Mean platelet volume (MPV), which reflects platelet size and activity, is known to be elevated in patients with type 2 diabetes mellitus. Although increased MPV has been linked to poor glycemic control and diabetic vascular complications, evidence regarding its association with hard kidney outcomes remains limited. We aimed to investigate the relationship between MPV and kidney events in patients with type 2 diabetes mellitus.
We retrospectively analyzed longitudinal data from 1,076 Japanese patients with type 2 diabetes mellitus enrolled in the Fukushima Cohort Study. Participants were categorized into quartiles based on baseline MPV levels. The primary endpoint was kidney events, defined as a ≥50% decline in estimated glomerular filtration rate (eGFR) from baseline or progression to end-stage kidney disease requiring kidney replacement therapy. The secondary endpoint was new-onset cardiovascular events.
During a median follow-up of 5.3 years, 97 patients experienced kidney events. The second quartile (Q2) had the lowest incidence of kidney events. Compared with Q2 as the reference, patients in the highest quartile (Q4) had a significantly increased risk of kidney events (adjusted hazard ratio 2.05, 95% confidence interval 1.13–3.72). Higher MPV levels were also significantly associated with an increased risk of cardiovascular events.
Elevated MPV was independently associated with both kidney and cardiovascular events in Japanese patients with type 2 diabetes mellitus. MPV may serve as a simple and useful biomarker for predicting kidney disease progression in this high-risk population.
We aimed to explore the association of the triglyceride-glucose (TyG) index and homeostasis model assessment of insulin resistance (HOMA-IR) with subclinical left ventricular function in the general population.
A total of 2,850 participants with left ventricular ejection fraction ≥50% were recruited from 2017 to 2019 in Danyang. Speckle-tracking echocardiography (Philips CX50) was used to measure global longitudinal strain (GLS). Subclinical left ventricular systolic dysfunction (LVSD) was defined as GLS < 18%.
In univariate analyses, higher TyG index and HOMA--IR were significantly associated with reduced GLS, lower E/A ratio and e', and higher E/e' ratio (P < 0.001). After adjustment for confounders, HOMA-IR remained significantly associated with lower GLS (P = 0.002), whereas the TyG index showed stronger correlations with E/e' ratio (P < 0.01). The inclusion of log-transformed HOMA-IR significantly improved model fit in analyses incorporating GLS and TyG index (P = 0.004) but not in those with E/e' ratio and TyG index (P = 0.65). Conversely, the TyG index enhanced model performance for the E/e'–HOMA-IR association (P < 0.001) but not for GLS–HOMA-IR relationships (P = 1). In addition, participants in the highest versus lowest HOMA-IR quartile demonstrated significantly increased odds ratio of subclinical LVSD (OR = 2.22, 95% CI: 1.26–3.92; P = 0.006), while the TyG index showed no significant association with its prevalence (P = 0.98).
In a community-based population, elevated HOMA-IR demonstrated a robust association with subclinical LVSD, whereas the TyG index exhibited a more pronounced correlation with early diastolic dysfunction.
The association between estradiol/testosterone (E2/T) ratio and metabolic dysfunction-associated steatotic liver disease (MASLD) remains controversial. Moreover, few studies have explored their relationship in men with type 2 diabetes mellitus. We aimed to investigate the association of the E2/T ratio with MASLD in type 2 diabetes mellitus male patients.
This real-world observational study was performed in 1441 male type 2 diabetes mellitus patients. MASLD was determined by abdominal ultrasonography. The clinical characteristics and prevalence of MASLD were compared across the E2/T ratio quartiles. The association of the E2/T ratio and quartiles with MASLD was also evaluated using binary logistic regression.
After adjusting for age and diabetes duration (DD), MASLD prevalence significantly increased across the E2/T ratio quartiles (37.7%, 42.6%, 53.1%, and 69.3%, respectively, P < 0.001 for trend). Fully adjusted logistic regression showed that both the E2/T ratio (OR: 2.201, 95% CI: 1.380–3.511, P = 0.001) and quartiles (P = 0.001) were positively associated with MASLD in males with type 2 diabetes mellitus. Furthermore, C-reactive protein (CRP) levels were significantly higher in patients with MASLD compared with those without (P < 0.001), and obviously increased across the E2/T ratio quartiles after controlling for age and DD (P = 0.016 for trend).
The E2/T ratio was independently and positively associated with the increased risk of MASLD in male type 2 diabetes mellitus patients, which may be attributed to the close association between the E2/T ratio and inflammation. The E2/T ratio may serve as a simple and practical indicator to assess the risk of MASLD in male type 2 diabetes mellitus patients.
To assess racial and ethnic differences in gestational diabetes mellitus (GDM) prevalence and perinatal outcomes among U.S. women with normal prepregnancy body mass index (BMI).
Retrospective, population-based cohort study using 2021–2023 US National Vital Statistics System data. Included singleton live births to women aged 18–44 years with BMI 18.5–24.9 kg/m2. Exclusions were preexisting hypertension or diabetes, multiple gestations, missing covariates, or implausible data.
Race/ethnicity: White, Black, Asian, and Other (Native American/Alaska Native, Native Hawaiian/Pacific Islander, and multiracial).
Primary outcome: GDM prevalence by race. Logistic regression estimated adjusted odds ratios (aORs) with White women as the reference. Secondary outcomes: preterm delivery macrosomia, NICU admission, and neonatal respiratory failure.
A total of 3,754,684 women, GDM prevalence was highest in Asians (12.5%). Compared with White women, Asians had nearly threefold higher odds of GDM (aOR, 2.95; 95% CI, 2.91–3.00). GDM was associated with preterm delivery (aOR, 1.23; 95% CI, 1.22–1.25), NICU admission (aOR, 1.26; 95% CI, 1.24–1.28), and neonatal respiratory failure (aOR, 1.27; 95% CI, 1.22–1.32), in all racial groups. Macrosomia was increased only in Black (aOR, 1.55; 95% CI, 1.43–1.68) and Other (aOR, 1.21; 95% CI, 1.08–1.34).
Among women with normal BMI, substantial racial disparities in GDM prevalence and outcomes exist, with Asian women at the highest risk. Our results support earlier and ethnicity-tailored GDM screening among women with normal BMI—particularly Asian women—plus proactive counseling on glucose monitoring and culturally adapted lifestyle interventions during pregnancy.
Type 1 diabetes mellitus (T1DM) arises from autoimmune destruction of pancreatic β-cells. Pleomorphic adenoma gene-like 1 (PLAGL1) overexpression has been linked to β-cell apoptosis, but molecular mechanisms remain incompletely understood. This study explored whether PLAGL1 exacerbates T1DM by promoting oxidative stress-induced DNA damage and activating the cGAS/STING inflammatory pathway.
The mouse β-cell line NIT-1 was transfected with PLAGL1 overexpression plasmids or specific siRNA. Mitochondrial and nuclear DNA damage was assessed through comet assays, 8-OHdG ELISA, and Western blot analysis of key DNA repair proteins, including XRCC1, OGG1, and PARP1. Oxidative stress was evaluated by measuring superoxide dismutase (SOD) activity and the glutathione redox state (GSH/GSSG ratio), while apoptosis was examined via expression levels of BCL2, BAX, and cleaved Caspase-3. To investigate pathway involvement, pharmacological inhibitors—RU.521 (targeting cGAS) and H-151 (targeting STING)—were applied. In NOD mice, PLAGL1 overexpression was combined with cGAS/STING inhibition; glucose tolerance was subsequently evaluated, and pancreatic tissue was subjected to histopathological examination.
Overexpression of PLAGL1 triggered substantial mitochondrial and nuclear DNA damage, which was accompanied by elevated oxidative stress and compromised DNA repair. Consequently, cytoplasmic DNA accumulated, leading to activation of the cGAS/STING pathway and subsequent β-cell apoptosis and functional decline. Treatment with the cGAS inhibitor RU-521 or the STING inhibitor H-151 markedly attenuated apoptosis and restored insulin secretion in PLAGL1-overexpressing NIT-1 cells. In NOD mice, PLAGL1 overexpression accelerated diabetes progression, whereas inhibition of the cGAS/STING axis preserved β-cell mass, improved glucose homeostasis, and sustained insulin output. Histological evaluation further confirmed that inhibition of this signaling pathway helped maintain normal islet architecture.
Our findings demonstrated that PLAGL1 exacerbates β-cell loss in type 1 diabetes by driving oxidative DNA damage and activating the cGAS/STING signaling cascade. Therapeutic intervention targeting this axis may therefore represent a promising strategy to protect β-cells and attenuate disease progression.
The MiniMed™ 780G® is effective for improving glycemic control; however, few studies have specifically examined the impact of upgrading from MiniMed™ 770G® to MiniMed™ 780G® in adults. We determined the effects of upgrading from MiniMed™ 770G® to MiniMed™ 780G® (780G) on glucose management, psychological distress, daily life quality, and sleep in type 1 diabetes mellitus (T1DM).
In this single-center prospective study, we observed 21 adults who transitioned from the MiniMed™ 770G® to the 780G for 3 months. Glycemic outcomes, insulin delivery parameters, frequency of alarms, and sensor calibrations were assessed. Patient-reported outcomes were evaluated using the Problem Areas in Diabetes (PAID), the Diabetes Treatment Satisfaction Questionnaire status version, the Diabetes Therapy-Related Quality of Life, and the Pittsburgh Sleep Quality Index.
Glycated hemoglobin (HbA1c) decreased (7.5 ± 1.3%–7.0 ± 0.8%, mean difference: −0.5%, 95% Confidence Interval (CI): −0.9 to −0.1; P = 0.018). Time in tight range (TITR) showed trends toward improvement (44.9 ± 15.5%–48.9 ± 15.5%, mean difference: 4.0%, 95% CI: −0.7 to 8.6; P = 0.090). Alarm frequency declined (11.9 ± 8.7–7.1 ± 5.5 times/day, mean difference: −4.8, 95% CI: −7.0 to −2.6; P = 0.0002), and calibration frequency decreased (3.6 ± 2.2–0.8 ± 0.6 times/day, mean difference: −2.8, 95% CI: −3.7 to −1.9; P < 0.0001). The PAID score improved, decreasing from 38.7 ± 19.9 to 31.7 ± 19.3 (mean difference: −7.0, 95% CI: −14.7 to 0.7; P = 0.074).
Favorable changes in HbA1c, TITR, and PAID scores suggest potential glycemic and psychological benefits.
To compare the efficacy and safety of insulin degludec/insulin aspart biosimilar B01711 (HS-IDegAsp) with originator insulin degludec/insulin aspart-Ryzodeg (NN-IDegAsp) in Chinese patients with type 2 diabetes mellitus (T2DM) who were inadequately controlled on once- or twice-daily (BID) premixed or basal insulin ± oral antidiabetic drugs (OADs).
In this multicenter, randomized, open-label, parallel-group, active-controlled, phase 3 study, 367 participants with T2DM were randomized 1:1 to receive BID injections of HS-IDegAsp (n = 183) or NN-IDegAsp (n = 184) for 24 weeks. Insulins were administered subcutaneously with breakfast and the main evening meal at the same titration target. The primary endpoint was the change from baseline in glycated hemoglobin (HbA1c) to week 24.
At Week 24, the least squares (LS) mean change in HbA1c from baseline was −1.12% (95% CI −1.24 to −1.01) and −1.23% (95% CI −1.34 to −1.11) with HS-IDegAsp and NN-IDegAsp, respectively. The LS mean difference (HS-IDegAsp minus NN-IDegAsp) at Week 24 was 0.10% (95% CI −0.06 to 0.27), demonstrating that HS-IDegAsp was non-inferior to NN-IDegAsp. There was no statistically significant difference (P > 0.05) in fasting plasma glucose or proportion of patients achieving HbA1c < 7.0% at Week 24 between both groups. Safety and immunogenicity were similar between both groups.
HS-IDegAsp demonstrated comparable efficacy and safety to NN-IDegAsp during the 24-week treatment period in Chinese patients with inadequately controlled T2DM previously treated on once- or twice-daily premixed or basal insulin, with or without OADs.
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