Diabetic corneal neuropathy and diabetic retinopathy are ocular complications occurring in the context of diabetes mellitus. Diabetic corneal neuropathy refers to the progressive damage of corneal nerves. Diabetic retinopathy has traditionally been considered as damage to the retinal microvasculature. However, growing evidence suggests that diabetic retinopathy is a complex neurovascular disorder resulting from dysfunction of the neurovascular unit, which includes both the retinal vascular structures and neural tissues. Diabetic retinopathy is one of the leading causes of blindness and is frequently screened for as part of diabetic ocular screening. However, diabetic corneal neuropathy is commonly overlooked and underdiagnosed, leading to severe ocular surface impairment. Several studies have found that these two conditions tend to occur together, and they share similarities in their pathogenesis pathways, being triggered by a status of chronic hyperglycemia. This review aims to discuss the interconnection between diabetic corneal neuropathy and diabetic retinopathy, whether diabetic corneal neuropathy precedes diabetic retinopathy, as well as the relation between the stage of diabetic retinopathy and the severity of corneal neuropathy. We also endeavor to explore the relevance of a corneal screening in diabetic eyes and the possibility of using corneal nerve measurements to monitor the progression of diabetic retinopathy.

The changes in amino acid (AA) levels have been observed in pregnant women with gestational diabetes mellitus (GDM). However, it remains unclear whether the AA levels in offspring of GDM mothers are affected by GDM. This study aimed to investigate the changes in AA metabolism in offspring of pregnant women with GDM undergoing different glycemic control treatment regimens.

272 pregnant women treated at our hospital were selected and divided into the GDM and the non-GDM groups. The GDM group was further subdivided into three treatment groups: exercise-diet therapy, metformin therapy, and insulin therapy. The levels of 11 AAs of their offsprings were detected using tandem mass spectrometry and the differences in neonatal AA metabolism between the three treatment groups and the non-GDM group were compared.

There were significant differences in the levels of Arg, Cit, Met, Orn, and Pro of their offsprings between different treatment groups and the non-GDM group (P < 0.05). After controlling for relevant confounding factors, the differences in Arg and Orn remained statistically significant in the three treatment groups compared to the non-GDM group (P < 0.05); Cit remained statistically significant in the exercise-diet group (P < 0.05); and Met and Pro remained statistically significant in the exercise-diet group and insulin group (P < 0.05).

Regardless of the glycemic control treatment regimens used for GDM, AA metabolism related to the arginine family is influenced.

Previous studies have suggested that pesticide exposure and gut microbiome alterations are associated with gestational diabetes mellitus (GDM) risk. Understanding the complex interactive effect of these factors on GDM is essential. In a cohort of 852 pregnant women, we assessed pesticide levels in serum and analyzed the gut microbiota using 16S rRNA and shotgun metagenomic sequencing. We explored the interactions between pesticides and gut microbiota, assessed their roles in GDM development, and proposed a predictive model based on identified biomarkers. We identified an environmental risk score (ERS), denoting the pesticide mixture level significantly associated with GDM, with the gut microbiota, particularly involving the Dorea branch, playing a crucial mediating role. In addition, we found an interactive effect of pesticide exposure and gut microbiota on GDM risk. Notably, low Prevotella enrichment combined with high ERS arisen from pesticide levels led to a 10.36-fold increased GDM risk. The identified pesticide and gut microbial biomarkers achieved high predictive accuracy for GDM (AUC: 0.833, 95% CI: 0.748-0.918). Collectively, maternal pesticide exposure may induce disrupted microbiome-dependent glycemic alteration, necessitating future assessment of clinical implications. Potential GDM markers can serve as targets for therapeutic intervention caused by pesticides, leading to prevention.

The prevalence of gestational diabetes mellitus (GDM) is currently on the rise globally, which heightens the risk of adverse pregnancy outcomes and subsequently increases the likelihood of cesarean delivery. GDM can induce hyperglycemic conditions in cesarean wounds, leading to delayed wound healing and complications such as itching, pain, and scarring. These complications significantly impact the quality of life and mental health of mothers. Furthermore, there is a lack of effective clinical prevention strategies. Consequently, the need to improve wound healing after cesarean sections in women with GDM is a pressing concern that warrants our attention. To maximize the therapeutic impact and extend the bioavailability of calycosin-7-glucoside (CG), it was integrated into a hybridized hydrogel (GOHA) as a drug carrier to create the GOHACG hydrogel. Bases on our tests, the GOHACG hydrogel demonstrated a strong capacity for water absorption, appropriate pore size, and good biocompatibility to adjust to the in situ surroundings of the wound. GOHACG also promoted epidermal regeneration, collagen deposition, angiogenesis, and the conversion of macrophages from the M1 to M2 phenotype. Indicating a reduction in the inflammatory response, accelerated wound repair, and minimized skin scarring in a postcesarean delivery model involving gestational diabetic mellitus mice. In brief, the GOHACG possesses significant properties that enhance wound healing in GDM model, suggesting its potential effects in treating wound healing of GDM.

The aim of this study was to evaluate and compare the usefulness of the C-reactive protein (CRP)-triglyceride glucose (TyG) index (CTI) and other insulin resistance (IR) or inflammatory indexes for predicting recurrent cardiovascular events in percutaneous coronary intervention (PCI)-treated patients. In addition, the mediating effects of systemic inflammation, represented by high-sensitive CRP (hs-CRP), on TyG index-associated adverse cardiovascular events across different subgroups were also evaluated.

The formula for calculating the CTI was 0.412 × ln [high-sensitivity CRP (mg/L)] + ln [triglyceride (mg/dl) × fasting glucose (mg/dl)/2]. The primary endpoint was defined as the incidence of major adverse cerebrovascular and cardiovascular events (MACCEs), including cardiovascular death, nonfatal acute myocardial infarction (AMI), nonfatal ischemic stroke and repeat coronary revascularization.

Among the 2383 PCI-treated patients, 413 experienced MACCEs during a median of 34 months follow-up. Correlation analysis showed CTI was significantly associated with cardiometabolic factors. The CTI was the strongest predictor for MACCEs (adjusted HR 1.85, 95% CI 1.44-2.38) among the inflammatory and IR indicators. CTI had an incremental effect on the predictive ability of the prognostic model for MACCEs (NRI: 0.220, p < 0.001; IDI: 0.009, p < 0.001). Subgroup analysis revealed that the prognostic value of the CTI remained significant across all subgroups (all p < 0.05) whereas the predictive abilities of other IR or inflammatory indicators were more or less influenced by the metabolic abnormalities. Finally, mediation analysis revealed that the effects of systemic inflammation on TyG index-associated MACCEs were more prominent in patients with metabolic disorders.

CTI was a practical indicator for evaluating cardiometabolic diseases. Among the IR and inflammatory indicators, CTI was the most promising index for predicting recurrent cardiovascular risks in PCI-treated patients. TyG index-associated cardiovascular risks were partially mediated by systemic inflammation in patients with metabolic abnormalities.

Increasing evidence has suggested that maternal gestational diabetes mellitus (GDM) can influence the neonatal gut microbiota. However, the initial microbial colonization of neonates is still unclear. The discrepancy in results between studies may be due to many other prenatal characteristics. This study aimed to investigate whether perinatal characteristics affect the association between maternal GDM status and early neonatal gut microbiota. This nested case-control study was based on a cohort of mothers and children (2016YFC1000304). Meconium samples were collected from neonates of mothers with (n = 114) and without GDM (n = 133) within 24 h after birth, and then assessed via 16S rRNA gene amplicon sequencing. Differences in the diversity and composition of the neonatal gut microbiota were compared according to maternal GDM status and other perinatal characteristics. The gut microbiota of neonates born to mothers with GDM presented lower alpha diversity with the Chao1 index (P = 0.0235). Principal coordinate analysis revealed that the meconium samples were clustered by maternal GDM status only with unweighted UniFrac distances (R2 = 0.011, P = 0.003). In other groups, such as maternal age ≥ 35 years old and maternal prepregnancy BMI ≥ 24 kg/m2, meconium was not clustered by maternal GDM status. Linear discriminant analysis revealed that 81 taxa were significantly different between the GDM group and the control group. Based on delivery mode, there were 226 representative taxa in the control group, whereas in the GDM group, there were no representative taxa. In addition, based on neonatal sex, there were 79 representative taxa in the GDM group and seven in the control group. Other perinatal characteristics, such as maternal prepregnancy BMI, age, gestational weight gain, and birth weight also influenced the differential taxa of the neonatal gut microbiota between the two groups. In our cohort, newborns from mothers with GDM and without GDM had similar composition but different abundances of the gut microbiota. Maternal prepregnancy BMI, age, gestational weight gain, and neonatal delivery mode, sex, and birth weight had different influences on the diversity and differential taxa of the neonatal gut microbiota. The results of this study suggest that when studying the association between GDM and neonatal gut microbiota, it is necessary to consider the concomitant perinatal characteristics.

This study uses 16S rRNA gene amplicon sequencing to analyze 247 meconium samples with or without maternal gestational diabetes mellitus (GDM) and make a multi-group comparison. We found that newborns from mothers with GDM and normoglycemic mothers had similar compositions but different abundances of the gut microbiota. Other than the maternal diabetes status, maternal body mass index, age, gestational weight gain, and neonatal delivery mode, gender and birth weight all contribute to neonatal gut microbiota. Compared with former related studies, our sample size was larger, and meconium was collected within 24 h after birth to avoid the influence of the living environment, feeding methods, mother's lifestyle, or diet. The results of this study will provide some information on the association between maternal GDM and neonatal gut microbiota colonization in early life and highlight the influence of non-negligible concomitant perinatal characteristics.

Elevated intracranial pressure (ICP) is a veritable and potentially modifiable predictor of adverse stroke outcome. Sonographically measured optic nerve sheath diameter (ONSD), a non-invasive proxy for ICP, could potentially be utilized as an objective measure of severity and outcome among acute stroke patients.

To evaluate the relationship between admission ONSD, stroke severity, and functional outcomes among patients with acute stroke.

A prospective cohort study was conducted among patients with neuroimaging-confirmed acute strokes admitted to a tertiary hospital in Ghana. The ONSD of each patient was measured within 24 h of admission. Multivariable linear regression was conducted to determine the relationship between admission ONSDs, Glasgow Coma score (GCS), and modified Rankin Score (mRS) at days 30, 60, and 90.

We enrolled 116 patients comprising 69 ischaemic strokes, mean (SD) age 62.6 years ± 12.8 versus 47 hemorrhagic strokes, aged 50.9 years ± 12.2 years (p = 0.000). Presence of neuroimaging features of raised ICP was associated with elevated admission ONSD (β 1.253 (95 % CI: 0.229-2.277), p = 0.017). A higheradmission ONSD was an independent predictor of lowerGlasgow Coma scorein individuals with ischemic strokes (adjusted β -8.602 (95 % CI -16.077- -1.127), p = 0.025) but not hemorrhagic strokes. For individuals with hemorrhagic strokes, higher admission ONSD was an independent predictor of month 1 mRS (β 5.363 (95 % CI 0.804-9.922), p = 0.022) and month 2 mRS (β 10.546 (95 % CI 0.595-20.498), p = 0.039). However, for ischemic strokes, elevatedadmissionONSD was an independent predictor of mRS at month 2 (β 16.501 (95 % CI 5.202-27.800), p = 0.005) and month 3(β 16.643 (95 % CI 3.666-29.620), p = 0.014).

Sonographically determined ONSD is an independent predictor of stroke severity and functional outcomes in this Ghanaian cohort. Randomized control trials exploring the potential role of ONSD in guiding clinical decisions during acute stroke management are warranted, especially in resource-limited settings.

This study assessed the mediating role of cognitive emotion regulation strategies in the relationship between illness uncertainty and diabetes health-promoting self-care behaviours.

A cross-sectional study was conducted with 433 T2DM outpatients using the Mishel Uncertainty in Illness Scale, the Diabetes Health Promotion Self-Care Scale, and the Cognitive Emotion Regulation Questionnaire (CERQ). Data were analysed using SPSS (v.29) for descriptive and Pearson correlation tests, and Process Macro for SPSS (Model 4, v.4.2) for mediation analysis.

There is a statistically significant, weak negative relationship between illness uncertainty and diabetes health promotion self-care scores (r = -0.105, p = 0.029). CERQ showed a weak negative correlation with illness uncertainty scores, whereas the questionnaire demonstrated a statistically significant, moderate positive correlation with diabetes health-promoting self-care (p < 0.05). The relationship between illness uncertainty and diabetes health- promoting self-care was mediated by CERQ such as self-blame (β= 0.083, 95 % CI= 0.019 - 0.155), acceptance (β= -0.031, 95 % CI= -0.061 - -0.007), rumination (β= -0.107, 95 % CI= -0.179 - -0.048), and positive reappraisal (β= -0.043, 95 % CI= -0.091 - -0.001).

Illness uncertainty negatively impacts self-care behaviours in T2DM patients. CERQ, including self-blame, acceptance, rumination, and positive reappraisal, play a mediating role, highlighting their potential in interventions to improve self-care.

Subclinical hypothyroidism is associated with metabolic diseases; however, it remains controversial in older individuals.

This work aimed to investigate the relationship between thyrotropin (TSH) levels and metabolic diseases.

In this cross-sectional study, sampling was conducted from nationally representative general communities from 31 provinces in mainland China. A total of6791 older (aged ≥65 years) and 55 303 young participants (aged 18-64 years) were selected after excluding individuals with overt hyperthyroidism or overt hypothyroidism. According to the kit, TSH reference range (0.27-4.2 mU/L) and the age-specific TSH range previously formulated (an upper limit of 8.86 mU/L for older adults and 6.57 mU/L for young adults), the older adults and young adults were separately divided into 4 groups based on their TSH levels. Main outcome measures included anthropometric assessments, serum concentrations of thyroid functions, and various metabolic parameters.

In contrast to young adults, there was no significant increase in the prevalence of any metabolic disorders assessed in the slightly elevated TSH group (TSH 4.21-8.86 mU/L) compared to the euthyroid group (TSH 0.27-4.2 mU/L) among older adults. After adjusting for interference factors, a TSH level higher than 8.86 mU/L was found to be an independent risk factor for low high-density lipoprotein cholesterol (OR, 1.84; 95% CI, 1.14-2.98) and dyslipidemia (OR, 1.49; 95% CI, 1.09-2.04) when compared to the euthyroid group in older adults.

Slightly elevated TSH levels are not associated with an increased risk of metabolic diseases in older adults. Therefore, we recommend raising the upper limit of the TSH range for individuals aged 65 years and older.

The main purpose of this study was to assess relationships between absolute and relative handgrip strength (HGS) versus other markers of health (body composition) and physical fitness (VO 2 max, vertical jump) in 220 (112 male) healthy young adults (25±10 years). HGS was measured using a hand dynamometer. Absolute HGS represented the highest grip strength measurement (kg) of the right and left hand combined, while relative HGS represented the absolute HGS divided by body weight (kg/kg). Body composition (lean and fat mass) was measured using dual energy x-ray absorptiometry. VO 2 max was measured using a treadmill peak speed protocol (ml/kg/min), while vertical jump was assessed using a countermovement jump (cm). Absolute HGS (mean=86±22 kg) was positively related with lean mass (r=0.82, p<0.001) and vertical jump (r=0.63, p<0.001), while relative HGS (mean=1.2±0.2 kg/kg) was negatively related with body fat (r=-0.69, p<0.001), but positively correlated with VO 2 max (r=0.47, p<0.001), and vertical jump (r=0.45, p<0.001). Linear models suggest that lean mass, body fat, and vertical jump predicted 69% of variance for absolute HGS (adjusted R 2 =0.71, p<0.001), while lean mass and body fat predicted 49% of variance for relative HGS (adjusted R 2 =0.49, p<0.001). Lower relative HGS scores (<1.0 kg/kg) were associated with higher body fat levels and may represent a quick, simple, marker of health.

Background: Alpha-1-acid glycoprotein (AGP) is a glycoprotein synthesized mainly by the liver. Nonalcoholic fatty liver disease (NAFLD) and liver fibrosis (LF) are associated with metabolic disorders. The aim of this study was to examine the potential correlation between AGP and both NAFLD and LF. Methods: The data were derived from the 2017-2023 National Health and Nutrition Examination Survey (NHANES). The linear association between AGP and NAFLD and LF was examined by multivariate logistic regression models. Non-linear relationships were described by fitting smoothed curves and threshold effect analysis. Subgroup analysis was also performed to assess potential regulatory factors. Results: The study included 2270 females. AGP was found to be significantly and positively associated with NAFLD [OR = 12.00, 95% CI (6.73, 21.39), p < 0.001] and LF [OR = 2.20, 95% CI (1.07, 4.50), p = 0.042]. Furthermore, the association between AGP and NAFLD was significantly different in the diabetic subgroup (p < 0.05 for interaction). Additionally, we found an inverted U-shaped relationship between AGP and controlled attenuation parameter (CAP), with an inflection point at 1.20 g/L. Conclusions: We found a significant positive correlation between AGP and both NAFLD and LF, and there was an inverted U-shaped relationship between AGP and CAP.

Human adenovirus 36 (HAdV-36) is associated with obesity, potentially by promoting adipocyte proliferation and differentiation. Although linked to increased fat storage, HAdV-36 is also correlated with improved insulin sensitivity. Given its potential role in modulating adipose tissue and promoting a less inflammatory metabolic profile, its impacts on pro- and anti-inflammatory cytokine secretion remain unclear.

This nested case-control study compared cytokine levels (IL-10, IL-2, IL-6, IL-8, and TNF-α) between patients with and without HAdV-36 infection. A total of 76 participants were included, with 37 in the control group (HAdV-36 negative) and 39 classified as cases (HAdV-36 positive).

HAdV-36 seropositive individuals exhibited significantly lower IL-6 levels and higher IL-8 levels than seronegative participants. Additionally, they had lower glucose levels, suggesting a potential link between HAdV-36 and metabolic regulation.

These findings support the hypothesis that HAdV-36 may influence inflammatory and metabolic responses by modulating cytokine expression and glucose levels. Further research is needed to clarify the underlying mechanisms and their implications for metabolic health.

Acute kidney injury (AKI) following cardiac surgery is common and is associated with poor outcomes. The combination of urinary tissue inhibitor of metalloproteinase 2 (TIMP-2) and insulin-like growth factor-binding protein 7 (IGFBP7) is a strong predictor of AKI after cardiac surgery. However, most studies have focused on non-Asian populations, and comparisons with other AKI biomarkers or the optimal timing for measurement have yet to be explored.

We prospectively enrolled adult patients at Kochi Medical School Hospital in Kochi, Japan, to assess the predictive values of [TIMP-2]•[IGFBP7], TIMP-2, IGFBP7, neutrophil gelatinase-associated lipocalin (NGAL), and liver fatty acid-binding protein (L-FABP) measured preoperatively and at 2, 4, 6, and 8 h, as well as on day 1 and day 2 after postoperative intensive care unit (ICU) admission, using receiver operating characteristic curve (ROC) analysis.

Of the 38 patients, 13 (34.2%) developed AKI: seven (18.4%) with stage 1, four (10.5%) with stage 2, and two (5.2%) with stage 3. ROC analysis showed that the area under the curve (AUC) for predicting any stage of AKI peaked at 0-4 h, with the highest value at 2 h after ICU admission. Among the biomarkers, [TIMP-2]•[IGFBP7] showed the best AUC at 2 h after ICU admission, followed by TIMP-2, IGFBP7, L-FABP, and NGAL.

Our study demonstrated the good predictive performance of urine biomarkers, including [TIMP-2]•[IGFBP7], TIMP-2, IGFBP7, NGAL, and L-FABP, for any stage of cardiac surgery-associated AKI (CSA-AKI). The combination of TIMP-2 and IGFBP7 measured 2 h after postoperative ICU admission effectively predicted CSA-AKI, identifying patients at higher risk.

Immune imbalance is the core pathophysiological mechanism of the deterioration of β-cell function driven by lipid metabolism disorders. Toll-like receptor 4 (TLR4) inflammatory signaling is a key pathway that mediates lipotoxic injury in β-cells, but the underlying mechanism needs to be further elucidated. Transmembrane protein 24 (TMEM24) is a key transporter that regulates pulsatile insulin secretion, but its pathophysiology in lipotoxicity remains unclear. In this study, we investigate whether TLR4-mediated lipotoxicity is affected by the inhibition of TMEM24 expression. The PPI network shows that TLR4 is associated with both insulin secretion and ER stress proteins in islets from obese rats. Using in vitro lipotoxic β-cell models, we found that TMEM24 is the target signal of palmitic acid (PA)-induced insulin secretion impairment in islet β-cells, and TLR4 plays a mediating role in this process. Mechanistically, TLR4 mediates lipotoxicity by binding to TMEM24 and downregulating its protein expression to suppress PI3K/AKT signaling, leading to β-cell dysfunction. TLR4 knockout ameliorates islet function impairment through TMEM24/PI3K/AKT signaling in HFD-induced obese rats. Taken together, our results show that TLR4 mediates lipotoxicity in islet β-cells by inhibiting the TMEM24/PI3K/AKT pathway, and the mechanism of TLR4-mediated lipotoxicity is elucidated from the perspective of insulin vesicular secretion.

Diabetic patients frequently face difficulty in identifying and adhering to dietary regimen, including its quality and quantity. This study assessed the knowledge and attitude to dietary regimen among patients with type 2 diabetes mellitus in Delta State University Teaching Hospital, Oghara, as implication for glycemic control. The objectives of the study were to evaluate the knowledge on dietary regimen, assess the attitude to dietary regimen among diabetic patients, and determine the relationship between the knowledge and attitude to dietary regimen among diabetic patients.

Descriptive survey design was used for the study. Convenience sampling technique and a sample size of 150 were used. Self-developed questionnaire was administered. Data was collected, analyzed, and presented in tables.

Findings from the study shows that 80% of the respondents have knowledge on adherence to dietary regimen while 61.3% of the respondents finds keeping to dietary regimen for managing diabetes difficult. Meanwhile, highest responses were attributed to family support, this was followed by support group and enlightenment programs, while the least measure was found in mass campaign.

It therefore shows that although there is high knowledge base on dietary regimen, diabetic patients often find difficulty in adhering to the prescribed regimen. Hence, it is important that measures to promote positive attitude to dietary regimen among diabetic patients be devised to enhance management outcomes.

Smoking was identified as a risk factor for the development of liver fibrosis in patients with metabolic dysfunction-associated steatotic liver disease (MASLD). However, the association between smoking cessation history and the development of liver fibrosis remains unclear. This study was intended to analyze the association between smoking cessation history and significant liver fibrosis in adult MASLD participants in the United States.

This study utilized data from 2643 patients with MASLD from the National Health and Nutrition Examination Survey (NHANES). Significant liver fibrosis was detected based on transient elastography measurements. According to the smoking questionnaire data, patients were categorized as non-smokers, ex-smokers and current smokers. A multivariate logistic regression analysis, adjusted for weights, was performed to investigate the relationship between smoking cessation history and the presence of significant liver fibrosis in participants with MASLD.

A total of 2643 patients with MASLD were included in this study. Compared with non-smokers, ex-smokers had a slightly elevated risk of developing significant liver fibrosis (OR: 1.07, 95% CI: 1.02-1.13). Specifically, a positive correlation was observed between patients who quit smoking for < 20 years and significant liver fibrosis (OR: 1.07, 95% CI: 1.01-1.15). Furthermore, MASLD patients who started regularly smoking at an age of ≤ 20 years (OR: 1.09, 95% CI: 1.02-1.16) and had a smoking duration of ≥ 10 years before quitting (OR: 1.10, 95% CI: 1.02-1.18) were also highly correlated with an increased likelihood of developing significant liver fibrosis.

This study revealed that individuals with MASLD who have ceased smoking exhibit an elevated risk for significant liver fibrosis when compared to those who never smoked. It is highly emphasized that MASLD patients who quit smoking for < 20 years, started regularly smoking at an age of ≤ 20 years, and had a smoking duration of ≥ 10 years before quitting should be extremely vigilant regarding the risk of significant liver fibrosis.

To investigate the effectiveness of maternal hemoglobin A1c (HbA1c) in the diagnosis of gestational diabetes mellitus (GDM) in the second trimester.

A total of 3000 pregnant women between 24 and 28 weeks of gestation were included in the study. Screening for gestational diabetes was performed using maternal HbA1c in 1200 pregnant women who either refused or could not tolerate the OGTT. The HbA1c value for the diagnosis of GDM was set at ≥ 5.7% in accordance with a meta-analysis by Paula B. Renz et al. A total of 154 pregnant women with HbA1c ≥ 5.7% were diagnosed with gestational diabetes, and their data were recorded prospectively. These data were compared with obstetric outcomes in 250 pregnant women diagnosed with diabetes by performing a 100-g OGTT after a 50-g glucose challenge test (GCT).

There were no significant differences between two groups in terms of maternal age, gestational age at diagnosis, gravidity, and parity. Body mass index (BMI) was found to be significantly higher in pregnant women with HbA1c levels ≥ 5.7% (p < 0.001). Polyhydramnios was more common in the HbA1c ≥ 5.7% group and oligohydramnios was more common in the OGTT group (p < 0.001). Neonatal hypoglycemia was found to be significantly higher in the OGTT group (p < 0.05). The median HbA1c value were different in each group (OGTT group 5.6%, HbA1c group 5.8%; p < 0.001).

HbA1c testing has lower accuracy rates than OGTT in diagnosing GDM because it may miss diagnosis in some groups.

Recent evidence links diet and physical activity with type 2 diabetes mellitus (T2DM) remission, but emerging findings suggest that immune system dysregulation may play a crucial role. This study aimed to investigate the associations between neutrophils and T2DM remission.

We conducted a comprehensive analysis of newly-diagnosed T2DM patients (N = 183) from the CORDIOPREV study, without glucose-lowering treatment, and were randomized to follow either a Mediterranean or low-fat diet. Patients were classified into two groups: Responders, who achieved T2DM remission (n = 73), and Non-Responders, who did not achieve remission during the 5-year dietary intervention (n = 110). Neutrophil count and their related-ratio (NER, NBR, NLR and NHR, normalized with erythrocytes, basophils, lymphocytes, and HDL respectively) were measured at the baseline and 5 years of follow-up.

The lowest baseline tertile of neutrophil count was associated with an increased likelihood of T2DM remission among patients following a Mediterranean diet (but not for low-fat diet) when compared with the highest tertile [adjusted HR of 4.23 (95% CI: 1.53-11.69)], in which similar results were observed for NER and NHR. When considering clinical and neutrophil variables, the predictive capacity of this model yielded an AUC of 0.783 (95% CI: 0.680-0.822). Furthermore, after 5-years, Responders exhibited lower neutrophil count compared to Non-responders (p = 0.006) and a significant decrease in neutrophil count (p = 0.001) compared to baseline. This decrease in neutrophil count in Responders who consumed a Mediterranean diet exhibited a significant increase in Insulin Sensitivity and Disposition Index (p = 0.011 and p = 0.018) after the follow-up period.

These findings suggest that neutrophil count can help in identifying patients that are more likely to achieve T2DM remission following a Mediterranean diet, suggesting a role on insulin sensitivity and β-cell function. Further research holds promise for providing valuable insights into the pathophysiology of T2DM.

ID: NCT00924937; URL Clinical trial: https://clinicaltrials.gov/study/NCT00924937?cond=NCT00924937&rank=1 .

Exposure to benzene, toluene, ethylbenzene, xylenes, and n-hexane (BTEX-H) may contribute to the development of diabetes. Oil spill response and cleanup (OSRC) workers are exposed to BTEX-H but there are few relevant studies. We studied incident diabetes over 10 years of follow-up among OSRC workers.

This analysis includes 21,726 participants (82.2 % male, mean age 39.9 years; 66.5 % White race) in the Gulf Long-term Follow-up Study - a prospective cohort of Deepwater Horizon (DWH) oil spill OSRC workers followed from 2011 to 2013 through 2021. Individual estimates of cumulative work-related exposures to specific BTEX-H chemicals and an aggregate sum (total BTEX-H) were derived from a job-exposure matrix that linked exposure group estimates derived from exposure measurements to self-reported DWH work histories. We used Cox models to estimate associations of quartiles of exposure to individual BTEX-H chemicals and total BTEX-H with diabetes incidence. We used quantile-based g-computation, quantifying associations with exposure to the BTEX-H chemicals, treating them as separate components in a mixture. We examined differences in associations by neighborhood disadvantage using the Area Deprivation Index (ADI) and by self-classified race in stratified analyses.

Exposure to the BTEX-H chemicals was associated with diabetes, with elevated hazard ratios for third and fourth quartiles of exposure compared to the first quartile. For example, total BTEX-H, Q3 and Q4 HRs were 1.10 95 %CI (0.91, 1.33) and 1.27 95 %CI (1.05, 1.53), respectively. The HR associated with a three-quartile increase in the BTEX-H mixture was 1.31 95 %CI (1.07, 1.59). Stratified analyses showed little variation by race and suggestions of variation by ADI.

Exposures to BTEX-H chemicals were associated with incident diabetes among OSRC workers for the individual BTEX-H chemicals, total BTEX-H, and the BTEX-H mixture. The range of exposures in this study make these findings relevant to other low to moderate exposure settings.

C-reactive protein-triglyceride-glucose index (CTI) has been proposed as a novel biomarker for insulin resistance and inflammation. However, the association between CTI and the risk of stroke, particularly in individuals with different glycemic status, remains unclear.

A total of 10,443 middle-aged and elderly participants were enrolled from the China Health and Retirement Longitudinal Study (CHARLS). The primary endpoint was the occurrence of stroke events. The CTI was calculated using the formula 0.412* Ln (CRP [mg/L]) + Ln (TG [mg/dl] × FPG [mg/dl])/2. The Kaplan-Meier curves, Cox proportional hazard models, and restricted cubic spline analysis were applied to explore the association between CTI and the risk of stroke according to gender, age and glycemic status.

During a median follow-up of 9 years, 960 (9.2%) participants experienced a stroke. Our findings revealed a significant positive linear relationship between CTI and the occurrence of stroke. The association was similar between male and female, despite the HR tended to be higher in females (HR 1.22, 95% CI 1.09, 1.36) than males (HR 1.15, 95% CI 1.02, 1.29), and similar in middle-aged (HR 1.25, 95% CI 1.11, 1.41) and elderly participants (HR 1.12, 95% CI 1.00, 1.26). In different glycemic status, high levels of CTI were found to be linked to an increased risk of stroke in individuals with normal glucose regulation (NGR) (HR 1.33, 95% CI 1.11, 1.59) and prediabetes mellitus (Pre-DM) (HR 1.20, 95% CI 1.04, 1.39). However, this association was not observed in individuals with diabetes mellitus (DM).

Our findings revealed a significant positive linear relationship between CTI and the occurrence of stroke. The association between CTI and stroke was similar between male and female, and similar in middle-aged and elderly participants. In different glycemic status, the association was significant in individuals with NGR and Pre-DM.

Preeclampsia (PE) and gestational diabetes mellitus (GDM) are common pregnancy disorders with shared pathophysiological mechanisms. This study examined the association between SIRT1 polymorphisms (rs12778366 and rs7895833) and relative telomere length (RTL) in women with PE and GDM. The DNA from pregnant women with GDM with and without PE was analyzed. The RTL and genotyping were measured using quantitative real-time PCR. The women with GDM and PE had significantly shorter telomeres. The rs12778366 TC genotype was associated with a 4.48-fold increased risk of PE (OR = 4.48; 95% CI 1.54-13.08; p = 0.003). The PE group had a higher prevalence of the heterozygous TC rs12778366 genotype with short telomeres. The SIRT1 variant rs12778366 is associated with shorter telomeres and an increased risk of developing preeclampsia, suggesting it may be a useful biomarker for preeclampsia risk assessment in GDM pregnancies.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is associated with an elevated risk of cardiovascular conditions, such as lower extremity arterial disease (LEAD). The Fibrosis-4 (FIB-4) index, a non-invasive marker of liver fibrosis, may have predictive value for LEAD in patients with MASLD. This study aimed to explore the association between FIB-4 and LEAD in a cohort of patients with MASLD.

This cross-sectional study included 481 participants with MASLD, selected from a comprehensive health check-up database. Participants were categorized into three groups based on their FIB-4 index (< 1.3, 1.3-2.66, > 2.66) and underwent duplex ultrasonography to diagnose LEAD. Logistic regression models were employed to evaluate the association between FIB-4 and LEAD, adjusting for demographic, metabolic, and lipid-related factors. Subgroup analyses were performed by sex, age, diabetes mellitus status, hypertension, dyslipidemia, smoking status.

The prevalence of LEAD increased with FIB-4 levels, from 51.3% in the low FIB-4 group to 86.5% in the high FIB-4 group (p < 0.001). In fully adjusted models, higher FIB-4 levels were significantly associated with LEAD (adjusted odds ratio [OR]: 3.54, 95% confidence interval [CI]: 1.39-9.01) in the high FIB-4 group compared to the low group. As a continuous variable, each unit increase in FIB-4 was associated with a 66% higher likelihood of LEAD (adjusted OR: 1.66, 95% CI: 1.12-2.26, P < 0.001). Subgroup analyses did not reveal significant interactions (P for interaction > 0.05).

Higher FIB-4 levels are independently associated with the prevalence of LEAD in MASLD patients, although subgroup analyses did not reveal significant interactions. This suggests that further studies with larger sample sizes are needed to explore these relationships more comprehensively.

The prevalence and clinical characteristics of chronic kidney disease (CKD) among patients with ketosis-onset diabetes (also known as ketosis-prone diabetes) remain unclear. Furthermore, the classification of ketosis-onset diabetes remains controversial and requires further investigation.

To investigate the prevalence and clinical features of CKD in patients with newly diagnosed ketosis-onset diabetes.

This real-world study included 217 patients with type 1 diabetes mellitus (T1DM), 698 with ketosis-onset diabetes, and 993 with non-ketotic T2DM. The prevalence and clinical characteristics of CKD were compared among the three groups. Risk factors associated with CKD were evaluated using binary logistic regression for each group.

After adjusting for age and sex, the prevalence of CKD among patients with ketosis-onset diabetes (17.8%) was significantly higher than that in those with T1DM (8.3%, P = 0.007), but was not statistically different compared to those with non-ketotic T2DM (21.7%, P = 0.214). Furthermore, some risk factors for CKD, including age, and serum uric acid and C-reactive protein levels, in patients with ketosis-onset diabetes were similar to those with T2DM, but significantly different from those with T1DM.

The prevalence, clinical characteristics, and risk factors for CKD among patients with ketosis-onset diabetes were more similar to those with non-ketotic T2DM but considerably different from those with T1DM. These findings further support the classification of ketosis-onset diabetes as a subtype of T2DM rather than idiopathic T1DM.

Cardiovascular-Kidney-Metabolic (CKM) syndrome is characterized by the interrelatedness of chronic kidney disease (CKD), cardiovascular disease (CVD), and metabolic disorders. The relationship between estimated glucose disposal rate (eGDR) and CVD risk in CKM syndrome remains unclear.

We analyzed data from 7,849 participants aged ≥ 45 years in the China Health and Retirement Longitudinal Study (CHARLS). The eGDR was calculated using waist circumference, hypertension, and HbA1c. Cox regression and restricted cubic spline (RCS) regression analyses examined the association between eGDR and CVD (stroke or cardiac events).

During a mean follow-up of 8.29 ± 1.67 years, among 7,849 participants (mean age 62.4 ± 8.7 years; 52.82% male), 1,946 CVD events occurred, including 1,504 cardiac events and 663 strokes. CKM stages 0-3 comprised 492 (6.27%), 1,404 (17.89%), 5,462 (69.59%), and 491 (6.26%) of participants, respectively. A U-shaped relationship between eGDR and CVD risk was identified (turning point: 11.82 mg/kg/min). Below this turning point, each unit increase in eGDR decreased CVD risk by 12% (HR: 0.88, 95% CI: 0.86-0.90, P < 0.0001); above it, each unit increase raised the risk by 19% (HR: 1.19, 95% CI: 1.04-1.37, P = 0.0135).

Our findings reveal a U-shaped relationship between eGDR and CVD risk in CKM syndrome stages 0-3. A higher or lower eGDR was associated with an increased CVD risk.

Type 2 diabetes (T2D) complications pose a significant global health challenge. Omics technologies have been employed to investigate these complications and identify the biological pathways involved. In this review, we focus on four major T2D complications: diabetic kidney disease, diabetic retinopathy, diabetic neuropathy, and cardiovascular complications. We discuss advancements in omics research, summarizing findings from genetic, epigenomic, transcriptomic, proteomic, and metabolomic studies across different ancestries and disease-relevant tissues. We stress the importance of integrating multi-omics techniques to elucidate the biological mechanisms underlying T2D complications and advocate for ancestrally diverse studies. Ultimately, these insights will improve risk prediction for T2D complications and inform translation strategies.

Gestational diabetes mellitus (GDM) increases maternal risks such as hypertension and future type 2 diabetes while also contributing to fetal complications such as large-for-gestational-age infants and stillbirth. The placenta which is crucial for fetal development, exhibits structural and functional changes in GDM, but the impact of these alterations on placental trophoblast function remains unclear. During their differentiation villous cytotrophoblast display several characteristics of senescent cells however the role of senescence pathways in placental function remains unexplored in GDM. Here we investigate whether placental senescence pathways are altered in GDM, utilizing term villous tissue and primary trophoblasts to assess molecular changes, and determined fetal sex-based differences. Our data suggest that both p21 and p16 mediated senescence pathways are activated during trophoblast differentiation and are dysregulated in GDM placenta in a sexually dimorphic manner. We also provide evidence for increased activation of p53-Lamin A/C and p16-RB pathways in trophoblast from GDM placentas. Reduced expression of p21 and its downstream effects on GCM1 expression and βhCG secretion outline how altered physiological senescence can affect trophoblast differentiation and function. This is a seminal study highlighting how placental senescence pathways are altered in pregnancies complicated by GDM.

Type 1 diabetes (T1D) is an autoimmune disease caused by T-cell mediated destruction of the pancreatic insulin-producing beta cells. Currently, the development of autoantibodies is the only measure of beta-cell autoimmunity used in the clinic. Despite T-cells' well-accepted role in the autoimmune pathogenesis of human T1D, autoimmune T-cell responses against beta cells remain very difficult to measure. An assay capable of measuring beta-cell antigen-specific T-cell responses has been a long-sought goal. Such an assay would facilitate the direct monitoring of T1D-associated T-cell responses facilitating, earlier diagnosis and rapid evaluation of candidate immune therapies in clinical trials. In addition, a simple and robust assay for beta-cell antigen-specific T-cell responses would be a powerful tool for dissecting the autoimmune pathogenesis of human T1D. Here, we review the challenges associated with measuring beta-cell antigen-specific T-cell responses, the current assays which are used to achieve this and, finally, we discuss BASTA, a promising emerging assay for measuring human beta-cell antigen-specific CD4+ T-cell responses.

Machine learning (ML) models are being increasingly employed to predict the risk of developing and progressing diabetic kidney disease (DKD) in patients with type 2 diabetes mellitus (T2DM). However, the performance of these models still varies, which limits their widespread adoption and practical application. Therefore, we conducted a systematic review and meta-analysis to summarize and evaluate the performance and clinical applicability of these risk predictive models and to identify key research gaps.

We conducted a systematic review and meta-analysis to compare the performance of ML predictive models. We searched PubMed, Embase, the Cochrane Library, and Web of Science for English-language studies using ML algorithms to predict the risk of DKD in patients with T2DM, covering the period from database inception to April 18, 2024. The primary performance metric for the models was the area under the receiver operating characteristic curve (AUC) with a 95% confidence interval (CI). The risk of bias was assessed using the Prediction Model Risk of Bias Assessment Tool (PROBAST) checklist.

26 studies that met the eligibility criteria were included into the meta-analysis. 25 studies performed internal validation, but only 8 studies conducted external validation. A total of 94 ML models were developed, with 81 models evaluated in the internal validation sets and 13 in the external validation sets. The pooled AUC was 0.839 (95% CI 0.787-0.890) in the internal validation and 0.830 (95% CI 0.784-0.877) in the external validation sets. Subgroup analysis based on the type of ML showed that the pooled AUC for traditional regression ML was 0.797 (95% CI 0.777-0.816), for ML was 0.811 (95% CI 0.785-0.836), and for deep learning was 0.863 (95% CI 0.825-0.900). A total of 26 ML models were included, and the AUCs of models that were used three or more times were pooled. Among them, the random forest (RF) models demonstrated the best performance with a pooled AUC of 0.848 (95% CI 0.785-0.911).

This meta-analysis demonstrates that ML exhibit high performance in predicting DKD risk in T2DM patients. However, challenges related to data bias during model development and validation still need to be addressed. Future research should focus on enhancing data transparency and standardization, as well as validating these models' generalizability through multicenter studies.

https://inplasy.com/inplasy-2024-9-0038/, identifier INPLASY202490038.

Lipoprotein(a) [Lp(a)] is associated with the development of coronary artery calcification (CAC), yet its exact function is not fully understood. This study sought to assess the relationship between Lp(a) levels and the risk of CAC in elderly diabetic patients.

This cross-sectional study included 486 elderly diabetic patients. The exposure factor was Lp(a) levels, categorized into three groups (T1, T2, T3). The outcome was the presence of CAC. The relationship between Lp(a) levels and CAC was evaluated using several statistical methods, including univariate and multivariate logistic regression, multivariable stratified analysis, receiver operating characteristic (ROC) curve analysis, and restricted cubic spline (RCS) analysis.

The highest Lp(a) group (T3) showed significantly higher prevalence of CAC compared to the T1 and T2 groups. Univariate logistic regression indicated a significant link between Lp(a) and CAC. Furthermore, multivariate logistic regression supported the finding that elevated Lp(a) levels correlated with a heightened risk of CAC in all models. Specifically, each unit rise in Lp(a) was associated with a notable increase in CAC risk, and Log10Lp(a) and each 1 standard deviation increase in Lp(a) also significantly elevated CAC risk. Multivariable stratified analysis demonstrated significant differences in CAC risk across various subgroups, including age ≤70 years, males, females, smokers, hypertensive, non-hypertensive, hyperlipidemic, non-hyperlipidemic, non-stroke, and non-chronic kidney disease patients. ROC curve analysis showed that adding Lp(a) to the baseline model improved the area under the curve from 0.741 to 0.755. RCS analysis indicated a significant, approximately linear association between Log10Lp(a) and CAC risk (p nonlinear = 0.115).

In an elderly diabetic population, elevated levels of Lp(a) were strongly linked to a greater risk of CAC. Integrating Lp(a) measurements with conventional risk factors improves the predictive accuracy for CAC.

Saponins are compounds composed of lipophilic aglycones linked to hydrophilic sugars. Natural saponins are isolated from plants and some Marine organisms. As important cholesterol-lowering drugs, natural saponins have attracted wide attention for their therapeutic potential in a variety of cholesterol-related metabolic diseases. To review the effects of natural saponins on cholesterol-related metabolic diseases, and to deepen the understanding of the cholesterol-lowering mechanism of saponins. The literature related to saponins and cholesterol-lowering diseases was collected using keywords "saponins" and "cholesterol" from PubMed, Web of Science, and Google Scholar from January 2000 to May 2024. The total number of articles related to saponins and cholesterol-lowering diseases was 240 after excluding irrelevant articles. Natural saponins can regulate cholesterol to prevent and treat a variety of diseases, such as atherosclerosis, diabetes, liver disease, hyperlipidemia, cancer, and obesity. Mechanistically, natural saponins regulate cholesterol synthesis and uptake through the AMPK/SREBP2/3-hydroxy-3-methyl-glutaryl coenzyme A reductase pathway and PCSK9/LDLR pathway, and regulate cholesterol efflux and esterification targeting Liver X receptor/ABC pathway and ACAT family. Natural saponins have broad application prospects in regulating cholesterol metabolism, for the development of more cholesterol-lowering drugs provides a new train of thought. However, it is still necessary to further explore the molecular mechanism and expand clinical trials to provide more evidence.

Chronic kidney disease (CKD) is a well-recognized complication in patients undergoing liver transplantation (LT), particularly those with metabolic dysfunction-associated steatohepatitis (MASH), a leading cause of cirrhosis in the modern era. This study sought to refine risk stratification for CKD events post-LT in cirrhosis patients with MASH by leveraging baseline renal function at transplant.

A total of 717 MASH cirrhosis patients who had LT (1997-2017) at 7 US centers (NailMASH Consortium) were analyzed. Patients were categorized by estimated glomerular filtration rate (eGFR) at transplant: low (LGFR, eGFR ≤30 mL/min/1.73 m²), medium (MGFR, eGFR >30-≤60 mL/min/1.73 m²), and high (HGFR, eGFR >60 mL/min/1.73 m²). Time-related eGFR intercepts, slopes, and assessments of advanced-stage CKD (aCKD) events, defined as 2 eGFR levels <30 mL/min/1.73 m² separated by ≥90 d, were examined.

Post-LT, LGFR group showed increased eGFR, whereas the HGFR group experienced a decline. The 3-mo mark was identified as a "reset point," signifying a new reference level, beyond which a different rate of decline was observed. After 3 mo, mean eGFRs of the LGFR group approached MGFRs, whereas the mean eGFR of the HGFR group continued to decrease but remained higher than other groups during a 60-mo follow-up. LGFR patients had significantly higher aCKD probability than MGFR and HGFR groups. Subanalysis at 3 mo post-LT revealed more aCKD events in the LGFR group compared with MGFR and HGFR groups ( P  < 0.0001).

The study underscores renal impact of LT in MASH cirrhosis, indicating unique eGFR trajectories post-LT tied to baseline eGFR, with a reset point at 3 mo. Monitoring post-LT renal function, especially in those at aCKD risk, is crucial. Renal-sparing immunosuppression may help, regardless of baseline eGFR. Further studies are needed for interventions addressing renal dysfunction of patients with MASH post-LT.

Introduction The triglyceride glucose (TyG) index and modified TyG-indices have been suggested as a reliable indication of insulin resistance. The present study aimed to investigate the predictive utility of TyG index and modified TyG indices (TyG-waist circumference, TyG-body mass index, TyG-waist-to-hip ratio, and TyG-waist-to-height ratio) for assessing glycemic control in type 2 diabetes mellitus (T2DM). Methods The present hospital-based cross-sectional study recruited 383 T2DM patients. On the basis of HbA1c levels, patients were grouped into poor glycemic control (n=168) and good glycemic control (n=215). Baseline and biochemical parameters including TyG and modified TyG indices were compared between the groups. We used a Spearman correlation analysis to look for an association between TyG and TyG-related indices and glycemic control. We conducted receiver operating characteristic curve analysis to evaluate the predictive capability of TyG-index and modified TyG indices in assessing poor glycemic control in T2DM. Results T2DM with poor glycemic control had significantly elevated TyG and modified TyG indices when compared to those with good glycemic control. The TyG index and modified TyG indices showed a strong correlation with glycemic control in individuals with T2DM. The TyG index exhibited greater predictive capacity for poor glycemic control as compared to the modified TyG indices. Conclusion Patients with T2DM who are treated in clinical settings with limited resources may benefit from using the TyG index to evaluate their glycemic control.

To investigate the association between the Weekend Warrior (WW) pattern and diabetes prevalence in American adults.

Cross-sectional analysis of data from the 2007-2016 National Health and Nutrition Examination Survey (NHANES).

We examined the relationship between four physical activity (PA) patterns-inactive, insufficiently active, WW, and regularly active-and diabetes prevalence. Multivariable logistic regression, marginal average population effects (MAPE), subgroup, and sensitivity analyses were performed to assess these associations. Odds ratios (ORs) and average marginal effects (AME), along with 95 % confidence intervals (CIs) were calculated.

Individuals engaging in the WW pattern (OR = 0.60, 95 % CI: 0.40 to 0.89, p = 0.013; AME = -0.05, 95 % CI: -0.09 to -0.02, p = 0.004) and the regularly active pattern (OR = 0.69, 95 % CI: 0.60 to 0.80, p < 0.001; AME = -0.04, 95 % CI: -0.06 to -0.03, p < 0.001) showed significantly lower diabetes prevalence than those classified as inactive. Compared to individuals classified as inactive, those categorized as insufficiently active demonstrated no significant difference in diabetes prevalence. No significant difference was observed between the WW and regularly active patterns (OR = 0.86, 95 % CI: 0.56 to 1.35, p = 0.5; AME = -0.01, 95 % CI: -0.06 to 0.03, p = 0.501). Subgroup interaction analyses revealed no significant effect modification (all p for interaction >0.05), and sensitivity analyses confirmed the robustness of these findings.

Both the WW and regularly active patterns are associated with a lower prevalence of diabetes compared with inactive individuals.

Progression of prediabetes to type 2 diabetes has been associated with β-cell dysfunction, whereas its remission to normoglycemia has been related to improvement of insulin sensitivity. To understand the mechanisms and identify potential biomarkers related to prediabetes trajectories, we compared the proteomics and metabolomics profile of people with prediabetes progressing to diabetes or reversing to normoglycemia within 1 year.

The fasting plasma concentrations of 1,389 proteins and the fasting, 30-min, and 120-min post-oral glucose tolerance test (OGTT) plasma concentrations of 152 metabolites were measured in up to 134 individuals with new-onset diabetes, prediabetes, or normal glucose tolerance. For 108 participants, the analysis was repeated with samples from 1 year before, when all had prediabetes.

The plasma concentrations of 14 proteins were higher in diabetes compared with normoglycemia in a population with prediabetes 1 year before, and they correlated with indices of insulin sensitivity. Higher levels of dicarbonyl/L-xylulose reductase and glutathione S-transferase A3 in the prediabetic state were associated with an increased risk of diabetes 1 year later. Pathway analysis pointed toward differences in immune response between diabetes and normoglycemia that were already recognizable in the prediabetic state 1 year prior at baseline. The area under the curve during OGTT of the concentrations of IDL particles, IDL apolipoprotein B, and IDL cholesterol was higher in new-onset diabetes compared with normoglycemia. The concentration of glutamate increased in prediabetes progressing to diabetes.

We identify new candidates associated with the progression of prediabetes to diabetes or its remission to normoglycemia. Pathways regulating the immune response are related to prediabetes trajectories.

Background/Objectives: Type 1 diabetes (T1D) is a chronic autoimmune condition characterized by the destruction of pancreatic β-cells, leading to insulin deficiency. Current therapies, such as islet transplantation, face significant challenges, including limited donor availability and the need for lifelong immunosuppression. Encapsulation technologies offer a promising alternative, providing immune protection and maintaining β-cell viability. In this study, we propose an encapsulation device featuring a spiral tubular semipermeable polyethersulfone (PES) membrane reinforced with a rigid biocompatible resin scaffold. Methods: The PES membrane was engineered with a tailored porosity of 0.5 µm, enabling efficient nutrient and oxygen exchange while preventing immune cell infiltration. Using INS-1E insulin-secreting cells aggregated into size-controlled islet-like spheroids (ILSs), we evaluated the device's performance. Results: The device achieved high ILS viability and insulin secretion over 48 h at therapeutic densities, maintaining functionality comparable to free-floating ILSs (control). The PES membrane, with its mechanical stability and biocompatibility, ensured durability without compromising diffusion dynamics, overcoming a critical limitation of other encapsulation approaches. Importantly, the device geometry allowed for the encapsulation of up to 356,000 islet equivalents (IEQs) in a single capillary fiber, reaching therapeutic thresholds for T1D patients. Conclusions: this device, with its innovative design, enables high-density encapsulation while preserving ILS functionality and scalability, making it a potential platform for clinical application. This work highlights the potential of PES-based encapsulation devices to overcome key barriers in T1D treatment, paving the way for personalized, long-term solutions to restore insulin independence.

The study aimed to assess the effect of COVID-19 on hepatic lipid (HL) content, fibrosis risk, and adiposity in persons with type 2 diabetes.

Participants with type 2 diabetes with a history of mild COVID-19 (n=15, age 58±12 years, body mass index 30.9±5.2 kg/m2) were examined before (baseline) and 1 year (12±2 months) after (follow-up) recovery from COVID-19. Investigations for changes in metabolic risk comprised clinical examination, fasting blood sampling and MR-based measurements. Potential changes were corrected with the time course of the respective parameters in a group of participants who did not contract COVID-19 over the same time course (n=14, 61±6 years, 30.0±4.6 kg/m2).

COVID-19 resulted in a relative increase in HL content of 56% (95% CI 18%, 106%; p=0.04) measured as proton density fat fraction (HL-PDFF), corrected for the time course in the absence of COVID-19. While no changes in hepatic stiffness and volume, intramyocellular lipids, whole-body, subcutaneous and visceral adipose tissue volumes as well as homeostatic model assessment of insulin resistance and beta-cell function were observed.

History of COVID-19 in persons with type 2 diabetes is associated with higher HL-PDFF after 1 year following recovery from infection.

NCT01055093.

Non-alcoholic fatty liver disease (NAFLD) is a prevalent liver disorder strongly associated with metabolic dysfunction, particularly in elderly populations where it presents with higher prevalence and severity. This study aimed to investigate the association between serum uric acid (SUA) levels and NAFLD in older adults, focusing on the independent effect of hyperuricemia on NAFLD risk. We enrolled 469 individuals aged ≥ 65 years who underwent community health checkups. The exposure variable was baseline SUA levels, while the outcome variable was the occurrence of NAFLD. Covariates included age, sex, BMI, blood pressure, diabetes status, lipids (TC, TG, LDL, HDL), glycemic indices (FPG, HBA1C), and physical activity. Multivariable logistic regression was applied to estimate the independent effect of SUA levels and hyperuricemia on NAFLD. Hyperuricemia was significantly associated with increased NAFLD risk (adjusted OR 2.16, 95% CI 1.28-3.67). Stratified analysis revealed a stronger association in individuals with elevated triglycerides (TG ≥ 2.26 mmol/L, OR 7.07, 95% CI 1.72-29.18). However, the association between SUA as a continuous variable and NAFLD risk was attenuated after adjusting for metabolic factors. Hyperuricemia independently increases NAFLD risk in older adults, particularly in those with elevated triglycerides, suggesting a potential synergistic effect. These findings highlight the importance of incorporating SUA assessments into routine metabolic evaluations and developing targeted interventions to mitigate NAFLD risk.

Type 2 diabetes accounts for over 90% of all diabetes cases and is caused by a combination of behavioral risk factors. It is currently a serious health issue, particularly among women of reproductive age, as it is associated with reproductive disorders. Preventing it requires knowledge, but there is limited data on behavioral risk factors in Ethiopia.

To assess knowledge of the behavioral risks of type 2 diabetes mellitus and its associated factors among women of reproductive age.

A community-based cross-sectional study was conducted, with all women in the town serving as the source population. A multistage sampling method was utilized to recruit kebeles, and a systematic random technique was employed to select households at every 13th interval. We completed interview questionnaires for 623 samples. The crude odds ratio was calculated using a bivariate logistic model, and multivariate analysis was performed to control for confounding and identify associated factors among model-fitting variables using an adjusted odds ratio (AOR).

The knowledge of behavioral risk factors (BRF) among women of reproductive age (WRA) is 47.0% [95% CI, 43.5-50.9], and significant associations were found with the following factors: average family income of between 3000 and 5000 Ethiopian Birr(ETH) 1.81 [95% CI, 1.03-3.18], > = 5001 ETH 1.93 [95% CI, 1.02-3.68], diabetes mellitus (DM) in the friend or relatives 4.03 [95% CI, 1.56-10.46], family history of DM 9.47 [95% CI, 4.74-18.90], source of information: health workers 1.87 [95% CI, 1.04-3.34] and friend or relatives 1.65 [95% CI, 1.04-2.62].

Knowledge of behavioral risk factors for type 2 diabetes was poor among study participants. Factors such as family income, diabetes mellitus (DM) in friends or relatives, family history of DM, and sources of information were strongly associated with good knowledge. It is essential to emphasize health education about behavioral risk factors for women.