EDC-associated product use impacts postpartum glucose metabolism is unknown.

We included 270 participants from the Boston, MA-based Environmental Reproductive and Glucose Outcomes (ERGO) pregnancy cohort with data on self-reported personal care product use at ≤4 pregnancy visits (median: 11, 19, 26, 36 weeks of gestation) and 1 postpartum visit (median: 9 weeks). We quantified postpartum hemoglobin A1c (HbA1c), fasting insulin, fasting- and 2-h glucose post-75-g oral glucose tolerance test, and calculated homeostatic model assessment for insulin sensitivity (HOMA2-S) and beta-cell function (HOMA2-B). Using covariate-adjusted linear regression, we estimated visit-specific associations of product use with postpartum glycemic outcomes.

Associations of product use with postpartum glycemic measures were mixed. Users of certain hair products had lower postpartum insulin sensitivity compared to non-users (e.g., Visit1 hair gel/spray: 22.8% difference [95% CI: 39.2, -1.9] in mean HOMA2-S). Conversely, users of products like deodorant, liquid- and bar soap, had higher insulin sensitivity and lower glucose levels (e.g., postpartum deodorant: 32.1% difference [95% CI: 7.0, 63.1] in mean HOMA2-S; -3.1 mg/dL [95% CI: 6.3, -0.04] mean fasting glucose). Associations with other products were inconsistent across timepoints or null.

Use of certain personal care products during the perinatal period was associated with altered postpartum glucose metabolism. Larger studies are needed to understand the impacts of product use patterns on glycemic outcomes.

This systematic review aims to map the existing literature on salivary biomarkers in adults with metabolically unhealthy obesity (MUO), identify key biomarkers associated with this high-risk group, and highlight areas requiring further research to advance this emerging field.

Obesity is characterized by an abnormal accumulation of body fat and chronic inflammation. However, not all individuals with obesity experience metabolic dysfunction. This review focuses on MUO, which is strongly linked to metabolic disorders such as insulin resistance, cardiovascular disease, type 2 diabetes, and systemic inflammation. Linking MUO and salivary biomarkers may enhance our understanding of how systemic health influences salivary composition and could enable the early identification of high-risk individuals through non-invasive saliva testing. This review synthesized findings from recent studies and identified key salivary biomarkers consistently elevated in individuals with MUO, including 8-OHdG, IL-6, IL-8, resistin, TNFR1, PTX-3, AEA, OEA, TNF-α, and sICAM-1. These biomarkers are associated with inflammation, oxidative stress, and metabolic dysregulation. The majority of studies utilized cross-sectional designs and used various saliva collection methods. Salivary biomarkers hold promise as non-invasive indicators of obesity-related metabolic dysfunction, particularly in MUO. However, their clinical diagnostic utility remains uncertain due to heterogeneity in study designs, a lack of biomarker validation, and limited longitudinal studies. Further research is needed to establish their bona fide diagnostic potential.

Ferroptosis is a critical factor in the impairment of osteoblast function in osteoporosis. Metformin (Met), a biguanide antidiabetic drug, has demonstrated anti-osteoporotic effects and has been confirmed to exert therapeutic benefits in diabetic osteoporosis (DOP). Nevertheless, the underlying mechanisms through which Met affects bone metabolism remain ambiguous.

This study seeks to elucidate the function of Met in DOP and to explore the potential mechanisms through which it mediates treatment effects.

In vitro, we utilized osteoblasts to explore the impact of Met on osteoblast differentiation and anti-ferroptosis in a high glucose and palmitic acid (HGHF) environment. In vivo, we developed a DOP model utilizing a high-fat diet along with streptozocin injections and evaluated the bone-protective effects of Met through micro-CT and histomorphological analyses.

Met inhibits HGHF-induced ferroptosis in osteoblasts, as indicated by the elevation of ferroptosis-protective proteins (GPX4, FTH1, and SLAC7A11), along with decreased lipid peroxidation and ferrous ion levels. Furthermore, Met augmented the levels of osteogenic markers (RUNX2 and COL1A1) and enhanced alkaline phosphatase activity in osteoblasts under HGHF conditions. Mechanistic investigations revealed that Met activates the AMPK/Nrf2 pathway, effectively preventing ferroptosis progression. Additionally, in vivo results demonstrated Met alleviates bone loss and microstructural deterioration in DOP rats.

Met can activate the AMPK/Nrf2 pathway to prevent ferroptosis, thereby protecting against DOP.

This study aims to investigate the association between the Inflammatory Burden Index (IBI) and the prevalence of pre-diabetes (pre-DM) and diabetes mellitus (DM) in the U.S. population from 1999 to 2010. By analyzing relevant data collected during this period, the study seeks to understand IBI's role in the onset of pre-DM and DM and its potential implications for public health.

A cross-sectional analysis was conducted using data from the National Health and Nutrition Examination Survey (NHANES) between 1999 and 2010. A total of 29,554 participants were included, with diabetes status determined by self-reported diagnoses and clinical indicators (such as glycosylated hemoglobin and fasting blood glucose). The Inflammatory Burden Index (IBI) was calculated using C-reactive protein (CRP) multiplied by the neutrophil-to-lymphocyte ratio. The generalized additive model (GAM) was employed to examine the relationship between increasing IBI and the incidence of pre-DM and DM.

The study included 29,554 participants, with 14,290 (48.4%) men and 15,264 (51.6%) women, and a mean age of 48.3 years (SD = 19.1). The findings revealed a significant association between IBI and the risk of pre-DM and DM. In the fully adjusted model, a stronger relationship was observed between pre-DM, DM, and IBI. The prevalence of pre-DM and DM was significantly higher in the fourth quartile (Q4) compared to the first quartile (Q1), with a 26% prevalence of pre-DM and an 18% prevalence of DM when IBI was greater than 1.04.

Our study demonstrates a significant correlation between IBI and the risk of pre-DM and DM in the U.S.

Given these findings, we recommend that IBI be considered as a key indicator for the management and treatment of pre-DM and DM in clinical settings.

Obesity is a major health problem associated with global metabolic dysfunction and increased inflammation. It is thus critical to identify the mechanisms underlying the crosstalk between immune cells and adipose tissue that drive cardiovascular and metabolic dysfunction in obesity. Expression of the kallikrein-related serine protease 7 (KLK7) in adipose tissue is linked to inflammation and insulin resistance in high fat diet (HFD)-fed mice. Here, we engineered mice with a macrophage-specific KLK7 knockout (KLK7MKO) to investigate how KLK7 loss impacts immune cell function and obesity-related pathology. Compared to control mice, we observed lower levels of systemic inflammation, with less infiltration and activation of inflammatory macrophages in HFD-fed KLK7MKO mice, particularly in the epididymal adipose tissue. Mechanistically, we uncover that Klk7 deficiency reduces pro-inflammatory gene expression in macrophages and restricts their migration through higher cell adhesion, hallmark features of macrophages in obese conditions. Importantly, through analyses of 1143 human visceral adipose tissue samples, we uncover that KLK7 expression is associated with pathways controlling cellular migration and inflammatory gene expression. In addition, serum KLK7 levels were strongly correlated with circulating inflammatory markers in a second cohort of 60 patients with obesity and diabetes. Our work uncovers the pro-inflammatory role of KLK7 in controlling inflammatory macrophage polarization and infiltration in visceral obesity, thereby contributing to metabolic disease. Thus, targeting KLK7 to control immune cell activation may dissociate adipose dysfunction from obesity, thereby representing an alternative obesity therapy.

Type 2 diabetes mellitus (T2DM) is a pressing public health challenge in Latin America, with an increasing prevalence and negative impacts on population health. Achieving optimal blood glucose levels is critical for preventing complications, yet significant socioeconomic inequities persist in disease management and optimal glucose control. We aimed to investigate the patient characteristics associated with optimal fasting capillary glucose in individuals living with T2DM in a hard-to-reach setting in Esmeraldas, Ecuador.

We carried out a cross-sectional study of individuals with T2DM in the Eloy Alfaro health district of Esmeraldas, using a complex sample design with some limitations. Data collection took place between October 2020 and May 2022 and involved face-to-face interviews to collect sociodemographic and clinical data and a Fasting Capillary Blood Glucose test. Perceived social support was measured with the Multidimensional Scale of Perceived Social Support (MSPSS). We estimated the prevalence of optimal glucose levels according to patient characteristics and calculated odds ratios (OR) with 95% confidence intervals using multivariable logistic regression.

Of the 474 participants surveyed, only 18.1% (86; 95%CI: 14.9-21.9) had optimal fasting capillary glucose levels. In this sample, optimal glucose was nearly four times more frequent among men compared to women (aOR = 3.92, 95%CI: 2.08-7.40, p < 0.001). Furthermore, older age (aOR = 1.03, 95%CI: 1.01-1.05, p = 0.006), living in an urbanised setting (aOR = 2.04, 95%CI: 1.22-3.40, p = 0.006) and unemployment (aOR = 0.48, 95%CI: 0.25-0.94, p = 0.031) were also linked to optimal blood glucose levels. While perceived social support in this population was moderate (median = 2.33, on a scale of 1 to 4), high family support appeared to reduce optimal glycaemic levels (aOR = 0.35, 95%CI: 0.18-0.70, p = 0.003).

The intricate interplay of factors influencing diabetes management and optimal blood sugar suggests that targeted, context-specific and gender-sensitive public health strategies may be needed to address diabetes disparities in vulnerable populations.

Early diabetes screening is critical in sub-Saharan Africa (SSA), where the prevalence is increasing, yet a large proportion of cases remain undiagnosed. This study aimed to evaluate the performance of fasting plasma glucose (FPG) in screening diabetes and/or prediabetes compared to the 2-hour plasma glucose (2-h PG)-level in SSA.

Data from a population-based, cross-sectional diabetes screening survey involving 1550 individuals in Butajira, Ethiopia, and Enugu state, Nigeria were analyzed. Fasting plasma glucose and a 2-hour 75-g oral glucose tolerance test (OGTT) were utilized for diabetes screening. In addition, we determined and plotted the receiver operating characteristic curve for FPG against the reference standard 2-h PG to evaluate the screening tool's sensitivity and specificity.

The mean (SD) age of the study participants was 44.5 (± 16.43) years, with men comprising 50.4% of the cohort. Among 1550 individuals analyzed, 4.6% and 16.8% demonstrated diabetes and prediabetes, respectively, as identified by either FPG or 2-h PG. The agreement between FPG and 2-h PG in identifying diabetes and prediabetes was moderate, with kappa statistic of 0.56 (95% CI, 0.51 - 0.61; p<0.0001) for diabetes and 0.45 (95% CI, 0.40 - 0.50; p<0.0001) for prediabetes. FPG failed to detect 34.1% of all prediabetes and 44.4% of all diabetes cases. The sensitivity of FPG in identifying diabetes cases was 44.3% at a cut-off 126 mg/dL with a specificity of 99.3%. We identified the optimal FPG cut-off for detecting newly identified diabetes cases using 2-h PG to be 105 mg/dL associated with a sensitivity and specificity of 67.2% and 94.0%, respectively.

FPG was able to correctly identify 99.3% of individuals with no diabetes but a significant percentage of diabetes cases would have remained undiagnosed if only FPG had been utilized instead of the 2-h PG. The use of 2-h PG test is recommended to diagnose diabetes in older individuals, females and non-obese persons who would be missed if tested by only FPG. Lowering the cut-off value for FPG to 105 mg/dL substantially increases the identification of individuals with diabetes, thus improving the effectiveness of FPG as a screening test for type 2 diabetes.

Polycystic ovary syndrome (PCOS) is a common endocrine disorder that increases the risk of gestational diabetes mellitus (GDM). This study aims to assess the correlation between PCOS and GDM and to identify associated healthcare needs.

A mixed-methods approach was used. The retrospective study analyzed 2635 medical records of women aged 19-45 who underwent fertility treatments (2020-2023). The prospective study (2023-2024) assessed PCOS and GDM knowledge, nutrition, and physical activity among three groups: PCOS, GDM, and normal pregnancies.

Women with PCOS had a significantly higher BMI (p < 0.001) and an increased risk of GDM (28.1% vs. 10.6%, p < 0.001), with a 2.94-fold higher likelihood (95% CI: 2.22-3.90). Preterm birth (p = 0.029) and multiple pregnancies (p = 0.014) were also more common. The GDM group demonstrated better nutritional habits (p = 0.017), while the PCOS group showed higher physical activity levels (p < 0.001). Greater disease knowledge correlated with healthier behaviors.

PCOS is a strong risk factor for GDM and adverse pregnancy outcomes. Targeted education and lifestyle interventions are crucial for improving maternal and neonatal health. Future research should focus on long-term metabolic management in women with PCOS.

This editorial comments on the study by Pierzynowska et al investigating the acini-islet-acinar (AIA) reflex, which integrates the exocrine and endocrine functions of the pancreas. The study investigates whether exogenous amylase introduced to the interstitial fluid surrounding pancreatic islets can inhibit insulin release. Historically, high serum amylase levels were associated with pancreatitis, but recent findings suggest that low amylase levels are more linked to metabolic diseases like diabetes and obesity. In their experiment, six pigs were used to examine the effects of amylase infusion on insulin release during an intravenous glucose tolerance test. The pigs received different treatments (amylase, saline, or bovine serum albumin), and blood samples were taken over two hours to measure insulin and glucose levels. The results showed amylase delayed glucose-stimulated insulin release, whereas bovine serum albumin increased insulin levels supporting the existence of the AIA reflex and suggesting amylase as a key metabolic regulator. Enzyme supplementation, particularly with α-amylases, may offer therapeutic benefits in preventing and managing metabolic disorders, including diabetes and obesity. Further research is warranted to explore the full scope of amylase's role in metabolic health and its therapeutic potential.

Familial hypercholesterolemia (FH) is a genetic condition characterized by elevated LDL-C and increased cardiovascular risk. Beyond LDL-C levels, the impact of genotype on glucose homeostasis has not been well evaluated. We aimed to evaluate the impact of genotype on glycemic status and on atherosclerotic injury in FH subjects.

We conducted a cross-sectional study on 322 FH subjects not on lipid-lowering therapy and without history of cardiovascular disease. Biochemical and genetic analyses as well as vascular profile assessment were obtained from all subjects. The study population was divided into two groups according to genotype: LDL receptor (LDLR) group and non-LDLR (NLDLR) group.

The LDLR group exhibited a higher prevalence of low glycemic status (LGS) than the NLDLR group (44.1% vs. 26%, p < 0.01), whereas a high glycemic status (HGS) was more prevalent in the NLDLR group compared with LDLR group (74% vs. 55.9%, p < 0.01). The NLDLR group exhibited a higher prevalence of peripheral atherosclerotic plaques than the LDLR group (93.4% vs. 73%, p < 0.05), while coronary artery calcification (CAC) presence was more prevalent in the LDLR group compared with the NLDLR group (74.7% vs. 48%, p < 0.01). In a secondary analysis the study population was stratified into three groups based on LDLR genotype: NLDLR, LDLR defective, LDLR null groups. The prevalence of LGS progressively increased from the NLDLR to the LDLR null group, while HGS showed an inverse trend (p for trend < 0.05). Peripheral atherosclerotic plaque prevalence decreased from the NLDLR to the LDLR null group (p for trend < 0.05), while CAC prevalence increased progressively in the three groups (p for trend < 0.01). Logistic regression analysis showed that FH groups with an LDLR mutation were inversely associated with HGS (p for both < 0.01) and the LDLR null group exhibited the strongest association.

FH subjects with NLDLR mutations exhibited a worse glycemic profile, while null LDLR mutations showed the strongest inverse association with HGS. The integrations of genetic, lipid and glucose data could be useful to better identify the metabolic profile and the atherosclerosis distribution in FH subjects.

WHAT IS CURRENTLY KNOWN ABOUT THIS TOPIC?: Familial hypercholesterolemia (FH) is characterized by elevated LDL-C levels. LDLR null mutations protected pancreatic β-cells from cholesterol accumulation. NGS has improved FH diagnosis by analysis of all genes implicated in the lipid disorder. WHAT IS THE KEY RESEARCH QUESTION?: What is the impact of FH genotype (monogenic with or without LDLR mutation/polygenic) on glycemic status? WHAT IS NEW?: FH population was characterized by a heterogeneous glycemic profile according to LDLR mutation. LDL-C and plasma glucose could modulate the distribution of subclinical atherosclerosis. HOW MIGHT THIS STUDYINFLUENCE CLINICAL PRACTICE?: Genetic, lipid, glucose data could better identify the metabolic and atherosclerotic profiles in FH.