Objective:To translate and psychometrically validate the Persian version of the Instrument for Self-care in Preventing Diabetic Foot (P-ISPDF) as a reliable, culturally appropriate tool for assessing foot-specific self-care behaviors among Persian-speaking adults, predominantly those with type 2 diabetes mellitus. Methods:The ISPDF was translated using a forward-backward procedure, followed by expert review (n=5) and cognitive debriefing with patients (n=10). A split-sample design was used: exploratory factor analysis (EFA; n=289) and a series of confirmatory factor analyses (CFAs), including first-order, second-order, and a hierarchical general-factor model in an independent sample (n=250). Items were rated on a 5-point Likert scale (1-5). Reliability (Cronbach's alpha, McDonald's omega, intraclass correlation coefficient [ICC]) and validity (EFA, CFA) were evaluated using SPSS 25, AMOS 24, and JASP. Results:EFA supported a three-factor structure: self-care maintenance (10 items), monitoring (9 items), and management (7 items). The hierarchical measurement model showed good fit (χ 2/df=2.80, CFI=0.974, TLI=0.954, RMSEA=0.060). Cronbach's alpha was 0.93 for the total scale, with subscale alphas ranging from 0.81 to 0.92. Test-retest reliability was excellent (two-way mixed-effects, absolute agreement ICCs 0.93-0.98 with 95% CIs reported). Conclusion:The P-ISPDF demonstrated strong reliability and preliminary structural validity. However, due to mixed evidence regarding convergent validity and the absence of external validation, the findings should be interpreted with caution. Further psychometric refinement and longitudinal studies are needed to establish its clinical utility.
Studies suggest that alterations of intestinal barrier function and a subsequent increased translocation of bacterial endotoxins may be critical in type 1 diabetes mellitus (T1DM) and may contribute to the proinflammatory state of patients. If Gram-positive derived bacterial toxins are also altered in the setting of T1DM is not yet clarified. In the present study, using a SEAP reporter assay and ELISA, markers of intestinal permeability, concentration of Toll like receptor (TLR) 2 ligands and soluble CD14 (sCD14) were assessed in serum of individuals with T1DM (n=19, m: 10/ f: 9) and age-matched healthy controls (n=18, m: 3/ f: 15) from the LatDiane study. BMI and HbA1c were significantly higher in individuals with T1DM. Serum concentrations of intestinal fatty acid binding protein (I-FABP) were significantly higher in individuals with T1DM than in controls as were concentrations of TLR2 ligands and sCD14 protein. A multivariable linear regression analysis revealed an independent association of T1DM with higher TLR2 ligand levels. Our findings indicate that not only bacterial endotoxin but also TLR2 ligands are elevated in patients with T1DM.
Purpose:Thyroid hormones are linked to prognostic outcomes for a range of diseases. The link between thyroid hormone levels and diabetic kidney disease (DKD) risk in euthyroid individuals with type 2 diabetes mellitus (T2DM) was investigated in this study. Patients and Methods:Overall, 2945 T2DM cases were enrolled and grouped as with or without DKD. Thyroid hormones were analyzed both as continuous variables and by quartiles. Logistic regression models and smooth curve fitting were applied to assess associations. Stratified analyses and interaction tests were also conducted to examine effect modification. Results:Patients with DKD had significantly decreased free triiodothyronine (FT3) levels compared to those without DKD, while free thyroxine (FT4) and thyroid-stimulating hormone (TSH) were comparable across groups. Relative to the bottom FT3 quartile (Q1), the respective adjusted odds ratios (ORs) for DKD in Q2, Q3, and Q4 were 0.63 (95% CI: 0.50-0.80, p < 0.001), 0.60 (95% CI: 0.47-0.77, p < 0.001), and 0.63 (95% CI: 0.49-0.82, p = 0.001). The relationship between FT3 and DKD followed a nonlinear, L-shaped pattern (p for nonlinearity < 0.001), with a threshold at approximately 3.09 pg/mL. Below this inflection point, an adjusted OR for DKD of 0.622 (95% CI: 0.515-0.751, p < 0.001) was evident. Subgroup analysis suggested that this association was generally consistent across most subsets of study subjects, but was not statistically significant in several strata. Conclusion:Lower FT3 levels are independently linked to greater prevalence of DKD in euthyroid individuals with T2DM. The observed L-shaped association suggests a threshold effect, with 3.09 pg/mL as the approximate inflection point.
Objective:To quantify the acute effects of exercise snacks on glucose and lipid metabolism in individuals with metabolic disorders (including those with type 2 diabetes, metabolic syndrome, and overweight or obesity) compared with sedentary behavior and continuous exercise, and to examine their effects across different exercise modalities. Methods:Following the PRISMA 2020 guidelines, four databases (PubMed, Embase, Web of Science, and Scopus) were searched up to February 4, 2026, to identify randomized crossover trials that examined the acute effects of exercise snacks on glucose and lipid metabolism in individuals with metabolic disorders. Risk of bias was assessed using the Cochrane Risk of Bias 2 tool, and the quality of evidence was assessed using the GRADE approach. The "meta" and "metafor" packages in R (version 4.5.2) were used to calculate pooled effect estimates (using Hedges' g as the effect size) and to conduct publication bias tests, subgroup analyses, and regression analyses. Results:The analysis included 20 randomized crossover trials (21 studies) involving 392 participants. Compared with prolonged sedentary behavior, exercise snacks significantly reduced postprandial glucose AUC (Hedges' g = -0.37, 95% CI -0.53 to -0.22, P < 0.01, I2 = 6.6%, moderate certainty of evidence) and insulin AUC (Hedges' g = -0.49, 95% CI -0.68 to -0.30, P < 0.01, I2 = 15.7%, moderate certainty of evidence), whereas no significant improvement was observed for triglycerides (Hedges' g = -0.014, 95% CI -0.18 to 0.15, P = 0.87, I2 = 0.0%, low certainty of evidence). Compared with a single session of continuous exercise, exercise snacks showed no statistically significant differences in postprandial glucose (Hedges' g = -0.14, 95% CI -0.73 to 0.45, P = 0.64, I2 = 57.6%, low certainty of evidence), insulin, or triglycerides. The included studies did not provide separate data for individuals with a confirmed diagnosis of MetS; therefore, the subgroup analysis was limited to overweight or obese individuals and those with T2DM. When stratified by study population, exercise snacks significantly reduced the postprandial glucose AUC in overweight or obese individuals (Hedges' g = -0.36, 95% CI: -0.52 to -0.20, P < 0.001), whereas the effect estimate in the T2DM group did not reach statistical significance (Hedges' g = -0.45, 95% CI: -1.47 to 0.56, P = 0.385), and the difference between the two subgroups was not significant (P between subgroups = 0.86). Insulin AUC was significantly reduced in both the overweight or obese group (Hedges' g = -0.42, 95% CI: -0.61 to -0.24, P < 0.001) and the T2DM group (Hedges' g = -1.15, 95% CI: -1.76 to -0.54, P < 0.001), and the difference between subgroups was significant (P = 0.03 between subgroups); however, the estimate for the T2DM subgroup was based on only one study. Regression analysis indicated that older participants experienced a greater reduction in insulin levels (β = -0.01, 95% CI -0.02 to 0.00, P = 0.02). Conclusion:In individuals with metabolic disorders, repeatedly interrupting sedentary behavior with short bouts of mild- to moderate-intensity aerobic exercise (2-5 minutes of activity every ≤30 minutes) can acutely reduce postprandial glucose and insulin responses. A meta-regression analysis suggests that studies involving participants with a higher average age showed a greater reduction in postprandial insulin AUC. No statistically significant differences in short-term glycemic control were observed between exercise "snacks" and a single continuous exercise session; however, this comparison was based on only four studies with small sample sizes and is therefore insufficient to demonstrate the non-inferiority or equivalence of the two exercise patterns. Exercise "snacks" can serve as a low-barrier complementary strategy to regular exercise and other lifestyle management approaches.
Aims:Current diabetes mellitus (DM) prevention and treatment strategies rely on risk factors adapted from developed countries, which may not be effective in most poor sub-Saharan Africa settings. This study investigated the association between diabetic treatment outcomes and complications with sociodemographic and diabetic risk factors among type 2 DM (T2DM) patients in Rwanda. Methods:This cross-sectional study analyzed the records of T2DM patients who accessed care at Kigali University Teaching Hospital (CHUK) between January and December 2020, using a non-random sampling technique. Treatment outcomes (improved or not improved based on glycemic control target) and complication outcomes (presence or absence of DM-related microvascular and macrovascular events) were the primary outcome variables. Data were analyzed using t-tests, chi-square tests, and multivariable analyses as appropriate. Results:After adjusting for confounders, only age remained significantly associated with treatment and complication outcomes. The adjusted prevalence ratio (PR) of treatment outcomes for patients aged <50 years was 1.43 (95% CI 1.07-1.92; p = 0.016) and for those aged 50-64 years was 1.12 (95% CI 0.83-1.52; p = 0.462), both relative to the ≥65 years reference category. The adjusted PR for complication outcomes was 0.59 (95% CI 0.40-0.86; p = 0.005) for patients aged <50 years and 0.72 (95% CI 0.57-0.91; p = 0.007) for those aged 50-64 years, compared with the ≥65 years reference category. The adjusted PRs for smoking, alcohol consumption, pharmacological therapy, non-pharmacological therapy, and diet were attenuated and no longer statistically significant (all p > 0.05). Conclusion:The outcomes of diabetic treatment in Rwanda are associated with the age of the patients, rather than the type of therapy or the assessed sociodemographic and risk factors. The causal interpretation and generalizability of this study are limited by its cross-sectional design, non-random sampling, and the single-center setting.
Insulin resistance is one of the main causes of type 2 diabetes mellitus and metabolic disorders. Histone deacetylase 9 (HDAC9) belongs to the class IIa histone deacetylase family. It remodels chromatin structure and modulates gene expression to regulate adipocyte differentiation, inflammatory responses, and hepatic glucose homeostasis, thereby inhibiting insulin signaling. However, the complete and precise molecular mechanisms underlying these processes remain unclear. This review systematically summarizes the molecular characteristics and regulatory mechanisms of HDAC9, and analyzes its biological functions under insulin resistance from the perspectives of chromatin remodeling and transcriptional regulation. This review further explores whether HDAC9 exacerbates insulin resistance through regulating adipocyte differentiation, mediating inflammatory responses and disrupting hepatic glucose metabolic homeostasis. Meanwhile, this review evaluates HDAC9-targeted therapeutic prospects for metabolic diseases and offer theoretical support for future precision interventions.
Objective:The functional status of regulatory T cells expressing the gut-homing receptor CCR9 (CCR9+ Tregs) in type 1 diabetes mellitus (T1DM) remains unclear. This study aims to investigate the functional alterations of CCR9+ Tregs in a T1DM model and evaluate the interventional effect of targeting the IL-21/IL-17 axis on their dysfunction. Methods:The spontaneous T1DM non-obese diabetic (NOD) mouse model was employed. CCR9+ and CCR9- Treg subsets were isolated from the spleen by flow cytometry. Their in vitro suppressive capacity on effector T cell (Teff) proliferation was assayed, and cytokine expression was analyzed using flow cytometry and qPCR. In vitro, CCR9+ Tregs were treated with different concentrations (50 and 100 ng/mL) of the anti-IL-21 monoclonal antibody (Avizakimab) to assess its effects on IL-21/IL-17A secretion and immunosuppressive function. In vivo, T1DM NOD mice were randomly assigned to a saline control group (n=3) and an Avizakimab treatment group (n=3, 10 mg/kg, tail vein injection, every other day for 2 weeks). Fasting blood glucose levels were monitored, pancreatic insulitis and pathological damage were evaluated by H&E staining, and the proportion of peripheral blood IL-17A+ cells was analyzed by flow cytometry. Results:Compared to CCR9- Tregs, CCR9+ Tregs exhibited a significantly reduced ability to suppress Teff proliferation, secreted less of the anti-inflammatory cytokine IL-10, and showed significantly upregulated expression of the pro-inflammatory cytokines IL-17A and IL-21. Avizakimab effectively and dose-dependently inhibited the abnormal secretion of IL-21 and IL-17A by CCR9+ Tregs in vitro and restored their suppressive function on Teff proliferation. In vivo, Avizakimab treatment significantly lowered fasting blood glucose levels in T1DM NOD mice, alleviated pancreatic insulitis and pathological damage, and downregulated the proportion of IL-17A+ cells in peripheral blood. Conclusion:In the T1DM milieu, CCR9+ Tregs become dysfunctional and shift towards a pro-inflammatory phenotype, thereby exacerbating the autoimmune response. The anti-IL-21 monoclonal antibody Avizakimab can reverse the dysfunction of CCR9+ Tregs and ameliorate disease symptoms by inhibiting the IL-21/IL-17 axis, providing a novel potential strategy for the immunotherapy of T1DM and highlighting the translational potential of targeting this axis.
Diabetic complications, driven by chronic hyperglycemia and complex pathogenic mechanisms, are a major global health challenge, yet the basis of tissue-specific injury and repair remains unclear. Wnt/β-catenin signaling has emerged as an important regulator in these complications, but its role is highly context dependent, promoting pathological remodeling in some tissues while impairing repair in others. This review is distinguished by its integration of current evidence on the dual and often opposing roles of Wnt/β-catenin signaling across six major diabetic complications: diabetic nephropathy (DN), diabetic retinopathy (DR), diabetic cutaneous ulcers (DCU), diabetic cardiomyopathy (DCM), diabetic neuropathy, and diabetic osteoporosis (DOP). We first outline the major pathological features and clinical significance of each complication, highlighting the recurring observation that hyperglycemia often causes aberrant activation of this pathway in DN, DR, and DCM, where it promotes epithelial-to-mesenchymal transition, extracellular matrix accumulation, fibrosis, inflammation, and pathological angiogenesis. In contrast, we then examine conditions in which Wnt/β-catenin signaling is suppressed, particularly in DCU, DOP, and certain forms or stages of DPN, leading to impaired wound healing, reduced bone formation, and defective nerve regeneration. We subsequently analyze the cell type- and stage-specific mechanisms underlying these divergent effects, including cross-talk with oxidative stress, the renin-angiotensin system, and transforming growth factor-β signaling. Following a detailed discussion of emerging therapeutic strategies, such as LRP6-targeting biologics, small-molecule modulators, and agents derived from traditional Chinese medicine, we summarize preclinical evidence showing that carefully tuned, context-specific modulation of Wnt/β-catenin can improve both pathological and functional outcomes. This review is intended to clarify the potential mechanisms linking Wnt/β-catenin signaling to diabetic complications and to guide the rational development of new therapies that take into account its tissue-specific and stage-specific effects.
Dandan Chi, Yuntao GuanDepartment of Endocrinology, The Second Affiliated Hospital of Dalian Medical University, Dalian, People’s Republic of ChinaCorrespondence: Yuntao Guan, Department of Anesthesiology, The Second Affiliated Hospital of Dalian Medical University, Dalian, People’s Republic of China, Tel +86 18842869236, Email 18842869236@163.com
Background:Polycystic ovary syndrome (PCOS) is a metabolic and endocrine disorder that affects women of reproductive age. There is no absolute treatment for PCOS, but it is managed symptomatically. Adopting a healthy lifestyle comprising a balanced diet and physical exercise is the major recommendation for management of PCOS. Objective:To evaluate the effectiveness of aerobic exercise as an intervention for improving metabolic profiles in women suffering from PCOS. Methods:A systematic search was performed in 4 databases; Scopus, MEDLINE (via PubMed), Embase, and Web of Science, since inception till 28.2.2025. Risk of bias was performed using Cochrane RoB 2.0 tool and meta-analysis was done by using random-effects models. Results:Twenty-five RCTs were included in the review for qualitative synthesis and 5 RCTs with a total of 192 participants were included for quantitative analysis. A low but statistically significant decrease was observed in waist-to-hip ratio). Lipid profile analysis revealed a significant reduction in low-density lipoprotein (LDL) cholesterol. Further, HIIT also improved insulin sensitivity, by decreasing fasting insulin levels and HOMA-IR. A non-significant reduction was observed in body mass index (BMI), waist circumference, total cholesterol, and fasting glucose. Changes in triglycerides, and HDL were also non-significant. Conclusion:Aerobic exercise, especially HIIT, appears effective in improving regional fat distribution, LDL cholesterol, and insulin resistance in PCOS women, though evidence for BMI and hormonal changes remains inconclusive. Larger, longer-term RCTs are needed to confirm these findings and clarify hormonal outcomes. Prospero Registration crd420251003425:
Background:Diabetic foot ulcers (DFUs) remain the leading cause of non-traumatic lower-extremity amputation (LEA). Most published risk-stratification tools require specialized testing and are difficult to apply in routine practice. We sought to build a simple nomogram for amputation risk using only routinely available clinical indicators. Methods:This single-center retrospective cohort study included 508 hospitalized patients with type 2 diabetes-related DFUs treated between January 2019 and June 2025. The cohort was randomly split into training (n=357, 84 amputations) and validation (n=151, 35 amputations) sets at a 7:3 ratio with stratification on outcome. The outcome was lower-extremity amputation (minor or major) during the index hospitalization. Twenty-four baseline variables were screened for selection in the training set (84 events) using two independent methods: LASSO regression with 10-fold cross-validation (at λ.1se) and 1000 bootstrap stepwise logistic regression replicates (selection frequency >80%). Variables retained by both methods were entered into the final multivariable logistic regression model, from which a nomogram was constructed. Discrimination was assessed by the area under the receiver operating characteristic curve (AUC); calibration was evaluated using calibration plots, the Hosmer-Lemeshow test, and the calibration slope; and clinical utility was assessed by decision curve analysis (DCA). Internal validity was further examined by bootstrap resampling with optimism correction. Results:Four variables were retained by both LASSO and bootstrap screening: serum albumin (protective), platelet count, smoking history, and hypertension (predictors of higher risk). The nomogram achieved an AUC of 0.788 (95% CI 0.735-0.840) in the training cohort and 0.755 (95% CI 0.671-0.839) in the validation cohort; the wide validation confidence interval reflects the limited number of validation events (n = 35). On bootstrap internal validation (1000 resamples), the optimism-corrected AUC was 0.776. Calibration was acceptable in both cohorts (Hosmer-Lemeshow P = 0.794; calibration slope 0.944 [bootstrap-corrected]), and DCA suggested potential clinical utility. Conclusion:A four-variable nomogram based on serum albumin, platelet count, smoking history, and hypertension estimated in-hospital LEA risk in hospitalised patients with type 2 diabetes-related DFUs with moderate discrimination and acceptable calibration, and decision curve analysis suggested potential clinical utility. Because every predictor is available from routine clinical history and standard laboratory testing, the model may support early in-hospital risk stratification rather than treatment decisions. As this was a single-centre study with internal validation only, external multi-centre validation is required before routine clinical use.
Obesity is a major metabolic disorder with increasing global prevalence and limited long-term therapeutic success. Growing evidence indicates that the gut microbiota (GM) plays an important role in energy metabolism, immune homeostasis, and neuroendocrine regulation, making it a potential target for obesity management. Traditional Chinese Medicine (TCM), characterized by holistic and multi-target regulation, has increasingly attracted attention for its potential to modulate host metabolism through interactions with the GM. This review summarizes current evidence on the relationship between GM and obesity and examines how TCM interventions may regulate obesity through microbiota-related mechanisms. Particular attention is given to microbial metabolites, intestinal barrier function, and gut-brain communication. We further reinterpret classical TCM concepts, especially spleen function and the theory of "the spleen stores intent", from the perspective of microbial activity and gut-brain interactions to establish a conceptual bridge between traditional theory and contemporary microbiome science. According to different therapeutic strategies in TCM, supplementing qi and strengthening the spleen may help restore microbial diversity and short-chain fatty acid production, thereby contributing to improved metabolic homeostasis through the G-protein-coupled receptors 41/43 (GPR41/43)-glucagon-like peptide-1 (GLP-1) pathway. Resolving turbidity to activate the spleen may alleviate metabolic inflammation by reducing lipopolysaccharide translocation, regulating Toll-like receptor 4 (TLR4)-mediated signaling, and modulating bile acid metabolism via the farnesoid X receptor (FXR)/Toll-like receptor 5 (TLR5) axis. Regulating qi and awakening the spleen may help stabilize gut-brain communication through modulation of gut-derived hormones and central appetite-related neuropeptides. Meanwhile, emerging evidence suggests that microbial biotransformation of herbal compounds may influence their bioavailability and therapeutic responsiveness, highlighting the bidirectional nature of TCM-microbiota interactions. Additionally, we introduce the "neuro-immune-microbiome axis" to explain how non-pharmacological therapies may indirectly remodel the GM. Overall, this review proposes an integrative framework linking TCM theory with microbiome research to better understand the therapeutic potential of TCM in obesity. While current evidence remains largely associative and relies heavily on preclinical studies, this perspective may provide new directions for microbiota-targeted and system-level strategies in obesity management.
Purpose:Sleep disturbance is common in adults with type 2 diabetes mellitus (T2DM), but associated psychosocial factors may vary by anxiety symptom status. We examined the prevalence of sleep disturbance and associated factors among adults with T2DM in Hainan Province, China. Patients and Methods:This multicenter cross-sectional study included 1200 adults with clinician-confirmed T2DM recruited from endocrinology departments of eight tertiary hospitals. Anxiety symptoms were defined as Generalized Anxiety Disorder-7 score ≥5, and sleep disturbance as Athens Insomnia Scale score ≥6. Multivariable logistic regression models were fitted separately for participants with and without anxiety symptoms. Secondary and sensitivity analyses examined continuous sleep scores, a higher anxiety threshold, and overlap from sleep-related questionnaire items. Results:Of 1200 participants, 309 had anxiety symptoms and 891 did not. Sleep disturbance affected 631 participants (52.6%) and was more prevalent among those with anxiety symptoms than among those without (82.2% vs 42.3%). In the anxiety-symptom subgroup, higher Patient Health Questionnaire-9, Beck Hopelessness Scale, and post-traumatic stress symptom scores were associated with greater odds of sleep disturbance. In the subgroup without anxiety symptoms, higher Patient Health Questionnaire-9 and Perceived Deficits Questionnaire scores and higher educational level were associated with sleep disturbance. Conclusion:Sleep disturbance was common, particularly among participants with anxiety symptoms. Anxiety-stratified analyses identified different exploratory patterns of associated factors. These cross-sectional findings may support more focused sleep and psychosocial assessment but do not establish causal relationships, validated clinical subtypes, or treatment recommendations.
Neuregulin 4 (Nrg4) is an adipocyte-secreted factor belonging to the epidermal growth factor (EGF) family, and has been implicated in the regulation of metabolic homeostasis, particularly insulin resistance (IR). Preclinical studies have demonstrated that Nrg4 activates ErbB4 receptor tyrosine kinase and downstream signaling pathways such as PI3K/AKT and AMPK/mTOR, leading to inhibition of inflammatory responses, regulation of autophagy, and protection of mitochondrial function, all of which can ameliorate IR in animal models. However, clinical evidence regarding Nrg4's association with insulin sensitivity in humans remains inconsistent and even contradictory. While some studies report reduced circulating Nrg4 levels in patients with type 2 diabetes and a positive correlation with insulin sensitivity, others have found a negative correlation, suggesting that Nrg4 may play context-dependent or even opposing roles. This review aims to provide a comprehensive overview of the physiological characteristics and signaling mechanisms of Nrg4, critically evaluate the evidence for its role in improving IR, and explicitly address the existing discrepancies between preclinical and clinical findings. Finally, we discuss the therapeutic potential and safety considerations of targeting Nrg4 for IR and related metabolic diseases, acknowledging the current limitations and unresolved controversies.
Categorical criteria for diagnosing metabolic syndrome often fail to capture the continuous nature of metabolic risk and underlying patient heterogeneity. This narrative review evaluates the methodological evolution of quantitative severity assessment, focusing on the transition from conventional statistical scoring to advanced machine learning applications. Initial statistical models established the foundation for continuous risk evaluation by mathematically weighting core diagnostic components. Supervised machine learning approaches subsequently enhanced predictive precision by processing multidimensional datasets, with high-performing models frequently achieving area under the curve values exceeding 0.88. Concurrently, unsupervised clustering algorithms provide a data-driven method to identify distinct clinical endotypes linked to specific prognostic outcomes. Current research advances the field by integrating routine clinical data with multi-omics profiles, medical imaging, and wearable sensor inputs to construct dynamic metabolic phenotypes. However, clinical translation demands rigorous validation against hard cardiovascular endpoints, algorithmic transparency via explainable artificial intelligence, and strict adherence to standardized reporting guidelines. Future implementation must prioritize prospective trials, harmonize endotype definitions, and embed these validated algorithms within electronic health record systems to realize precision metabolic healthcare.
Objective:This study aims to investigate the association between the cardiometabolic index (CMI) and the presence of diabetic retinopathy (DR) among individuals diagnosed with type 2 diabetes mellitus (T2DM). Methods:A retrospective analysis was performed on clinical data from 2571 T2DM patients in Anhui Medical University Affiliated Lu'an Hospital. Based on fundus examination, subjects were classified into a group without DR (NDR, n=1606) and a group with DR (n=965). Clinical data and laboratory parameters were collected, and CMI was calculated, and explore its correlation with DR. Results:Among the 2571 patients, CMI values were markedly elevated in the DR cohort compared to the NDR cohort (P<0.001). Trend analysis showed that DR prevalence increased progressively across CMI quartiles (12.8%, 22.2%, 49.4%, 65.8%, P < 0.001), with a significant positive linear correlation (r = 0.430, P < 0.001). Multivariable analysis identified female sex (OR = 1.240, P = 0.020), longer diabetes duration (OR = 1.060, P < 0.001), higher CMI (OR = 1.167, P < 0.001), and elevated UACR (OR = 1.001, P < 0.001) were independent risk factors for DR. RCS analysis indicated that DR risk increased markedly when CMI exceeded 1.01 (P for overall < 0.001). ROC analysis demonstrated that CMI showed superior predictive performance for DR (AUC = 0.760, sensitivity = 74.8%, specificity = 68.8%) compared with diabetes duration (AUC = 0.640), UACR (AUC = 0.624), and sex (AUC = 0.527). Conclusion:The higher level of CMI is significantly related to DR in T2DM patients, and this correlation is independent of diabetic retinopathy. Therefore, in clinical practice, CMI may become an effective metabolic indicator for evaluating the risk of DR.
Introduction:Hyperglycaemia is common during acute illness and may occur in individuals with previously known diabetes, previously undiagnosed diabetes, or stress‑related hyperglycaemia. In hospital settings, definitions vary across studies, and data on admission hyperglycaemia among adult medical emergency patients in Uganda remain limited. This study aimed to determine the prevalence of hyperglycaemia and identify factors associated with it among newly admitted adult medical patients at Mbale Regional Referral Hospital (MRRH). Methods:We conducted a prospective cross-sectional study among newly admitted adult medical patients at the emergency ward of Mbale Regional Referral Hospital in eastern Uganda. Socio‑demographic, clinical, and laboratory data were collected using a pretested structured tool. Hyperglycaemia was defined as a random capillary blood glucose of at least 7.8 mmol/L at admission. Glycated haemoglobin (HbA1c) was used to classify participants with hyperglycaemia as having probable previously undiagnosed diabetes mellitus if HbA1c was ≥6.5%, or stress hyperglycaemia if HbA1c was ≤6.4%. Modified Poisson regression was used to estimate adjusted prevalence ratios with 95% confidence intervals. Results:A total of 449 participants were enrolled, of whom 51.2% were female. The prevalence of hyperglycaemia at admission was 42.8%, while 14.5% of the total study population were classified as having previously undiagnosed diabetes based on admission glucose and HbA1c. Among participants with hyperglycaemia, 27.6% had known diabetes, 38.5% were classified as having stress hyperglycaemia, and 33.9% were classified as having previously undiagnosed diabetes. Factors associated with hyperglycaemia were prior diagnosis of diabetes mellitus [aPR 1.9, 95% CI: 1.7-2.4, p<0.001], Modified Early Warning Signs (MEWS) scores ≥5 [aPR 1.5, 95% CI: 1.2-1.9, p=0.002] and Tertiary level of education [aPR 1.6, 95% CI: 1.1-2.3, p=0.019]. Conclusion:This study found a high point prevalence of admission hyperglycaemia among newly admitted adult medical patients, including a substantial proportion classified as having probable previously undiagnosed diabetes mellitus. Hyperglycaemia was independently associated with tertiary education, prior diabetes diagnosis, and higher illness severity. These findings suggest that admission glucose assessment may be useful for identifying undetected hyperglycaemia, supporting emergency triage, and guiding post‑discharge metabolic follow‑up among acutely ill medical patients. Because this was a single‑site cross‑sectional study, further prospective studies are needed to validate these findings, examine patient outcomes, and clarify how admission glucose assessment may inform inpatient monitoring and follow‑up pathways.
This systematic review and meta-analysis aimed to examine the differential effects of metformin on progression to type 2 diabetes mellitus (T2DM) among individuals with different prediabetes subtypes, including impaired fasting glucose (IFG), impaired glucose tolerance (IGT), and combined IFG+IGT. Following PRISMA guidelines, ten databases, including PubMed and Cochrane, were systematically searched from inception to May 2025. Eighteen randomized controlled trials were included, and relative risks (RRs) with 95% confidence intervals (CIs) were calculated using fixed- or random-effects models as appropriate. Subgroup analyses were conducted by prediabetes subtype and intervention duration. Metformin reduced the risk of progression to T2DM by 35% compared with lifestyle intervention or placebo (RR = 0.65; 95% CI: 0.55-0.77; P < 0.00001), with moderate heterogeneity. The preventive effect was strongest among individuals with IFG (RR = 0.38; 95% CI: 0.24-0.61; P < 0.0001), followed by those with IGT (RR = 0.58; 95% CI: 0.43-0.79; P < 0.0004) and combined IFG+IGT (RR = 0.77; 95% CI: 0.70-0.86; P < 0.00001). An intervention duration of ≤24 months was associated with a greater effect in the IGT subtype (RR = 0.27; 95% CI: 0.16-0.44; P < 0.00001). Metformin also increased the proportion of individuals achieving normoglycemia (RR = 1.80; 95% CI: 1.39-2.34; P < 0.0001). This study was limited by reliance on published aggregate data without individual patient-level information to adjust for potential confounders, variation in prediabetes diagnostic criteria across the publication years of the included studies, and heterogeneity in effect size comparisons. Overall, metformin may delay progression from prediabetes to T2DM, with the greatest observed benefit among individuals with IFG. Given the study heterogeneity and variability in diagnostic criteria, these findings should be interpreted cautiously. From a nursing and chronic disease prevention perspective, metformin may be considered as an adjunctive intervention for individuals with IFG when lifestyle intervention alone is insufficient.
Background:Diabetic kidney disease (DKD) is a major microvascular complication of type 2 diabetes mellitus (T2DM). Chronic low-grade inflammation has been implicated in the development and progression of DKD. The systemic inflammatory response index (SIRI), a novel composite inflammatory biomarker, has demonstrated prognostic value in various inflammatory and metabolic disorders. However, evidence regarding the association between SIRI and DKD remains limited. Methods:This retrospective cross-sectional study included 2421 hospitalized patients with T2DM. DKD was defined according to established clinical criteria. Multivariable logistic regression models were used to evaluate the association between SIRI and DKD after adjustment for demographic and clinical covariates. Restricted cubic spline (RCS), receiver operating characteristic (ROC), subgroup, sensitivity, and mediation analyses were additionally performed. Results:Among the 2,421 participants, 892 (36.8%) were diagnosed with DKD. Higher SIRI levels were significantly associated with increased odds of DKD in multivariable logistic regression analyses. Participants in the highest SIRI category had substantially greater odds of DKD compared with those in the lowest category. RCS analysis demonstrated a nonlinear positive association between SIRI and DKD risk. ROC analysis showed that the combination of age, sex, and SIRI had better discrimination ability for DKD than SIRI alone. Subgroup analyses demonstrated generally consistent associations across predefined subgroups, although significant interactions were observed for age and HbA1c status. Mediation analysis indicated that eGFR partially mediated the association between SIRI and DKD, accounting for approximately 46% of the total effect. Conclusion:Elevated SIRI was independently associated with increased odds of DKD in patients with T2DM. The association appeared nonlinear and was partially mediated through renal function impairment. SIRI may serve as a convenient inflammatory biomarker for identifying patients at higher risk of DKD.
Min Cui, Qin ChenTongde Hospital of Zhejiang Province Affiliated to Zhejiang Chinese Medical University (College of Integrated Traditional Chinese and Western Medicine Clinical Medicine), Hangzhou, Zhejiang, 301012, People’s Republic of ChinaCorrespondence: Qin Chen, Tongde Hospital of Zhejiang Province Affiliated to Zhejiang Chinese Medical University, Hangzhou, Zhejiang, 301012, People’s Republic of China, Email chenqin2858@163.com
