BackgroundObstructive sleep apnea (OSA) is common in type 2 diabetes (T2D) and may contribute to its chronic complications. Whether STOP-Bang-defined OSA risk is associated with diabetic foot ulcer (DFU) severity and outcome remains unclear. We compared STOP-Bang score between T2D patients with and without DFU and explored the association between OSA risk and DFU severity and healing.MethodsWe conducted an observational study with a cross-sectional matched case-control comparison including 73 T2D patients with DFU and 73 T2D controls without DFU, matched by age, HbA1c, BMI and smoking. At the study visit, STOP-Bang-defined OSA risk was assessed as a continuous score and categorized as low versus moderate/high risk. In the DFU group, ulcer severity was graded at the same visit with the WIfI classification, and time to healing and amputation was recorded during clinical follow-up. Multivariable logistic regression identified predictors of moderate-to-high amputation risk.ResultsIn unadjusted analyses, DFU patients had higher STOP-Bang score than controls (4.3 ± 2.0 vs. 3.2 ± 2.2, p=0.004) and more often intermediate/high OSA risk (83.6% vs. 60.3%, p=0.002), although these differences were attenuated after accounting for sex imbalance. Among DFU patients, higher ulcer severity was associated with moderate/high STOP-Bang-defined OSA risk (97.1 vs. 71.8%; p=0.004). Median healing time was longer in those with moderate/high versus low STOP-Bang-defined OSA risk (120.0 vs. 65.0 days, p=0.032). In multivariable analysis, WIfI ulcer severity was associated with male sex, higher STOP-Bang category and poorer metabolic control.ConclusionSTOP-Bang-defined OSA risk was associated with greater DFU severity and delayed wound healing. Incorporating OSA risk stratification into routine assessment of patients with DFU may help identify individuals at higher risk of poor outcomes.

OBJECTIVES:To prospectively evaluate the relationship between 4-year changes in lung function and the progression of subclinical atherosclerosis among 1623 middle-aged adults with at least one cardiovascular risk factor participating in ILERVAS, and to determine whether individuals who develop airflow obstruction (AO) are especially susceptible to accelerated atherosclerosis progression. METHODS:This prospective cohort study included 1623 middle-aged adults from the ILERVAS cohort, recruited in primary care centers in the province of Lleida (Catalonia, Spain), with baseline assessments conducted between 2015 and 2018 and follow-up visits between 2019 and 2021 (mean follow-up, 3.99 [SD, 0.22] years). Pulmonary function was assessed by spirometry at baseline and at 4-year follow-up. Subclinical atherosclerosis was evaluated using vascular ultrasound of 12 carotid and femoral territories at baseline and at follow-up, with total plaque area quantified. Associations were analyzed using multivariable linear regression models, adjusting for clinical variables and baseline plaque burden. Analyses were stratified by smoking status. RESULTS:Median annual declines were -95mL (-2.04%) for FVC and -78mL (-2.00%) for FEV1. Categorization of annual pulmonary function decline by tertiles showed no significant association with plaque progression. In contrast, incident AO was associated with greater annual FEV1 decline (-146.73 vs -74.90mL; P<.001) and with greater plaque burden, reflected by an increase in affected vascular territories (0.26 [IQR, 0.00-0.75]; P<.001). Multivariable models confirmed larger annual increases in total (4.40mm2; P<.001), carotid (2.33mm2; P<.001), and femoral (1.99mm2; P=.031) plaque areas among participants with incident AO, with consistent results across smoking strata. Sensitivity analyses using a lower limit of normal-based definition of AO showed similar findings, with effect estimates consistent with the primary fixed-ratio analyses. CONCLUSIONS:In this two-time-point analysis, lung function decline was not independently associated with subclinical atherosclerosis progression. In contrast, incident AO was consistently associated with greater plaque progression across smoking strata. These findings support incident AO as a spirometric marker associated with vascular risk.

Introduction:Advanced liver fibrosis, a key complication of metabolic dysfunction-associated steatotic liver disease, has been increasingly linked to extrahepatic conditions, including type 2 diabetes, obesity, and cardiovascular disease. However, the specific association of liver fibrosis in the development and progression of subclinical atheromatous disease across vascular territories remains poorly understood. This study evaluates the utility of two non-invasive indices to predict liver fibrosis and their associations with subclinical atheromatous plaque burden and distribution. Methods:Atheromatous plaque burden (plaque presence, number, and total area) was assessed in the carotid and femoral territories via ultrasonography in 3,981 middle-aged participants without known cardiovascular disease, diabetes, or liver disease from the ILERVAS cohort (ClinicalTrials.gov Identifier: NCT03228459). The fibrosis-4 (FIB-4) and the NAFLD Fibrosis Score (NFS) were evaluated. FIB-4 risk categories were defined as low (<1.30), intermediate (1.30-2.67), and high (>2.67). Results:Participants in the intermediate and high-risk FIB-4 categories exhibited a higher prevalence of carotid atheromatous disease (56.8% vs. 49.5%, p<0.001), a greater number of plaques (p<0.001), and a larger total plaque area (p=0.007). Multivariable analyses confirmed FIB-4 as an independent predictor of carotid plaque burden (OR: 1.14, 95% CI 1.05-1.24, p=0.003), even adjusting for traditional cardiovascular risk factors. Moving from low to high FIB-4 cut-offs was associated with 12.6% higher odds of carotid atherosclerosis. NFS was also independently associated with carotid atheromatosis (OR 1.10, 95% CI 1.05-1.15, p<0.001). No significant associations were found in the femoral territory for either index. Conclusions:Estimated liver fibrosis, particularly FIB-4, is a valuable marker for identifying carotid subclinical atherosclerosis in populations without known liver disease. These findings highlight the importance of vascular territory-specific evaluations and support their utility in integrated liver and cardiovascular risk assessment strategies.

Background:Weight-loss outcomes after bariatric surgery (BS) show interindividual variability that is not fully explained by clinical factors. In the OBEGEN study we previously developed a clinical-genetic score combining three clinical variables with nine single nucleotide polymorphisms to predict weight-loss success at 12-18 months after BS. In the present study we evaluated the usefulness of this clinical-genetic score to predict longitudinal weight-loss trajectories up to five years after BS. Methods:Multicenter retrospective cohort study including 342 adults who underwent Roux-en-Y gastric bypass or sleeve gastrectomy (2018-2020) with available genetic data. Patients were classified as into higher or lower predicted response groups using the OBEGEN cut-off (0.662). The primary outcome was percentage total weight loss (%TWL) assessed from 6 months to 5 years. Longitudinal trajectories were analyzed using linear mixed-effects models adjusted for baseline BMI, sex, type 2 diabetes, and center. Secondary outcomes included the proportion achieving >20% TWL and recurrent weight gain. Results:Patients in the higher predicted response group achieved greater %TWL throughout follow-up than those in the lower predicted response group (adjusted β = 2.60%, p = 0.009). Differences emerged early after surgery and remained stable over time without progressive divergence. At 5 years, a higher proportion of patients in the higher predicted response group maintained >20% TWL (78.7% vs. 60.0%, p = 0.001). Discriminatory performance of response to BS was moderate but consistent (area under the receiver operating characteristic curve 0.674 at 1 year; 0.608 at 5 years). Conclusion:The OBEGEN clinical-genetic score stratifies patients into distinct medium-term weight-loss trajectories after bariatric surgery, supporting its utility as a preoperative tool for risk stratification and personalized management in obesity.

A close relation between intake and expenditure of energy exist in humans. Peripheral signals from the gastrointestinal tract (cholecystokinin, peptide YY, ghrelin, and glucagon-like peptide 1) and available metabolic fuels signals (leptin, insulin, and amylin) bind to their respective receptors located at the vagus nerve fiber terminals. In addition, GLP1, leptin, and ghrelin also regulate food intake through its receptors localized in the hypothalamus. Vagal afferents synapse on the brainstem to enhance or inhibit neurones in the nucleus tractus solitaries. From this nucleus, signal reflecting the availability and demand for metabolic fuel will go to the arcuate nucleus, that lies around the base of the third ventricle in the mediobasal hypothalamus. In the arcuate nucleus, two distinct set of neurons that are crucial for controlling food intake and regulating body weight: the POMC/CART (anorexigenic) and NPY/AgRP (orexigenic) neurons. In addition, many other microscopically defined nuclei and interconnected areas will integrate metabolic information and hedonic drives to finally regulate food intake.

Introduction and Objective: Metabolic dysfunction-associated steatotic liver disease (MASLD) has been linked to chronic kidney disease (CKD), with fibrosis as the potential pathogenic factor shared by both diseases. The Fibrosis-4 (FIB-4) index is a widely used non-invasive fibrosis marker; however, its association with renal outcomes remains uncertain. We evaluated the relationship between FIB-4, estimated glomerular filtration rate (eGFR) decline and albuminuria in the ILERVAS cohort. Methods: We included 3,940 adults aged 45-70 years from the ILERVAS study, all free of diabetes, CKD and chronic liver disease. FIB-4 was analysed categorically (<1.30 vs. ≥1.30) and continuously in regression models. Renal outcomes were eGFR and albuminuria (albumin-to-creatinine ratio ≥30 mg/g) at baseline and 4 years. Multivariable linear and logistic regression models were adjusted for age, sex, hypertension, presence of prediabetes, adiposity, lipids and smoking. Results: At baseline, 78.3% of participants were classified as low FIB-4 risk and 21.7% as indeterminate-high risk; the latter were older and had lower eGFR, whereas albuminuria prevalence was similar. At 4 years (n=1,593), eGFR remained lower in the indeterminate-high group, with no differences in albuminuria prevalence. In multivariable analyses, higher FIB-4 values and prediabetes independently predicted greater eGFR decline (β =−1.15 and -1.57; p=0.013 and 0.023, respectively). Age, female sex, baseline eGFR and hypertension also emerged as independent predictors of eGFR decline. Conclusion: In adults at low-to-moderate cardiovascular risk without diabetes or established liver/kidney disease, both higher FIB-4 values and prediabetes were independently associated with faster eGFR loss. FIB-4 may help to capture systemic metabolic factors related to fibrosis, suggesting its potential role in renal risk stratification. Disclosure A. Lecube: None. J.L. Mengíbar: None. R. Simo: Research Support; Current; Abbott, Dexcom, Inc., Novo Nordisk. Board Member; Current; D-Sight. C. Hernández: None. O. Simó-Servat: Advisory Panel; Current; Abbott Diabetes. Other - Speaker on a meeting; Ended; Tandem Diabetes Care, Inc. P. Gil-Millán: None. Á. Ortiz Zúñiga: None. A. Switzer-Rodriguez: None. Funding This research was supported by grants from the Diputació de Lleida.

Acquired hypothalamic obesity (AHO) is a complex neuroendocrine disorder characterized by rapid weight gain and multisystem dysfunction following hypothalamic damage. AHO represents the weight-related manifestation of the broader hypothalamic syndrome (HS), a heterogeneous spectrum of dysfunctions that can also encompass disturbances in pituitary function, energy expenditure, sleep, behavior, and thermoregulation, with obesity itself absent in some affected individuals. This narrative review provides an updated and integrative overview of AHO pathophysiology, clinical characterization, and current and emerging approaches to diagnosis, prevention, and treatment, with the aim of proposing a multidimensional framework to improve patient care. The literature, including seminal studies, recent systematic reviews, clinical trials, and expert consensus statements, was critically appraised with emphasis on clinical applicability and existing knowledge gaps. Current evidence highlights the limitations of BMI-based assessment and supports a multidomain clinical approach. In this context, a three-layer diagnostic model is proposed, integrating etiological factors, longitudinal anthropometric and metabolic assessment, and domain-specific clinical evaluation. Preventive strategies remain underexplored, although hypothalamus-sparing interventions, early monitoring of weight trajectory, and management in specialized Pituitary Tumor Centers of Excellence in surgical cases appear critical. Therapeutic options are limited, with modest evidence for conventional treatments; however, emerging therapies targeting the melanocortin pathway, including MC4R agonists, showed promising results. Overall, AHO requires a paradigm shift toward early identification, multidimensional assessment, and coordinated multidisciplinary care, with future research prioritizing preventive strategies and robust clinical trials to improve outcomes.

ABSTRACT Background Obesity management remains influenced by misconceptions about the disease, which compromise care quality. Introduction The OBEQUIDAD study explores the clinical management of people with obesity in Spain based on the perspectives of healthcare professionals involved in its treatment across different medical specialties. Methods A cross‐sectional online survey was conducted among endocrinologists, family and community medicine specialists, and internal medicine physicians actively treating people with obesity in Spain. The survey explored patient profiles, use of clinical practice guidelines, diagnostic approaches and therapeutic strategies, motivations for initiating obesity management interventions, and follow‐up practices. Results Among 352 respondents, 37% were family and community medicine specialists, 37% were endocrinologists, and 26% were internal medicine physicians. Most worked in the public sector (87%) and in non‐obesity specific medical consultations (82%). The most common patient profile attending for obesity included women (60%), individuals aged 40–64 years (51%) and people with Class I obesity (48%) who were diagnosed opportunistically (33%) or sought treatment themselves (31%). 95% of people with obesity have obesity‐related complications: dyslipidemia (55%), hypertension (52%) and type 2 diabetes mellitus (51%). Dietary and nutritional changes and increased physical activity were the most recommended obesity management interventions. The use of medical and surgical treatments was more frequent in Class II and III obesity, compared to Class I. Reducing the risk of cardiovascular complications and improving people with obesity's functional capacity and their quality of life were the main reasons to start obesity treatment. Conclusion Obesity management in Spain is mainly reactive, with care often initiated opportunistically or at the patient's request, often once comorbidities have developed. There is variability in the use of clinical practice guidelines, and treatment generally follows a stepwise approach.

Advanced glycation end-products (AGEs) activate specific receptors (RAGE) promoting inflammation and oxidative stress. The lungs, with high RAGE expression, may be particularly susceptible to AGE-related injury. This study assessed whether baseline skin AGE levels, measured by skin autofluorescence (SAF), predict pulmonary function decline in middle-aged adults with cardiovascular risk factors. This ancillary analysis of the ILERVAS cohort included adults aged 45-70 years with cardiovascular risk factors but without diabetes or chronic kidney disease. Baseline data included demographics, lifestyle, and fasting blood tests. SAF was measured using AGE Reader™, and spirometry performed at baseline and after a median follow-up of 4 years. Associations between baseline SAF and annual declines in FEV1, FVC, and FEV1/FVC were analysed using adjusted models and generalized additive models, stratified by smoking status. Among 658 participants (median age 56 years, 48% female), median baseline SAF was 1.90 AU [1.60; 2.20]. Baseline lung function was preserved, with median FEV1, FVC and FEV1/FVC of 2795 mL [2270; 3,341], 3,525 mL [2870; 4300], and 78.6% [74.4; 82.8]. Annual declines were -  81.9 mL [- 120.6; - 43.3] for FEV1, - 99.6 mL [- 159.3; - 37.9] for FVC, and - 0.04% [- 0.85; 0.70] for FEV1/FVC. No significant associations were found between SAF and spirometry changes. Results were consistent across smoking subgroups. Baseline skin AGE levels did not predict pulmonary function decline over four years in middle-aged adults with cardiovascular risk factors. While SAF reflects cumulative AGE exposure, it has limited prognostic value for lung function in this population.

Introduction and Objective: Diabetic retinopathy (DR) is one of the most frequent microvascular complications of type 1 diabetes (T1D) and advanced glycation end products (AGEs) play a major pathogenic role. The relationship between AGEs and the presence and the degree of DR in individuals with T1D has not been fully established. Objectives: To evaluate the association between cutaneous AGEs and both the presence and severity of DR. Methods: This cross-sectional study included adults with T1D using continuous glucose monitoring systems (GCM). Cutaneous AGEs were assessed by skin autofluorescence. Clinical variables including the presence and severity of DR and standard GCM-derived metrics were recorded. Descriptive analyses, non-parametric tests, multivariable logistic and ordinal logistic regression models were performed. Results: A total of 98 individuals with T1D were included (mean age 42.1 ± 13.5 years; mean diabetes duration 21.5 ± 11.6 years); 31 (31.6%) had DR: 11 (35.5%) mild DR, 13 (41.9%) moderate DR and 7 (22.6%) severe DR. AGEs were significantly higher in individuals with DR compared with those without (2.67 ± 0.53 vs 2.27 ± 0.57; p<0.001). In multivariable logistic regression analyses, AGEs were independently associated with the presence of DR (OR 3,88; CI95% 1,25-13,0; p = 0,022). In the adjusted ordinal logistic regression model, AGEs were independently associated with greater DR severity (OR 3.98; CI95% 1.37-12.15). Diabetes duration was also an independent predictor of severe DR (OR 1.08 per year; CI95% 1.03-1.13). We did not observe any independent relationship between HbA1c and CGM-derived metrics and the presence and degree of DR. Finally, a positive correlation was observed between AGEs and DR severity (p < 0.001). Conclusion: In individuals with T1D, cutaneous AGEs were independently associated with both the presence and severity of DR. Longitudinal studies are needed to determine the prognostic value of AGEs in DR progression. Disclosure A. Rojano-Toimil: Other - travel and congress support; Ended; Novo Nordisk, Lilly. P. Gil-Millán: None. Á. Ortiz Zúñiga: None. A. Lecube: None. O. Simó-Servat: Advisory Panel; Current; Abbott Diabetes. Other - Speaker on a meeting; Ended; Tandem Diabetes Care, Inc. C. Hernández: None. R. Simo: Research Support; Current; Abbott, Dexcom, Inc., Novo Nordisk. Board Member; Current; D-Sight.

AIMS:Prediabetes is a prevalent condition associated with increased cardiovascular and renal risk. However, the long-term impact of haemoglobin A1c (HbA1c) within the range defined as prediabetes on kidney function remains unclear. This study aimed to evaluate the association between prediabetes and renal function (estimated glomerular filtration rate [eGFR] and albuminuria) through cross-sectional and prospective analyses over 4 years in a cohort of individuals with no diagnosis of diabetes or established cardiovascular disease. MATERIALS AND METHODS:Analysis using data from 8153 participants in the ILERVAS cohort, a prospective cross-sectional study. Prediabetes was defined as HbA1c 5.7%-6.4% (ADA criteria). Kidney impairment was defined as eGFR <60 mL/min/1.73 m2 and/or urinary albumin-to-creatinine ratio (ACR) ≥30 mg/g at a single time point. A prospective study was conducted in 3222 participants, who were reassessed after 4 years. Associations were explored using multivariable regression models adjusted for confounders. RESULTS:At baseline, prediabetes was associated with higher kidney impairment prevalence (17.8% vs. 13.7%; p < 0.001), lower eGFR and increased ACR. Each 1% increase in HbA1c was linked to a 4.6 mL/min/1.73 m2 decrease in eGFR. Prediabetes remained independently associated with kidney impairment (OR 1.17; 95% CI: 1.03-1.34; p = 0.020) and lower eGFR (β = -0.76; 95% CI: -1.40 to -0.13; p = 0.019). At follow-up, prediabetes predicted further eGFR decline, and HbA1c increase was independently associated with eGFR decline. CONCLUSIONS:HbA1c-defined prediabetes is independently associated with early renal impairment and accelerated kidney function decline. These findings support incorporating renal risk assessment in prediabetes and suggest HbA1c as a marker for chronic kidney disease prevention strategies.

The evidence on weight-related stigmatization among U.S. Hispanic (HISP), non-Hispanic White (NHW), and non-Hispanic Black (NHB) adults with obesity is limited. We compare levels of prejudices, stigma, and internalization of negative bias across diverse minority groups using validated surveys. Observational study conducted at two academic centers, including adults ( ≥ 18 years of age) with body mass index (BMI) ≥ 30 kg/m2. We assessed 1) weight-related aversion/prejudices using Anti-Fat Attitudes (AFA) survey, 2) stigmatizing experiences with the Brief Stigmatizing Situations Inventory (SSI-B), and 3) internalization of negative weight bias with the Weight Bias Internalization Scale (WBIS) survey. Among 296 participants (age 54.9 ± 13 years, 59% females, 42% HISP, 23% NHW, 35% NHB), with obesity (BMI 36.7 ± 6.2), 72% perceived themselves as having overweight and only 24% as having obesity. Among the three groups, HISP had the highest AFA score (3.6 ± 1.3 vs. 3.3 ± 1.1 vs. 2.1 ± 1.2, p < 0.001), NHW had the highest SSI-B (1.2 ± 1.1 vs. 2.0 ± 1.4 vs. 1.2 ± 1.4, p < 0.001), and NHB had the lowest WBIS (2.7 ± 1.2 vs. 3.0 ± 1.3 vs. 2.3 ± 1.2, p < 0.001) score. Among an ethnically diverse U.S. cohort of adults with obesity, most participants perceive themselves as having overweight and not obesity. HISP exhibited greater aversion and prejudices towards people with obesity, NHW reported more stigmatizing situations and NHB the lowest internalization of negative bias. These findings should be incorporated when developing or implementing culturally appropriate educational or interventional programs for people with obesity.

Introduction: Obesity is multifactorial and increasingly prevalent disease associated with chronic kidney disease (CKD). While cross-sectional studies support a link between adiposity and renal dysfunction, the long-term impact of total body fat on kidney function remains unclear. This study aims to evaluate the association between baseline adiposity, assessed by body mass index (BMI) and total body fat percentage, and renal function parameters, and to determine whether adiposity predicts CKD outcomes over 4 years in individuals without diabetes at low-to-moderate cardiovascular risk. Methods: This retrospective, multicenter study included 8,153 participants from the ILERVAS project in Lleida, Spain. Adiposity was measured using BMI and estimated body fat percentage (CUN-BAE formula). Renal function was evaluated by estimated glomerular filtration rate (eGFR) and albumin-to-creatinine ratio (ACR). A subset of 3,222 individuals was reevaluated after 4 years. Multivariable regression models and ROC analysis were performed to explore associations and predictive performance. Results: CKD prevalence was 15.1%, higher in individuals with obesity (17.2%) than in those with overweight (13.7%) or normal weight (13.9%, p < 0.001). Body fat percentage showed a stronger inverse correlation with eGFR than BMI and was independently associated with eGFR decline. Baseline body fat percentage and its increase over time were associated with eGFR decline. Neither adiposity measure independently predicted CKD presence nor albuminuria. Conclusions: Higher total body fat is associated with impaired renal function and its progression over time, independently of traditional CKD risk factors. These findings support incorporating body fat assessment in CKD prevention beyond BMI-based strategies.

INTRODUCTION:The aims of the study were to describe a biopsy procedure to obtain subcutaneous adipose tissue (SAT) samples for fibrosis assessment in patients with adipose-based chronic disease (ABCD) and to explore potential associations between SAT fibrosis and comorbidities. METHODS:Single-center, cross-sectional study conducted at the Arnau de Vilanova University Hospital (Lleida, Spain) between January and December 2024. We included patients aged 18-65 years attending their first appointment in the Obesity Unit. Between-group comparisons were performed using Student's t-test for continuous variables and chi-square tests for categorical variables, and correlations were assessed using Spearman's rank correlation coefficient. RESULTS:58 patients were recruited and 50 were included in the final analysis. Most were female (76.0%), with a mean age of 47.1 years (SD: 10.8), and a mean BMI of 46.3 kg/m2 (SD: 5.0). The biopsy technique evolved over time, reducing the procedure duration from 55 min to under 10 min without any adverse events. SAT fibrosis was observed in 10 patients (20.0%), who showed a higher prevalence of type 2 diabetes (50.0% vs. 15.0%, p = 0.017), significantly higher aspartate transaminase and gamma-glutamyl transferase, and elevated signs of liver fibrosis. CONCLUSION:SAT fibrosis was associated with ABCD comorbidities and could serve as a tool for risk stratification beyond traditional indicators.

Background:The management of type 2 diabetes mellitus (T2DM) remains a complex clinical challenge, particularly for patients requiring multiple daily insulin injections (MDI). Advances in precision medicine and continuous glucose monitoring (CGM) have created opportunities to personalize treatment and potentially reduce the therapeutic burden on people with T2DM. Assessing β cell function and autoimmunity could help identify patients with T2DM eligible for simplified regimens without compromising glycemic control. Objective:The aim of this study is to test a simple personalized medicine protocol in routine clinical practice for people with T2DM treated with MDI. The intervention is based on evaluating C-peptide and glutamic acid decarboxylase autoantibody status with the goal of improving diagnostic accuracy and optimizing treatment. Methods:This is a pragmatic before-and-after intervention study involving people with T2DM currently receiving MDI across primary care centers and a referral hospital in the Lleida health care region in Catalonia (Spain). Eligible participants will undergo clinical and laboratory assessment, including C-peptide and glutamic acid decarboxylase autoantibody testing, and wear a CGM device. On the basis of a predefined algorithm, patients may either continue or discontinue prandial insulin. The primary outcome is the proportion of patients in whom prandial insulin is discontinued and remains discontinued over 6 months. Secondary outcomes include changes in hemoglobin A1c, CGM metric variables, quality of life, adherence, and treatment satisfaction. Results:Recruitment was completed on March 31, 2025. The follow-up phase is ongoing and expected to conclude by September 30, 2025. Data analysis will begin thereafter. Conclusions:This study will evaluate the feasibility and impact of implementing a personalized therapeutic approach for persons with T2DM receiving MDI in real-world clinical settings. If effective, this strategy could contribute to safer, simpler, and more individualized diabetes care.

Obesity-related chronic kidney disease (Ob-CKD) is an alteration that affects a wide variety of patients with chronic kidney disease (CKD) at different levels: without ultrastructural lesions (hyperfiltration and/or albuminuria), with obesity-related glomerulopathy (glomerular hypertrophy, podocytopathy, matrix mesangial expansion, focal and segmental glomerulosclerosis, tubular-interstitial fibrosis, vascular lesions, and tubular atrophy), associated with other kidney diseases, in persons with CKD in dialysis programs, as well as patients with transplanted kidneys. The S.E.N. (Sociedad Española de Nefrología), SLANH (Sociedad Latinoamericana de Nefrología e Hipertensión), and SEEDO (Sociedad Española para el Estudio de la Obesidad) Consensus report on Ob-CKD proposes a classification based on kidney alterations and CKD stage (CKD, dialysis, or kidney transplant) with the clear aim to unify nomenclature and subsequently the management of persons with Ob-CKD. The document defines a classification of Ob-CKD. As seen with current times in terms of new strategies for Ob-CKD treatment, the consensus also recognizes that an effective management of obesity in persons with CKD, when available, should be treated by a multidisciplinary team that incorporates nutrition, physical activity, pharmacotherapy, as well as bariatric surgery, if indicated. In addition, the consensus also mentioned the new therapeutic approach with incretin-based therapies that has demonstrated to decrease body weight and have a beneficial effect on cardiorenal events and reduction in cardiovascular death in patients with obesity and CKD.

Introduction: Current obesogenic environments, along with intrinsic factors, contribute to the obesity pandemic, which impacts the quality of life and healthcare for individuals with obesity. In addition, discrimination and stigma related to obesity remain widespread in our society. In this scenario, the Spanish Society for the Study of Obesity (SEEDO), in collaboration with 38 recognized scientific societies and 12 patients' organization, has elaborated the Spanish guideline for obesity management in adults, referred to as the GIRO guideline. GIRO aims to drive a shift in obesity management and serve as a guide for healthcare professionals (HCPs) to address this chronic and multifactorial disease. METHODS:A comprehensive systematic review was conducted and completed with experts' contribution, with a particular focus on Spanish society. The quality of evidence was assessed using the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) system. Experts selected the recommendations and determined their strength through consensus. RESULTS:A total of 121 recommendations were proposed, including 32 adopted from the Canadian Adult Obesity Clinical Practice Guidelines and 89 specific recommendations created for the Spanish context, and were distributed across five areas of application: (1) recognition of obesity as a chronic disease, (2) obesity assessment, (3) multidisciplinary approach to obesity treatment, (4) recommendations for obesity management in special populations, and (5) implementation of the GIRO guideline and future challenges. CONCLUSION:The GIRO recommendations are intended to serve as a useful and interactive tool for HCPs, policymakers, and other stakeholders to ensure access to and quality of healthcare for individuals living with obesity. .

Zinc-alpha2-glycoprotein (ZAG) is a soluble glycoprotein primarily produced in adipocytes and the liver, with key roles in lipid metabolism, including lipolysis and the browning of adipose tissue. Despite extensive studies on its role in rodents, the relationship between ZAG and insulin in humans remains unclear. Given the emerging interest in ZAG’s involvement in metabolic diseases such as metabolic-dysfunction-associated steatotic liver disease, this study aimed to investigate the acute effects of insulin on ZAG levels both in vivo and in vitro. We recruited 24 healthy, individuals who were non-obese and assessed the impact of oral glucose overload, a standardized liquid nutritional supplement, and intravenous glucagon on circulating ZAG levels. In parallel, we explored the effects of insulin on ZAG production in cultured HepG2 cells. Our findings revealed a consistent acute reduction in serum ZAG levels following all in vivo tests, coinciding with increased insulin levels. In vitro, insulin rapidly downregulated ZAG protein and mRNA levels in HepG2 cells, with significant reductions observed within 15 min, followed by partial recovery after 2 h. These results suggest a potential acute inhibitory effect of insulin on ZAG production, supporting its role in promoting energy storage by suppressing lipolysis postprandially. This study provides new insights into the complex interplay between insulin and ZAG in regulating energy balance and highlights the potential of ZAG as a therapeutic target in metabolic diseases.