Currently, the diagnosis and monitoring of diabetes mellitus (DM) primarily rely on clinical symptoms, blood glucose measurements, and laboratory blood tests. With the continuous advancement of medical imaging, magnetic resonance imaging (MRI) is increasingly being applied to the study of diabetes and its associated complications. Given that the pancreas plays a pivotal role in the pathogenesis and progression of DM, quantitative MRI techniques have emerged as powerful tools; they provide not only fundamental structural information but also visualize the pathophysiological alterations of the pancreas throughout the disease course. This literature review suggests that quantitative pancreatic MRI holds great promise as a novel, non-invasive biomarker for evaluating diabetic pathophysiology, facilitating early diagnosis, and monitoring therapeutic efficacy. Advancing this field further, the integration of artificial intelligence and radiomics offers powerful tools for automated high-throughput mining of these datasets, though its clinical translation remains preliminary. Current implementation gaps-most notably the critical need for multi-center external validation and standardized models-must be recognized before these deep imaging phenotypes can be reliably utilized in clinical settings.

This study evaluated the clinicopathological profiles and prognostic trajectories of nondiabetic renal disease (NDRD) subtypes coexisting with type 2 diabetes mellitus (T2D).

The study cohort comprised of 123 patients with predominant NDRD subtypes: IgA nephropathy (T2D-IgAN, n = 52), membranous nephropathy (T2D-MN, n = 48), and podocytopathies (T2D-Podo, n = 23). Multivariate Cox regression was used to identify prognostic factors for renal outcomes over a median follow-up period of 80 months (interquartile range 62-102).

T2D-MN patients exhibited distinct characteristics compared to T2D-IgAN and T2D-Podo, including advanced age, higher incidence of nephrotic-range proteinuria and elevated total cholesterol. This group also demonstrated a greater susceptibility to atherosclerotic plaque formation. Pathological analysis revealed more severe glomerular sclerosis, interstitial inflammation, and C3 deposition in T2D-IgAN. Multivariate Cox regression identified three independent predictors of renal endpoints: glomerular C3 deposition (HR 3.021, 95% CI: 1.084-8.419), preserved estimated glomerular filtration rate (>60 mL/min/1.73 m²; HR 0.296, 95% CI: 0.110-0.796), and prolonged T2D duration (>10 years; HR 4.168, 95% CI: 1.389-12.503).

These findings suggest that integrating clinical and pathological parameters enhances the prognostic accuracy of NDRD in patients with diabetes, enabling timely therapeutic interventions to mitigate complications in high-risk cases.

Diabetes mellitus is a common metabolic disease affecting more than 500 million people worldwide. Macrophages, driving inflammation, immune dysregulation, and tissue injury, contribute to diabetes progression and diabetic complications. Nanomedicine offers unique advantages in drug delivery, tissue accumulation, and macrophage targeting, making it particularly suitable for modulating macrophage-mediated pathological processes in diabetes. In this review, we describe the role of macrophages in the pathological progression of diabetes mellitus and further summarize current strategies for using nanoparticles to target macrophages. We highlight the diagnostic and therapeutic potential of macrophage-targeted nanoparticles in diabetes and its related complications. Finally, we discuss key translational challenges, including biodistribution, off-target uptake, long-term immunological safety, toxicity, and clinical applicability. This review provides a distinct framework for understanding how macrophage-targeted nanomedicine can be developed to improve diabetes diagnosis, therapeutic modulation, and the management of diabetic complications.

Depression and impaired health-related quality of life are common after acute myocardial infarction (AMI) and have been associated with worse clinical and functional outcomes. However, local data describing these dimensions during the post-infarction period in public healthcare settings remain limited.

We conducted a cross-sectional observational study using data from the Prospective Myocardial Infarction Registry (REPRIM), including patients with ST-segment elevation myocardial infarction (STEMI) treated in a public tertiary care setting in Chile between 2019 and 2020. Health-related quality of life was assessed 30 days after the index event using the SF-36 questionnaire, and depressive symptoms were evaluated with the 17-item Hamilton Depression Rating Scale (HAM-D). Associations between quality of life and depressive symptoms were explored using multivariable linear regression models adjusted for age, sex, diabetes mellitus, hypertension and left ventricular ejection fraction, and mortality was described during the available follow-up.

During the study period, 121 patients with acute myocardial infarction were identified. Of the 100 patients included in REPRIM, 68 met the criteria for this subanalysis (alive at 30 days, successful contact and complete questionnaire data). Most patients exhibited at least mild depressive symptoms (94.1%), with a median HAM-D score of 12 (interquartile range 10-15). Higher depressive symptom severity was significantly associated with lower physical (PCS) and mental (MCS) component scores of the SF-36 in unadjusted analyses (ρ = -0.46 and ρ = -0.58, respectively; p < 0.001) and remained independently associated after multivariable adjustment [β = -1.26 [95% CI -2.06 to -0.46] for PCS; β = -1.50 [95% CI -2.40 to -0.61] for MCS; both p < 0.01]. Patients with moderate or higher depressive symptoms had significantly worse quality-of-life scores compared with those with mild symptoms. Mortality analyses were descriptive due to the limited number of events.

In this cross-sectional study of STEMI survivors treated in a public hospital, depressive symptoms were highly prevalent at 30 days and were consistently associated with poorer physical and mental health-related quality of life. These findings highlight the substantial burden of depressive symptoms early after myocardial infarction and support the relevance of integrating mental health and quality-of-life assessment into post-infarction follow-up within public healthcare systems, while acknowledging the limitations of our small, single-centre study.

Radiofrequency ablation is a useful alternative to surgery for small renal cell carcinoma in nonsurgical candidates; however, its long-term clinical outcomes remain controversial. This study evaluated the long-term outcomes of radiofrequency ablation in patients with pathologically diagnosed T1a renal cell carcinoma.

This single-center retrospective study included 60 consecutive patients (median age, 67.0 years) who underwent radiofrequency ablation for 62 pathologically diagnosed T1a renal cell carcinomas between 2002 and 2014, all without prior renal cell carcinoma or other active malignancies. Tumor diameters ranged from 1.0 to 3.9 cm (median, 2.3 cm), and 22 (35.5%) renal cell carcinomas were centrally located. Overall and cancer-specific survival, local tumor control, and complications were evaluated.

Complete tumor ablation was achieved in 53 renal cell carcinomas (85.5%) after the initial radiofrequency ablation and in all renal cell carcinomas after the second radiofrequency ablation. The local tumor control rates were 96.3% (95% confidence interval, 91.2%-100%) and 91.6% (95% confidence interval, 83.6%-99.6%) at 5 and 10 years, respectively. During a median follow-up period of 9.0 years (range, 1.3-16.5 years), renal cell carcinoma-related death in only one (1.7%) patient. Overall and cancer-specific survival rates were 98.3% (95% confidence interval, 94.9%-100%) and 100% at 5 years, and 85.7% (95% confidence interval, 75.0%-96.4%) and 97.4% (95% confidence interval, 92.5%-100%) at 10 years. Univariate analysis identified diabetes mellitus (p = 0.007) and chronic kidney disease (p = 0.039) as significant prognostic factors. No procedure-related deaths or major complications were observed. Dialysis was initiated in four (6.7%) patients.

Radiofrequency ablation is a safe procedure with strong anticancer effects and contributes to the long-term prognosis of patients with T1a renal cell carcinoma.

Malaysia has the highest obesity prevalence in Southeast Asia, driving the burden of type 2 diabetes mellitus (T2DM) and its healthcare costs. Long-term real-world cost-effectiveness data on bariatric surgery from Malaysia are absent. We evaluated the clinical outcomes, safety, and exploratory cost-effectiveness of bariatric surgery in Malaysian patients with obesity and T2DM.

Retrospective cohort study of 180 patients undergoing laparoscopic sleeve gastrectomy or Roux-en-Y gastric bypass at HCTM, Universiti Kebangsaan Malaysia (2014-2016), with 5-year clinical follow-up. BMI and HbA1c were analysed using generalised estimating equations (GEE) with a Gaussian family, identity link and exchangeable working correlation. An exploratory cost-effectiveness analysis compared 20 surgical patients with 20 matched conventional-management patients (2012-2014) over a 10-year horizon from the healthcare-payer perspective. The incremental cost-effectiveness ratio (ICER) was expressed per 1% HbA1c reduction, with one-way deterministic and probabilistic sensitivity analyses.

Mean BMI decreased from 49.29 ± 8.97 to 25.33 ± 4.25 kg/m² at 5 years; HbA1c fell from 6.37 ± 1.37% to 5.62 ± 0.68% (both GEE p<0.001). The complication rate was 2.2%, and 76% of patients were discharged ithin 2 days. The base-case ICER was RM 4683 per 1% HbA1c reduction; probabilistic analysis yielded a median ICER of RM 4828 (95% credible interval: cost-saving to RM 32,286) and a 59% probability of cost-effectiveness at a willingness-to-pay threshold of RM 7500 per 1% HbA1c reduction.

In this single-centre Malaysian cohort, bariatric surgery produced durable improvements in BMI and HbA1c with low complication rates and a favourable exploratory ICER. Findings should be interpreted in light of the retrospective design and small economic cohort, and confirmed in multicentre prospective studies.

This study aimed to investigate the expression levels and significance of Protein Arginine Methyltransferase 1 (PRMT1) in patients with diabetic kidney disease (DKD).

236 patients with Type 2 Diabetes Mellitus (T2DM) who were admitted to Hebei Provincial People's Hospital from October 2023 to May 2025 were enrolled in this study. According to the urinary albumin-creatinine ratio (UACR), they were divided into normal albuminuria group (D1), microalbuminuria group (D2) and macroalbuminuria group (D3). 93 healthy people undergoing routine examination during the same period served as normal control (NC). Collect clinical data, use Enzyme-Linked Immunosorbent Assay (ELISA) to detect serum PRMT1. Detection of glucose and lipid metabolism and renal function indicators were used to evaluate intergroup differences and explore the relationship between PRMT1 and DKD.

Serum PRMT1 level rose gradually from NC group to D1, D2 and D3 groups (P<0.05), in T2DM patients, there was a significant positive association between PRMT1 expression and UACR (P < 0.05). Multivariate logistic regression analysis demonstrated that elevated PRMT1 expression was independently associated with both early and clinical DKD, and receiver operating characteristic (ROC) analysis indicated PRMT1 had discriminative ability for DKD.

Serum PRMT1 concentrations were significantly elevated in patients with DKD compared with those with type 2 diabetes without nephropathy and healthy individuals, and levels increased with advancing disease severity, which implies that PRMT1 could be a valuable diagnostic marker for DKD.

Cardiovascular complications of diabetes mellitus (DM) are responsible for morbidity and mortality in DM patients. Recent evidence highlights the pathophysiological role of the renin-angiotensin-aldosterone system in DM. This study determined whether chronic angiotensin (1-7) (Ang (1-7); 576 μg/kg, s.c., 4 weeks) treatment improves vascular reactivity in mesenteric small resistance arteries of streptozotocin-induced diabetic rats using a wire myograph system and to investigate the underlying mechanisms. Increased sensitivity to vasoconstrictors and decreased responses to endothelium-dependent vasodilators in diabetic rats compared to control rats were partially reversed by Ang (1-7) treatment. Nω-nitro-L-arginine methyl ester (L-NAME, 10^-4 M) incubation significantly decreased vasorelaxant responses to acetylcholine (ACH, 10^-10-10^-5 M) in all groups except the diabetic group. Superoxide dismutase (SOD, 50 U/mL) incubation produced significant increases in vasorelaxant responses to ACH only in the diabetic groups. Glibenclamide (10^-5 M), 4-aminopyridine (4-AP, 5 mM), indomethacin (INDO, 10^-5 M), or catalase (CAT, 200 U/mL) incubations did not alter ACH responses in any experimental groups, whereas charybdotoxin (ChTX, 10^-7 M) or apamin (APA, 10^-7 M) produced significant decreases in ACH-induced vasorelaxation, similar in extent in the control and diabetic rats. Following co-incubation with L-NAME and INDO, ACH-induced vasorelaxation in 30 mM KCl pre-contracted arterial rings did not differ significantly between the groups. These findings indicate that improved nitric oxide bioavailability and reduced superoxide activity contribute to the beneficial vascular effects of Ang (1-7) in diabetic rat resistance arteries. Further in vivo studies are warranted to clarify its therapeutic relevance. SUMMARY: Ang (1-7) improves vascular function in diabetic rat resistance arteries. Treatment increases NO bioavailability and reduces oxidative stress. Vasoconstrictor sensitivity is decreased, improving endothelium-dependent vasorelaxation. Ang (1-7) restores vascular responses to endogenous vasoactive agents. Findings suggest Ang (1-7) as a potential target for diabetes-related vascular issues.

Type 2 diabetes mellitus (T2DM) is increasingly recognized as a heterogeneous, multisystem disease that extends beyond chronic hyperglycemia to encompass cardiovascular disease, chronic kidney disease, and metabolic dysfunction-associated steatotic liver disease. Central to this expanded disease spectrum is insulin resistance arising from coordinated metabolic, inflammatory, neuroendocrine, and immune disturbances across multiple organs. Rather than a uniform defect in insulin signaling, insulin resistance represents a dynamic, tissue-specific, and stage-dependent process involving multiorgans, with substantial interorgan crosstalk. This review synthesizes contemporary mechanistic insights into the pathogenesis of insulin resistance in T2DM, integrating molecular pathways, organ-specific dysfunction, and systemic metabolic networks. Ectopic lipid accumulation, mitochondrial dysfunction, chronic low-grade inflammation, immune dysregulation, and gut dysbiosis are highlighted as convergent processes that impair insulin action and drive clinical heterogeneity. Insulin resistance is further contextualized within the cardiovascular-kidney-metabolic syndrome framework, which unifies metabolic, renal, and cardiovascular disease through shared upstream mechanisms. In addition, how contemporary glucose-lowering therapies exert benefits beyond glycemic control by targeting insulin resistance, metabolic reprogramming, and interorgan crosstalk is discussed. Collectively, insulin resistance is positioned as a central pathophysiological driver of T2DM and its complications, supporting a shift toward mechanism-based, organ-protective, and precision-oriented therapeutic strategies.

The impacts of cardiometabolic risk factors (CMRFs) and the biomarkers on disease severity in metabolic dysfunction-associated steatotic liver disease (MASLD) remain elusive. Accordingly, a multicenter study by recruiting MASLD patients from a nationwide registry database was conducted with a total of 2882 MASLD patients (54.1% males, mean age = 55.6 ± 13.9 years, mean body mass index [BMI] = 28.1 ± 4.9 kg/m²) being recruited. The proportions of patients carrying CMRFs of overweight/obesity, hypertension, hypertriglyceridemia, low high-density lipoprotein cholesterol level, and diabetes/prediabetes were 91.2%, 74.5%, 54.8%, 59.6%, and 74.5%, respectively. There was a significant linear trend between significant fibrosis and CMRFs (5.1%, 27%, and 54.6% in patients with one CMRF, 3 CMRFs, and ≥ 4 CMRFs, respectively, p = 0.009). The adjusted odds ratios (aOR) with 95% confidence intervals (CIs) for advanced fibrosis in patients of hemoglobin A1c (HbA1c) 5.7%-6.5%, 6.5%-8.0%, and > 8.0% were 1.02 (95% CI = 0.68-1.53, p = 0.93), 1.83 (95% CI = 1.16-2.88, p = 0.01), and 2.78 (95% CI = 1.45-5.34, p = 0.002), respectively. The significant risk factors for advanced fibrosis in MASLD were age > 60 years (aOR = 12.08, 95% CI = 6.23-23.46, p < 0.001), elevated transaminase level (aOR = 1.06, 95% CI = 1.05-1.09, p < 0.001), and diabetes (aOR = 1.51, 95% CI = 1.02-2.26, p = 0.04). In conclusion, there was a significant linear association between advanced fibrosis and the items of CMRFs. The HbA1c level could serve as a predictive biomarker for advanced fibrosis in MASLD with the implication that diabetes control is mandatory for patients with MASLD.