This systematic review aimed to evaluate the prevalence and risk factors of Incontinence-Associated Dermatitis (IAD) in elderly patients.

A systematic search was conducted across 10 databases, including PubMed, Embase, Web of Science, Cochrane Library, CINAHL, Ovid MEDLINE, Scopus, VIP, WanFang, and CNKI, from inception to November 2023. Two reviewers independently performed study screening, data extraction, and risk-of-bias assessment. Prevalence meta-analysis was restricted to cross-sectional studies, whereas risk factor synthesis included all eligible observational studies, with priority given to multivariable-adjusted effect estimates. Meta-analysis was conducted using RevMan 5.3 and R 4.4.2, with random-effects models applied for all pooled analyses. This review was conducted in accordance with PRISMA 2020 and prospectively registered in PROSPERO (CRD42023442585).

A total of 16 studies were included, involving 30,747 geriatric patients. For prevalence estimation (4 eligible cross-sectional studies, 18,619 incontinent geriatric patients), the pooled prevalence of IAD was 14.81% (95%CI: 4.16%-41.04%), with substantial heterogeneity (I²=98.4%, P < 0.001). For factor association analysis (11 case-control studies, 4 cross-sectional studies, 1 cohort study), 12 statistically significant factors associated with IAD were identified, including diabetes mellitus (adjusted OR = 2.17, 95%CI: 1.23-3.84), diarrhea (OR = 3.37, 95%CI: 2.38-4.78), incontinence frequency ≥ 3 times/day (OR = 4.70, 95%CI: 2.85-7.76), dual incontinence (OR = 4.03, 95%CI: 1.52-10.71); antibiotic use (OR = 3.26, 95%CI: 1.67-6.36); prolonged hospitalization (OR = 3.33, 95%CI: 2.60-4.26); presence of ≥ 3 comorbidities (OR = 2.53, 95%CI:1.48-4.32); mechanical ventilation (OR = 2.67, 95%CI: 1.20-5.93); and infection (OR = 2.93, 95%CI: 1.72-4.99) (all P<0.05). The certainty of evidence for primary outcomes ranged from very low to moderate per the GRADE framework.

IAD is common among elderly patients, with a pooled prevalence of 14.81%. Individualized prevention and management strategies should be implemented according to the identified risk factors.

Type 2 diabetes (T2D) subgroups defined by clinical variables differ in disease progression and treatment response. To uncover potential molecular drivers of this heterogeneity, we performed a multi-omics analysis of 826 drug-naïve T2D patients from two phase 3 trials of the insulin sensitizer chiglitazar. Here we show that severe insulin-resistant diabetes (SIRD) is characterized by distinct miRNA profiles (e.g., miR-122-5p) correlated with liver injury, and metabolic shifts in amino acids and primary bile acids. Mild obesity-related diabetes (MOD) showed the lowest level of phenylacetylglutamine, a metabolite known to promote cardiovascular disease. Severe insulin-deficient diabetes (SIDD) exhibited high pancreas-specific miR-7-5p, while mild age-related diabetes (MARD) presented the mildest abnormalities. Finally, integrating these multi-omics signatures into machine learning models enhanced prediction of insulin sensitizer efficacy over clinical data alone. Our findings define the distinct molecular signatures of T2D subgroups, facilitating the prediction of heterogeneous treatment responses and supporting personalized clinical management.

A woman in her 40s initially diagnosed with type 1 diabetes in 1994 exhibited an atypical 30-year metabolic course, characterised by fluctuating insulin sensitivity, prolonged insulin independence and later insulin resistance despite a non-obese phenotype.

Owing to the unusual clinical trajectory and a strong family history of young-onset diabetes, genetic testing identified a heterozygous pathogenic INSR mutation (p.M1180K), confirming Type A Insulin Resistance Syndrome (TAIRS).

Management evolved from insulin therapy to oral hypoglycaemic agents, including metformin and gliclazide alongside lifestyle modification resulting in partial glycaemic improvement.

This case underscores the diagnostic challenge of TAIRS, which is frequently misclassified as type 1 or type 2 diabetes and highlights the importance of early genetic evaluation and multidisciplinary care.

Diabetes mellitus continues to be a global public health concern, owing to its increasing incidence, complex etiology, and the limitations of standard therapy regimens. Conventional therapeutic strategies often face several limitations including poor bioavailability, frequent administration, and absence of real-time blood sugar regulation. Recent advancement of smart nanotechnology has provided new opportunities for prevention, diagnoses, and management of diabetes as a part of smart health concept and precision medicine. This review highlights the recent trends in the design and application of nanotechnology for managing diabetes specifically focusing on two areas, glucose monitoring and drug delivery. Novel drug delivery systems are revolutionizing diabetes treatment, providing better pharmacokinetic control, adherence of patients, reduction of side effects, and target/stimuli responsive therapy. Recent developments in this area include sustained release implants and depots for extended periods of glycemic control; nanoparticles and liposomes for improved oral absorption and protection of insulin against enzymatic hydrolysis; transdermal and microneedles for minimal invasive delivery of insulin and peptides; inhalable dosage forms for faster systemic absorption; and glucose responsive 'smart' devices which deliver drugs only when required due to hyperglycemia. The use of nanotechnology-based biosensors and wearable devices has enabled the development of glucose monitoring based on their improved sensitivity, specificity, and integration into digital healthcare applications. Nanotechnology, coupled with artificial intelligence, and real-world health data, enhances personalized diabetes management through predictive monitoring and adaptive insulin delivery systems. Despite tremendous achievements, still some concerns persist, related to clinical translation, biosafety issues, and regulations. With continued interdisciplinary research that integrates the materials science, bioengineering, and clinical medicine, smart nanotechnology holds substantial promise to shift diabetes care, enabling an improvement in diabetic treatment from symptomatic to a physiologically sounder approach.

In advanced diabetic kidney disease (DKD), tubulointerstitial fibrosis (TIF) is a key histopathological lesion accompanying progressive renal functional decline. However, the tubular mechanisms that drive tubulointerstitial fibrogenesis remain incompletely understood. N-acetyltransferase 10 (NAT10) mediates mRNA N4-acetylcytidine (ac4C) modification, but its role and therapeutic potential in DKD are unknown. We investigated NAT10 regulation and function using cultured tubular cells, diabetic mouse models, patient kidney specimens, and tubule-specific Nat10 knockout mice, together with pharmacological treatment using guanosine diphosphate disodium salt. High glucose or diabetes increased tubular NAT10 abundance in cultured cells, mouse kidneys, and human DKD tissues through activation of NF-κB signaling. Mechanistically, NAT10 in tubular cells stabilized Brd4 and Pfkm mRNAs through ac4C modification, activating the STAT3/TGF-β and lactate/H3K18 lactylation pathways. These pathways synergistically promoted fibroblast activation through NOTCH/SMAD3 signaling and formed a positive feedback loop with NF-κB. Tubule-specific Nat10 deletion reduced Brd4 and Pfkm expression, suppressed the associated signaling cascades, and mitigated kidney fibrosis in the DKD model. Consistently, guanosine diphosphate disodium salt alleviated renal injury and fibrosis in db/db mice. Thus, NAT10 drives tubular fibrosis through ac4C-dependent profibrotic signaling, supporting NAT10 inhibition as a potential therapeutic strategy for DKD.

Mitochondrial dysfunction is a hallmark of acute and chronic kidney diseases. This study investigates the expression landscape and potential association of FNDC5 with renal injury.

We integrated human scRNA-seq, mouse spatial transcriptomics (ischemia-reperfusion injury model), in vitro high-glucose (HG) models in proximal tubule cells and podocytes, and a constitutive Fndc5 knockout mouse model. Candidate transcription factor occupancy at the FNDC5 promoter was examined by ChIP-qPCR, and associations were assessed in a non-insulin-dependent diabetes mellitus mouse model.

scRNA-seq localized FNDC5 to specific tubules, showing downregulation in diabetic nephropathy. Spatial transcriptomics confirmed a distinct loss of cortical Fndc5 following ischemia-reperfusion injury. In vitro, HG treatment suppressed FNDC5, reduced cell viability, and triggered mitochondrial fragmentation, evidenced by increased DRP1 phosphorylation and downregulated MFN1/OPA1. ZEB1 and CREB1 were identified as candidate transcription factors showing occupancy at the FNDC5 promoter. Genetic deletion of Fndc5 reproduced this fission-permissive shift and reduced PGC1α expression under basal, non-diabetic conditions, providing loss-of-function evidence that Fndc5 deficiency is sufficient to reproduce this phenotype, independent of any additional metabolic stressor. In vivo, diabetic mice exhibited diminished FNDC5 levels, which correlated with an oxidative stress-associated marker (4-HNE) and reduced expression of the biogenesis-associated marker PGC1α.

FNDC5 downregulation is a conserved feature of renal injury associated with mitochondrial fission, and genetic loss-of-function data indicates that Fndc5 deficiency is sufficient to reproduce selected features of this fission-permissive mitochondrial phenotype; whether FNDC5 acts through a defined downstream pathway remains to be established.

Type 2 diabetes mellitus (DM) is a progressive disease worldwide that leads to various complications. Given the roles of the hormones amylin and irisin and the enzyme sirtuin 1 (SIRT1) in metabolism and oxidative stress, we focused on these parameters in the serum of patients.

We investigated the associations between serum amylin, irisin, and SIRT1 levels and diabetic nephropathy (DN), an important complication of DM.

Patients with DM (n = 50) and DN (n = 50) were included in this single-center cross-sectional study. Various parameters were measured from fasting blood and urine samples. Serum amylin, irisin, and SIRT1 levels were measured using enzyme-linked immunosorbent assay kits. In addition to demographic characteristics, fasting blood sugar, glycated hemoglobin, serum insulin, urine creatinine, and estimated glomerular filtration rate were used to classify participants.

After adjustment for age, diabetes duration, body mass index, fasting blood sugar, glycated hemoglobin, homeostasis model assessment of insulin resistance, triglycerides, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol, amylin levels were significantly lower, whereas irisin and SIRT1 levels were significantly higher, in the DN group than in the DM group. Multivariable logistic regression showed that higher amylin levels were associated with lower odds of DN, whereas higher irisin and SIRT1 levels were associated with higher odds of DN. Receiver operating characteristic curves were used to evaluate the ability of these biomarkers to discriminate between the DM and DN groups. In addition, mediation analysis showed associations among irisin, SIRT1, and DN.

These findings suggest that irisin and SIRT1 are associated with DN status in patients with diabetes and may provide insights into metabolic complications. However, longitudinal studies are needed to establish causality.

The interplay between sympathetic nervous system activation and metabolic disorders, particularly type 2 diabetes mellitus (T2DM) and hypertension, has been increasingly recognized as a critical factor in cardiovascular morbidity and mortality. This review explores the potential mechanisms linking sympathetic overactivity to insulin resistance (IR) and T2DM, highlighting the role of renal denervation (RDN) as a promising therapeutic intervention. Sympathetic activation contributes to metabolic dysregulation by increasing plasma fatty acids, enhancing hepatic gluconeogenesis, and impairing pancreatic insulin release, while also inducing vasoconstriction and reducing glucose uptake in skeletal muscle. RDN, a catheter-based procedure targeting renal sympathetic nerves, has shown efficacy in managing resistant hypertension and improving glucose metabolism by reducing sympathetic drive, normalizing hepatic gluconeogenesis gene expression, and enhancing insulin sensitivity. Experimental and clinical studies suggest that RDN may mitigate IR, improve glycemic control, and reduce renal complications in diabetic models, independent of obesity or glucose tolerance status. However, the long-term effects on glycemic control and broader clinical applicability require further investigation.

Type 2 diabetes mellitus (T2DM) is a highly prevalent and rapidly expanding global metabolic disorder. Medicinal mushrooms have recently been proposed as promising functional foods, owing to their broad range of bioactive compounds, including β-glucans and other polysaccharides, triterpenoids, phenolic metabolites, sterols, nucleoside analogs, and sulfur-containing antioxidants. Their bioactivity is increasingly understood as an emergent property of multi-scale interactions, in which structural glycan complexity, supramolecular organization, and chemically diverse low-molecular-weight metabolites act in a network-like fashion rather than through single-target mechanisms. This review provides an integrated synthesis of the antidiabetic potential of medicinal mushrooms, encompassing ethnopharmacological origins, chemical diversity, preclinical and clinical evidence, and mechanistic pathways. Preclinical studies consistently report improvements in glucose homeostasis, insulin sensitivity, lipid metabolism, and redox balance across diverse experimental models. These effects are associated with modulation of insulin-PI3K/Akt and AMPK signaling, Nrf2-dependent antioxidant responses, NF-κB-driven inflammatory pathways, and gut microbiota-host metabolic interactions involving short-chain fatty acids and incretin signaling. However, most mechanistic evidence remains pathway-associated rather than causally validated, and the clinical relevance of many findings is limited by uncertain dose-response relationships, sparse pharmacokinetic data, preparation heterogeneity, and incomplete safety evaluation. Mushroom-drug interactions, liver safety, and environmental contaminant screening of concentrated mushroom-derived products warrant particular attention. Together, these factors constrain clinical translation, further compounded by heterogeneity of interventions, lack of standardization, short trial durations, and limited integration of mechanistic endpoints. Overall, medicinal mushrooms show potential as multi-target functional foods capable of modulating core pathological networks in T2DM. Future progress will critically depend on rigorous standardization of bioactive preparations, mechanistically driven clinical trials, and systems-level multi-omics integration to establish causal links between fungal bioactives and metabolic outcomes.

Time-restricted eating (TRE), a novel dietary approach for the management of type 2 diabetes mellitus (T2DM), has been shown to affect the metabolic panel. Accordingly, this study aimed to evaluate the efficacy of the TRE on glycemic control, lipid profiles, anthropometric measurements, metabolic markers, and sleep-related outcomes in patients with T2DM.

A systematic search was conducted in PubMed, Embase, Web of Science, and the Cochrane Library from inception up to May 2026. A random-effects model was used, and effect sizes are reported with 95% confidence intervals (CIs). Because of substantial heterogeneity, pooled estimates are presented as hypothesis-generating rather than confirmatory.

Thirteen studies (n = 544 participants) were included from 915 records. The pooled analysis suggested that TRE may be associated with a reduction in glycemic control (HbA1c; WMD: -0.46%; 95% CI: -0.91, -0.00; p = 0.048) and in central adiposity (WC; SMD: -0.55; 95% CI: -1.09, -0.02; p = 0.042); however, these findings are based on low- to moderate-certainty evidence with very high heterogeneity (I ² > 90% for most outcomes). No significant effects were observed for fasting blood glucose (FBG), homeostatic model assessment for insulin resistance (HOMA-IR), lipid profile, blood pressure, dietary intakes, or sleep outcomes (p > 0.05). The reduction in body mass index (BMI) was not robust; it was entirely driven by a single study, as omitting this trial in the leave-one-out sensitivity analysis rendered the pooled estimate non-significant. Subgroup analyses based on duration, sample size, and age were underpowered and did not explain the heterogeneity. Quality assessment showed that most RCTs had a low risk of bias, but the GRADE certainty of evidence was downgraded to low or moderate for all outcomes, mainly due to serious inconsistency and imprecision.

TRE may offer a straightforward dietary approach that could have some benefits for glycemic control (HbA1c) and central adiposity (WC) in individuals with T2DM. However, due to substantial statistical heterogeneity, small sample sizes, the fragility of pooled estimates, and low-to-moderate GRADE certainty, the current evidence does not support a definitive clinical recommendation. For all other outcomes-weight, lipids, blood pressure, sleep, dietary composition, no consistent or robust evidence of an effect was found. High-quality, long-term RCTs are needed before firm conclusions can be drawn.