Heart failure (HF) and diabetes frequently coexist and are associated with worse outcomes, yet contemporary evidence on the prevalence and clinical correlates of diabetes in hospitalized patients with HF in China remains limited.

Data for this study were obtained from Zigong Fourth People's Hospital. A total of 2,008 adults hospitalized with HF were included, of whom 466 had diabetes. Demographic, clinical, hemodynamic and laboratory variables were extracted from the first admission records. We estimated the prevalence of diabetes and used univariate and multivariable logistic regression to identify factors associated with diabetes. Machine learning models were applied to rank variable importance, and restricted cubic splines were used to explore the shapes of these associations. Sex- and age-stratified analyses were further conducted to assess heterogeneity.

The prevalence of diabetes among hospitalized patients with HF was 23.21% (95% CI: 21.39-25.13). In multivariable models, female sex, higher systolic blood pressure, statin use, elevated white blood cell (WBC) count, and higher serum potassium were associated with greater odds of diabetes, whereas higher high-density lipoprotein cholesterol (HDL-C) was inversely associated with diabetes (OR = 0.53, 95% CI: 0.37-0.76). WBC, potassium and HDL-C consistently ranked among the top contributors in both machine learning models. Restricted cubic splines revealed a nonlinear association between WBC count and diabetes, while potassium and HDL-C showed monotonic relationships. In stratified analyses, potassium and HDL-C remained associated with diabetes in females and in patients aged ≥70 years.

In Chinese inpatients with HF, approximately one in four had concomitant diabetes. WBC count, blood pressure, potassium and HDL-C were associated with diabetes status, with some variation across sex and age groups. These findings provide additional evidence on the clinical characteristics associated with diabetes in hospitalized patients with HF.

To identify clinical, sociodemographic and glucometric factors associated with achieving international glycaemic targets derived from intermittently scanned continuous glucose monitoring (isCGM) in adults with type 1 diabetes mellitus (T1DM) treated with multiple daily injections (MDI) in Andalusia, a region with universal access to isCGM.

A cross-sectional, population-based study was conducted using centralized electronic health records from the Andalusian Public Health System (APHS). Adults with T1DM using isCGM for ≥1 year and integrated glucometric data in Electronic Health Records in APHS in the 14 days preceding the download were included. Four glycaemic endpoints were evaluated: time in range (TIR ≥ 70%), time above range (TAR < 25%), time below range (TBR < 5%), and achievement of full AGP profile. Univariate analyses and multivariable logistic regression models were used to identify independent predictors.

A total of 7,885 individuals were included. Overall, 24.8% achieved TIR ≥ 70%, 35.0% TAR < 25%, 72.9% TBR < 5%, and 12.3% met the full AGP profile. Lower HbA_1c, lower glycaemic variability and a higher number of daily scans were consistently associated with achieving glycaemic targets. Older age and male sex were independent predictors of TIR ≥ 70%. Socioeconomic status showed a significant association: individuals in the intermediate-income group had higher odds of achieving TIR, TAR and full AGP criteria. No socioeconomic associations were observed for TBR < 5%.

In a real-world setting with universal isCGM provision, clinical, sociodemographic and glucometric determinants independently influence the achievement of glycaemic targets in adults with T1DM. Integrating advanced monitoring metrics with explicit consideration of social determinants may enhance the precision and equity of glycaemic management strategies.

Sustained glycemic control in type 2 diabetes mellitus (T2DM) remains difficult in routine care. Long-term real-world evidence on diabetes management platforms in Traditional Chinese Medicine (TCM) hospitals is limited.

We conducted a real-world retrospective observational study at Guangdong Provincial Hospital of Traditional Chinese Medicine. Adults with T2DM enrolled in a hospital-based chronic disease management platform between January 2017 and December 2018 were followed for up to 36 months. Primary outcomes were longitudinal changes in glycated hemoglobin (HbA1c) and HbA1c target attainment (<7.0%). Secondary outcomes included fasting blood glucose (FBG), postprandial blood glucose (PBG), body mass index (BMI), and self-reported lifestyle and self-management behaviors. Linear mixed-effects models and generalized estimating equations were used for longitudinal analyses.

A total of 546 patients were included. HbA1c decreased significantly over 36 months, and the proportion achieving HbA1c <7.0% increased from 30% at baseline to 49% at 12 months and remained around 45% at 24 and 36 months. Patients with baseline HbA1c >9.0% showed the greatest absolute reductions, whereas those with baseline HbA1c <7.0% generally maintained near-target levels. Clinically meaningful HbA1c reductions were common among participants with paired measurements, and sustained HbA1c target attainment was also observed across follow-up visits. In contrast, longitudinal changes in FBG were not significant, while reductions in PBG and BMI were modest. Improvements in lifestyle and self-management behaviors were limited.

In this TCM hospital setting, platform-based chronic disease management was associated with sustained improvement in HbA1c over 3 years. Greater benefit was observed in patients with poor baseline glycemic control, although improvements in behavioral indicators and other metabolic measures were limited.

This study examined the association between plasma pentosidine concentrations-an advanced glycation end-product marker-and skeletal muscle morphometric indices, physical function, and sarcopenia among community-dwelling older adults without diabetes.

This cross-sectional study analyzed data from the 2023 Itabashi Longitudinal Study on Aging in Itabashi Ward, Tokyo, Japan. Participants aged ≥ 70 years were included. Associations between pentosidine concentrations and skeletal muscle morphometric indices and physical function were examined using multiple linear regression adjusted for age, sex, and estimated glomerular filtration rate (eGFR). To explore sex differences, pentosidine × sex interaction terms were tested. Multivariable logistic regression with the same covariates examined associations with impaired physical function, sarcopenia, and severe sarcopenia defined by the Asian Working Group for Sarcopenia 2019 criteria.

Among 424 participants (mean age 75.7 years; 48.3% women), the mean plasma pentosidine concentration was 5.59 μg × 10^-2/mL, with no sex difference. In quartile-based analyses adjusted for age and eGFR, higher pentosidine concentrations were associated with lower skeletal muscle mass index (SMI) and slower gait speed in women, but not in men. In multivariable analyses adjusted for age, sex, and eGFR, higher pentosidine concentrations were independently associated with lower SMI, lower whole-body and limb phase angles, and lower short physical performance battery scores. Pentosidine levels were not significantly associated with grip strength, chair rise performance, sarcopenia, or severe sarcopenia. No significant pentosidine × sex interactions were observed.

Higher plasma pentosidine concentrations were associated with lower skeletal muscle mass and unfavorable muscle-related indices in older adults without diabetes. Although stratified analyses suggested stronger associations in women, interaction testing did not support significant sex-specific effects.

Although continuous glucose monitoring (CGM) in adults with type 2 diabetes (T2D) has known glycemic benefits, the underlying behavioural and psychosocial processes driving these outcomes remain poorly understood. We examined how CGM influences patient-reported outcomes and whether changes in those outcomes predict glycemic improvement.

This 6-month prospective observational study included 115 adults with T2D and elevated HbA1c who did not use fast-acting insulin and initiated CGM through a real-world program. At baseline, 3- and 6-months, HbA1c, medication use/changes and key psychosocial and self-care behaviours were assessed. Longitudinal structural equation models assessed changes over time and predictors of HbA1c reduction. Post hoc moderation analyses explored whether the effect of self-care behaviour improvements on HbA1c outcomes depended upon new medication starts at baseline.

HbA1c declined significantly from 9.4% (79 mmol/mol) at baseline to 7.3% (56 mmol/mol) at both 3 and 6 months (ps < 0.001). Participants reported increased diabetes engagement, reduced distress, increased physical activity, fewer missed medications and less overeating (ps < 0.001). In multivariate models, greater HbA1c reduction was independently predicted by: (1) starting a new diabetes medication in the few months before baseline (b = -1.06, p < 0.001); (2) increases in physical activity (b = -0.13, p = 0.040); and (3) improvements in medication-taking (b = 2.33, p < 0.001). Post hoc moderation analysis revealed that behaviour changes were most predictive of glycemic benefit among participants who had not started a new diabetes medication pre-baseline.

Real-world CGM initiation was associated with significant improvements in glycemic control, self-care behaviours and psychosocial outcomes. Behaviour change-notably, improved diet and physical activity-was a key contributor to glycemic gains, particularly among those not undergoing medication adjustments prior to CGM initiation. These findings support CGM as a catalyst for engagement and behaviour change in T2D management.

BACKGROUND Elderly patients with both coronary heart disease (CHD) and diabetes mellitus (DM) undergoing off-pump coronary artery bypass grafting (CABG) face high risks of perioperative glucose fluctuations and impaired recovery. We evaluated the impact of a structured, multidisciplinary case management model on cardiac function and glycemic control in this population. MATERIAL AND METHODS This single-center, randomized controlled trial enrolled 168 elderly (≥65 years) patients with CHD and type 2 DM scheduled for off-pump CABG. Patients were randomized (1: 1) to a control group (CG, n=84; routine care) or an observation group (OG, n=84). The OG received routine care plus a 6-month multidisciplinary intervention including individualized cardiac rehabilitation, modified Mediterranean diet, psychological support, and intensified follow-up. The primary endpoint was 6-month left ventricular ejection fraction (LVEF); HbA1c was a key secondary endpoint. RESULTS All 168 randomized patients were analyzed. At 6 months, the observation group demonstrated significantly superior primary outcomes. LVEF was significantly higher in the OG (mean difference: 6.2%, P<0.001), and HbA1c was significantly lower (mean difference: 1.3%, P<0.001). The intervention group also showed significant improvements in secondary endpoints, including reduced left ventricular diameters (LVESD, LVEDD), an improved lipid profile (P<0.05), longer 6-minute walk test distance, and higher Diabetes-Specific Quality of Life (DSQL) and Activity of Daily Living (ADL) scores (P<0.0001). CONCLUSIONS Structured, multidisciplinary case management significantly improved cardiac function, metabolic control, and functional capacity in elderly diabetic patients after off-pump CABG, validating its efficacy for this high-risk group.

Endocrine disorders in pediatric patients often involve a variety of imaging modalities as part of diagnostic workups or disease surveillance. This pictorial essay and review of the literature highlights a wide range of imaging findings for central nervous system pathologies leading to endocrine-related diseases, as well as for glucose metabolism disorders that impact the brain. In this review focusing on the central nervous system, congenital, developmental, inflammatory, and neoplastic disorders of the pituitary and hypothalamus will be discussed, as well as brain findings that may be seen with diabetic ketoacidosis and with congenital hypoglycemia. Differential diagnostic considerations, appropriate imaging protocols, and clinical management strategies will be described.

Metabolic diseases (MetDs), characterized by metabolic dysregulation leading to abnormal blood glucose, lipid, and uric acid levels, frequently result in organ damage, functional impairment, and multiple complications. These conditions severely compromise quality of life and increase mortality risk, constituting a major global health burden. Icariin (ICA), a major bioactive compound derived from Epimedium species, has demonstrated substantial therapeutic potential in the management of MetD. Accumulating evidence indicates that ICA exerts beneficial effects by improving insulin resistance and modulating oxidative stress, fibrosis, inflammatory responses, and lipid metabolism. Through these mechanisms, ICA influences the pathogenesis and progression of diabetes mellitus, osteoporosis, metabolic dysfunction-associated steatotic liver disease, obesity, and various metabolic disorders. This review provides a comprehensive summary of recent advances in the application of ICA for the management of MetD, focusing on its molecular mechanisms, clinical applications, and research prospects. The aim is to establish a solid foundation for optimizing the therapeutic use of ICA in the management of MetDs.

Type 1 diabetes (T1D) has historically been framed as a disease initiated and maintained by dysregulated immunity that targets insulin producing β-cells. However, recent findings from human tissue analysis, single cell transcriptomics, and longitudinal cohort studies reveal that intrinsic β-cell stress responses contribute substantially to early disease development. These responses include endoplasmic reticulum stress, remodeling of the unfolded protein response, oxidative and metabolic strain, impaired proinsulin folding and processing, altered granule biogenesis, increased production of cytokines and chemokines, and significant enhancement of antigen presentation pathways. Together, these stress responses create a cellular environment that increases immunogenicity and influences the recruitment and activation of immune cells. This perspective provides a comprehensive integration of mechanistic and clinical evidence showing that β-cell intrinsic biology interacts closely with immune dysregulation to shape disease trajectory. Mechanistic insights from human islets are integrated with translational data from longitudinal clinical studies, revealing a coherent model in which β-cell stress appears early, informing biomarker patterns, influences disease heterogeneity, and provides promising therapeutic targets. This overview offers a unified, balanced conceptual framework to guide future research, early detection strategies, and treatment development.

Diabetic neuropathy (DN) is the most prevalent and debilitating complication of diabetes, with a notable absence of effective disease-modifying therapies in clinical practice. This article proposes a shift in the pathological progression of DN from focusing on "metabolic toxicity" to an integrated dysfunction within the "immune-metabolic network." We analyze the core mechanisms underlying this network and highlight how the diabetic microenvironment may drive immune cells to shift abnormally from the "Warburg effect" to "metabolic inflexibility" and "metabolic paralysis," ultimately failing to resolve inflammation and causing persistent tissue damage. Furthermore, we identify a "zero-sum game" between Schwann cells (SCs) in their roles in immune response and metabolic support. Pro-inflammatory signals trigger the collapse of the "lactate shuttle" mechanism, exposing neurons to the dual insults of "hunger" and "toxicity." At the molecular level, we highlight ZBP1 as a critical switch, sensing mitochondrial damage and is proposed to trigger the assembly of the PANoptosome complex, which forms the terminal execution pathway for neurodegenerative lesions. Given the current gap between animal models and clinical realities, we propose employing spatial transcriptomics to examine subpopulation differences between the nerve sheath and endoneurium, alongside the development of novel precision therapies targeting NLRP3 or utilizing metabolic reprogramming to restore immune repair functions. In conclusion, framing DN within the immune-metabolic network provides a new approach to overcoming the therapeutic impasse and developing truly effective interventions.