Search Results (228)

Metabolic syndrome (MetS) is a multifactorial disorder characterized by central obesity, insulin resistance, dyslipidemia, and hypertension, all of which increase the risk of type 2 diabetes and cardiovascular diseases. This study investigates the potential complementary effects of the standardized green and black ADM ComplexTea Extract (CTE) and the heat-treated postbiotic (BPL1^® HT) on the cardiometabolic alterations associated with MetS in a murine model. C57BL/6J mice were fed a high-fat/high-sucrose (HFHS) diet and treated with CTE, BPL1^® HT, or their combination for 20 weeks. Metabolic, inflammatory, oxidative, vascular parameters, and fecal microbiota composition were assessed. Both CTE and BPL1^® HT individually attenuated weight gain, organ hypertrophy, insulin resistance, and inflammation. However, their combined administration exerted synergistic effects, fully normalizing body weight, adipocyte size, lipid profiles, HOMA-IR index, and insulin sensitivity to levels comparable to lean controls. Co-treatment also restored PI3K/Akt signaling in liver and muscle, reduced hepatic steatosis, and normalized the expression of inflammatory and oxidative stress markers across multiple tissues. Furthermore, vascular function was significantly improved, with enhanced endothelium-dependent relaxation and reduced vasoconstrictor responses, particularly to angiotensin II. CTE, BPL1^®HT, and the blend prevented bacterial richness reduction caused by HFHS; the blend achieved higher bacterial richness than mice in Chow diet. Additionally, the blend prevented the increase in Flintibacter butyricus, which is associated with MetS clinical parameters, and showed a tendency to increase the abundance of Bifidobacterium. These findings suggest that the combination of CTE and BPL1^® HT offers a potential nutritional strategy to counteract the metabolic and cardiovascular complications of MetS through complementary mechanisms involving improved insulin signaling, reduced inflammation and oxidative stress, enhanced vascular function, and modulation of gut microbiota. Full article

Over a quarter of human pregnancies are associated with complications, including fetal growth restriction, pre-eclampsia and gestational diabetes. These are major causes of maternal and fetal morbidity and mortality, and also lead to a 3–5-fold increased risk of subsequent development of cardio-metabolic diseases. Although the mechanistic details remain elusive, a dysfunctional placenta is central to the pathophysiology of these conditions. The placenta ensures sufficient nutrient supply to the fetus without compromising maternal wellbeing. This balance is achieved by the secretion of large quantities of placental-derived peptide hormones into the maternal circulation. Consequently, the placenta is susceptible to endoplasmic reticulum (ER) stress, and we were the first to demonstrate the presence of ER stress in placentas from complicated pregnancies. The mouse placenta provides an ideal model for studying the impact of ER stress as it is composed of two distinct regions, an endocrine zone and a transport zone. Therefore, perturbation of placental endocrine function by ER stress can be generated without directly affecting its capacity for nutrient exchange. In this review, we summarise the current literature on how transgenic mouse models enhance our understanding of ER stress-mediated perturbation of placental endocrine function, and its contribution to the pathophysiology of pregnancy complications and life-long health. Full article

Background: Obesity and its accompanying complications have an influence on diurnal rhythm, potentially causing cardiometabolic disease. This study explores how weight loss due to bariatric surgery affects circadian rhythm disruptions measurable through wearable heart rate monitors. Methods: A single-center observational study was performed, in which patients who had undergone primary bariatric surgery 3 years ago with telemonitoring of vital parameters using a wireless accelerometer were eligible to participate. A Wilcoxon signed-rank test was conducted to evaluate the delta of, or amount of change in, circadian patterns between the baseline (before) and post-weight-loss peak, nadir, and peak–nadir heart rates. Results: In this cohort of 69 patients, 70% were female, with a median total weight loss of 31.4% towards a median BMI of 28.4 kg/m². Analysis revealed significant changes in peak–nadir excursions post-weight loss. Peak, nadir, and peak–nadir differences showed a significant reduction in values in the post-weight-loss group. No significant correlations between other clinical endpoints and change in peak–nadir excursion were found in the multivariable regression models. Conclusions: In conclusion, this study reveals significant changes in circadian heart rate patterns before and after weight loss due to metabolic surgery. The results could add to the health benefits of bariatric surgery, as it could lower the incidence of diseases associated with changes in diurnal rhythm due to obesity. However, a clear clinical explanation is lacking, as no correlation with total weight loss nor other variables was substantiated. Full article

Linear growth is traditionally attributed to the growth hormone (GH)/insulin-like growth factor-1 (IGF-1) axis, yet “growth without GH” is documented. We report five patients with severe GH deficiency—one congenital and four acquired, who reached normal or tall stature despite persistently low IGF-1. All patients had obesity and metabolic complications (insulin resistance, dyslipidemia, and/or fatty liver). Catch-up or sustained growth occurred before or independent of sex-steroid replacement in most cases. One patient with lifelong hypogonadism showed slow, prolonged growth with delayed epiphyseal fusion. Three patients also received recombinant human GH (rhGH), without a significant impact on overall growth velocity, but with favorable metabolic outcomes. Findings support multifactorial drivers of linear growth beyond the GH/IGF-1 pathway. Likely contributors include insulin signaling associated with adiposity, permissive thyroid hormone action, local growth-plate paracrine pathways, and, in hypogonadism, delayed epiphyseal closure. Genetic modifiers that enhance chondrogenesis or delay growth-plate fusion may contribute. We also reviewed the published literature on “growth without GH,” integrating single-case reports and series to contextualize these mechanisms and outcomes. In conclusion, profound GH deficiency does not preclude near-normal or accelerated growth. In “growth without GH,” therapeutic priorities should pivot from stature to cardiometabolic risk reduction. rhGH may be considered to improve metabolism when individualized and closely monitored, recognizing that height velocity is often adequate. Notably, rhGH consistently improved lipid profiles and steatohepatitis in two patients, suggesting a primarily metabolic benefit. Lifelong follow-up from childhood into adulthood is essential. Full article

Background: Eosinophilic granulomatosis with polyangiitis (EGPA) is a rare vasculitis, and contemporary population data from Central and Eastern Europe are limited. Aim: To describe hospital-based incidence, patient characteristics and comorbidities among EGPA hospitalizations in Poland (2014–2023), including differences by age, sex and place of residence. Methods: This retrospective, population-based study used nationwide hospital discharge records with an EGPA diagnosis. First EGPA-coded hospitalizations were used to estimate annual incidence per 1,000,000 inhabitants. Demographics, duration of stay and accompanying comorbidities (cardiovascular disease, pulmonary disease, and asthma) were analyzed for all EGPA hospitalizations. Place of residence was classified as urban or rural. Group differences and temporal trends were assessed using appropriate parametric and non-parametric tests and regression models, with a two-sided p value < 0.05 considered statistically significant. Results: Between 2014 and 2023, 911 patients had a first EGPA-coded hospitalisation in Poland, corresponding to a mean annual hospital-based incidence of 2.38 per 1,000,000 inhabitants (range 1.28–3.38); incidence declined significantly from 2014 to 2019 (p < 0.001) and was disrupted during the COVID-19 period. Overall, 3524 EGPA hospitalisations were recorded, and women were more frequently hospitalised than men (54.5% vs. 45.2%; p < 0.001). Mean age at hospitalisation increased over time, with patients in 2023 being about 5–6 years older than in 2014 (p ≤ 0.009). Median length of stay was 8 days for first admissions and 5 days for all EGPA stays and shortened significantly over the study period (p < 0.001). Cardiovascular disease, pulmonary disease and asthma were present in 23.6%, 35.3% and 32.3% of patients, respectively. Cardiovascular disease was more common in men and in rural residents (both p < 0.001) and was associated with older age (p < 0.001), whereas pulmonary disease was associated with younger age (p < 0.001). Among women, the proportions with pulmonary disease and asthma decreased over time (p = 0.009 and p = 0.025). Conclusions: EGPA in Poland is rare, with hospital-based incidence comparable to other European and Asian populations. The hospitalized EGPA population is aging and cardiovascular comorbidity is increasingly prominent, especially in older and rural patients, while recorded pulmonary disease and asthma in women are decreasing. Full article

Introduction: Hyperuricemia is increasingly recognized as a metabolic disorder linked to dyslipidemia, insulin resistance, and vascular complications. In Saudi Arabia, the prevalence of hyperuricemia is rising with obesity and diabetes, yet its relationship with lipid-derived cardiometabolic indices remained understudied. This study aimed to examine the associations between uricemia status and lipid-derived cardiometabolic indices in a large adult cohort. Methods: This retrospective cross-sectional study analyzed data from 7652 adults, including 5385 normouricemic (NU) and 2267 hyperuricemic (HU). Key cardiometabolic indices, including the triglyceride-glucose index (TyG), non-high-density lipoprotein cholesterol (non-HDL-C), remnant cholesterol (RC), atherogenic index of plasma (AIP), and Castelli risk indices I and II (CRI-I, CRI-II), were calculated. Associations were evaluated treating HU as the exposure and the lipid-derived cardiometabolic indices as the outcomes. Multivariable regression analyses, receiver operating characteristic (ROC) curves, and prevalence-based association estimates were used to assess these relationships. Results: HU individuals exhibited significantly higher TG along with lowered HDL-C. Median TyG (4.61), AIP (0.38), non-HDL-C (147 mg/dL), RC (18 mg/dL), CRI-I (4.30), and CRI-II (2.85) were higher in the HU group compared to NU group, with non-HDL-C and CRI-I falling within the abnormal range, AIP in the high-risk range, and TyG and CRI-II at borderline levels. Across the separately adjusted models, hyperuricemia showed consistent positive associations with RC, AIP, CRI-I, and CRI-II, whereas associations with TyG and non-HDL-C diminished after adjustment for renal or liver markers. ROC analysis demonstrated modest discriminatory ability of uric acid for elevated indices, with AIP (AUC = 0.641) and CRI-I (AUC = 0.640) exhibiting the highest performance. The prevalence of elevated indices was substantially higher in HU, particularly for CRI-II (44.0% vs. 25.9%) and CRI-I (28.2% vs. 13.7%). Conclusions: These findings highlight associations between HU and lipid-derived cardiometabolic indices, but further longitudinal research is required to determine whether HU has a clinical predictive value in cardiovascular risk assessment. Full article

Introduction: The PROMOTE cohort study is a prospective pregnancy cohort study that seeks to improve the understanding of cardiometabolic risk and determinants, such as diet, during pregnancy in a multi-ethnic population. Increasing age and obesity has resulted in an increased risk of cardiometabolic complications during pregnancy, including gestational diabetes. Trials of lifestyle interventions have so far produced mixed results, partly due to a wide variation in the methods, duration, adherence and type of dietary intervention. There is a need for high quality data about dietary habits in pregnancy, particularly in multi-ethnic populations. Objectives: In this study, we report the dietary habits of women in early pregnancy in the population of interest. We report early data seeking to assess the relationship between dietary patterns and risks of gestational diabetes. Methods and analysis: The PROMOTE cohort study is a prospective pregnancy cohort study recruiting pregnant participants with <16 weeks gestation in an area of high social and cultural diversity in western Sydney, Australia. The participants are surveyed about their physical activity levels, diet quality, emotional wellbeing and sociodemographic status using validated tools. Participants have consented to the use of routinely collected clinical and social data, including medical conditions, body mass index (BMI), blood pressure (BP) and glycaemia. The follow-up is from routinely collected data. This paper presents dietary data. Results: A total of 459 participants were recruited (n = 459), including 416 with GDM data available, at the conclusion of the first 2 years of recruitment. No participants met national dietary guideline recommendations. Fifty-six participants (n = 56, 13%) met a pragmatic composite standard of favourable diet, defined as two servings of vegetables and two servings of fruit per day, with a maximum of one discretionary serving per day. Over half the participants (n = 215, 51%) reported an adequate daily fruit intake. In total, 7 participants ate at least five servings of vegetables per day (n = 7, 1.7%), 61 participants (14.7%) ate three or more servings of vegetables per day and 212 (51.2%) participants reported one discretionary item per day. The data suggest that few women meet dietary recommendations in pregnancy. The association between dietary habits and GDM was unable to be assessed. The study was underpowered to detect an association due to the highly skewed distribution of dietary patterns in our population. Conclusions: The uptake of dietary recommendations was very low in our sample. This represents a major population health concern. Multi-level approaches are urgently needed to address poor dietary habits in pregnancy. Full article

Heart failure (HF) is a major cardiovascular complication in people with type 2 diabetes (T2D), where heart failure with preserved ejection fraction (HFpEF) is the most common presentation. Despite its high prevalence, HF in T2D often remains undiagnosed during its early stages due to nonspecific symptoms and the limitations of conventional diagnostic tools. Epicardial adipose tissue (EAT), a visceral fat depot surrounding the myocardium, has emerged as a mechanistic and clinically relevant contributor to myocardial dysfunction. In T2D, EAT expansion fosters a pro-inflammatory, fibrotic, and metabolically adverse milieu that may directly promote the onset and progression of HF. This perspective synthesizes current translational evidence on the role of EAT in the pathogenesis of HF among individuals with T2D. We highlight diagnostic challenges related to imaging-based quantification and the limited sensitivity of natriuretic peptide-based screening, while emphasizing the potential relevance of emerging biomarkers such as GDF-15, Galectin-3, sST2, LDL particle size, GGT, and soluble low-density lipoprotein receptor-related protein 1 (sLRP1) to enhance early detection and risk stratification. Additionally, therapeutic approaches—including lifestyle modification, SGLT2 inhibitors, and GLP-1 receptor agonists—are considered for their potential to modulate EAT volume and reduce cardiovascular risk. Advancing knowledge on EAT biology and its circulating biomarkers holds promise to refine HF risk stratification and support translational efforts toward precision cardiometabolic care. Full article

Background: Inflammation plays a key role in the pathogenesis of type 2 diabetes (T2D) and the associated cardiovascular complications. High-sensitivity C-reactive protein (hsCRP) is a widely used marker of systemic inflammation as well as a predictor of cardiovascular risk. Objective: There is increasing evidence that glucagon-like peptide-1 receptor agonists (GLP-1RAs), including semaglutide, may have effects on hsCRP levels, independent of their effects on glycemic control and body weight loss. This purpose of our study is to explore the effect of semaglutide on hsCRP levels in patients with type 2 diabetes. Additionally, we aimed to determine whether the observed effect of semaglutide on hsCRP is fully mediated by changes in HbA1c and body weight, or whether there is a direct effect suggesting the presence of an independent anti-inflammatory mechanism. Methods: The study included 70 outpatients with diagnosed type 2 diabetes undergoing therapy with metformin and/or a sulfonylurea. Semaglutide was added to the existing therapeutic regimen. All participants were followed up after a 6-month a period. At the beginning and at the end of the study, the hsCRP values, some selected indicators of glycemic control, and the anthropometric measurements were recorded. Results: The mean hsCRP value at baseline was 4.90 ± 1.21 mg/L, while after six-month therapy, it dropped to 2.23 ± 2.21 mg/L. Conclusions: The results of the analysis have a good potential to contribute to a better understanding of the pleiotropic effects of GLP-1 RAs and support the hypothesis of a direct anti-inflammatory role of semaglutide, which could have clinical significance in the context of cardiometabolic risk management in patients with type 2 diabetes. Full article

Numerous studies and international recommendations have investigated risk factors that put childhood cancer survivors (CCSs) at a higher risk of late-onset cancer therapy-related cardiovascular toxicities (CTR-CVTs). While anthracyclines and chest-directed radiotherapy are well-established high-risk treatments, other anticancer therapies, including alkylating agents, antimetabolites, targeted therapies, and hematopoietic stem cell transplantation, also carry potential cardiotoxic effects. The likelihood of developing CTR-CVT is further modulated by the presence of cardiometabolic risk factors, prior occurrence of CTR-CVT during treatment, and certain clinical conditions, which may predispose survivors to long-term cardiovascular complications. This state-of-the-art review summarizes current strategies for stratifying the risk for developing CTR-CVT in CCSs. We then propose a tailored, multimodal approach for guiding cardio-oncological assessments both during treatment and in long-term follow-up, including a structured echocardiographic protocol. Future perspectives include validation of this approach to optimize early detection and personalized management of CTR-CVT. Full article

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a chronic hepatic disease with a rising global prevalence (25–38% of the general population). As a new term, MASLD was introduced in 2023 to replace the previous nomenclature of non-alcoholic fatty liver disease (NAFLD) and metabolic dysfunction-associated fatty liver disease (MAFLD). This new term/definition introduced changes in the diagnostic criteria and underscores the direct link between cardio-metabolic risk and this prevalent liver disease. In this context, the present review examines the clinical and pathophysiological links between MASLD and cardiovascular disease (CVD), providing a robust evidence synthesis of primarily systematic review data on the association between MASLD and coronary artery disease (CAD), atrial fibrillation (AF), and heart failure (HF). This association appears to be not only synergistic, but also independent of other known CVD risk factors, highlighting MASLD as a key cardio-metabolic risk factor that merits prompt diagnosis and treatment. The development of MASLD-related cardiovascular morbidity increases with the severity of the underlying hepatic pathology, particularly with progression to steatohepatitis and fibrosis. Notably, growing evidence highlights the links between MASLD and CVD through cardiac structural, electrical, and functional alterations that can progress to CAD, AF, and new-onset HF. Recognizing these links in clinical practice underscores the importance of early detection and multi-disciplinary management of MASLD to prevent disease progression and CVD complications. Full article

Metabolic dysfunction–associated fatty liver disease (MAFLD) is now the leading indication for liver transplantation (LT), reshaping the landscape of transplant hepatology. Its close association with obesity, type 2 diabetes, cardiovascular disease, and extrahepatic malignancies poses unique challenges throughout the transplant continuum. This narrative review synthesizes current evidence across the pre-, peri-, and post-transplant spectrum, with a focus on practical implications for clinical management. We explore pre-transplant evaluation, focusing on how metabolic comorbidities, frailty, and organ allocation disparities intersect with emerging interventions such as GLP-1 receptor agonists, bariatric surgery, and structured weight loss programs. The increase in pediatric MAFLD, especially its early-onset aggressive form, indicates an evolving and concerning future burden on transplant programs. In the peri-operative and post-transplant periods, we address MAFLD recurrence, cardiometabolic complications, and the rising incidence of new cancers, particularly in relation to calcineurin inhibitor (CNI) exposure. Customized immunosuppression strategies, using mTOR inhibitors and mycophenolate mofetil, are discussed for their role in balancing graft protection with reducing cancer risk. We also review the application of machine perfusion technologies to optimize and expand the pool of steatotic donor livers. Future directions include the development of non-invasive diagnostic biomarkers, precision immunosuppression, and genomics-based risk stratification. Collectively, these insights emphasize the urgent need for multidisciplinary, patient-specific approaches and prospective, multicenter studies to optimize outcomes and equity in the era of MAFLD-driven liver transplantation. Full article

Background: Obesity is a risk factor for several non-communicable diseases and premature death. The Western-type diet, rich in calories and diverse in tastes, smells, and textures, promotes the onset and progression of obesity. We compared the effects of two Western-style palatable obesogenic diets—the cafeteria (CAF) diet, which allows for self-selection of calorie-dense food items consumed by humans, and the fast-food diet (FFD)—composed of a fixed combination of cheeseburgers and fries—on the manifestation of obesity-related complications. Methods: 3-month-old female rats consumed either the control (CTRL), FFD, or CAF diet for 12 months. Body weight was monitored weekly. At the end of the experiment, rats underwent metabolic and behavioral testing. Cardiometabolic markers and those characterizing glycoxidative and carbonyl stress, inflammatory status, and tryptophan metabolism were determined. Results: The CAF rats gain most weight (CTRL: +111 ± 40 g; FFD: +211 ± 77 g; CAF: 316 ± 87 g). CAF feeding produced a classical metabolic syndrome–like profile with severe obesity, insulin resistance, dyslipidemia, and liver steatosis, whereas the FFD model led to moderate obesity with preserved insulin sensitivity but elevated blood pressure and hepatic cholesterol accumulation. Thus, the CAF group developed a severe metabolic syndrome-like pathology assessed as continuous metabolic syndrome z-core (CTRL: −2.3 ± 1.0; FFD: −0.4 ± 1.9; CAF: 3.0 ± 2.4). Despite these differences, both diets promoted neuroinflammation and social deficits, likely mediated through gut microbiota–derived metabolites such as 5-HIAA and indoxyl sulfate. Conclusions: In female rats, self-selected CAF diet drives more severe and distinct pattern of metabolic syndrome-like pathology than a fixed FFD. Full article

Background/Objectives: Insulin resistance is a major public health issue in Mexico, closely linked to obesity, prediabetes, and type 2 diabetes. The euglycemic–hyperinsulinemic clamp is the diagnostic gold standard but is impractical for routine use. The triglyceride–glucose (TyG) index has been proposed as a simple alternative validated in diverse populations. We aimed to assess the utility of TyG relative to HOMA-IR and QUICKI as an early diagnostic tool in young Mexican adults. Methods: We performed an analytical cross-sectional study in young adults. Clinical, anthropometric, and fasting biochemical variables were collected to compute TyG. We compared TyG with HOMA-IR and QUICKI and evaluated diagnostic performance using receiver operating characteristic analysis to estimate area under the curve (AUC) and identify the optimal cut-off. Results: We analyzed 115 participants; 66.9% were insulin resistant by HOMA-IR, 79.1% by QUICKI, and 42.6% by TyG. TyG showed significant associations with anthropometric and biochemical measures. Diagnostic performance was good (AUC 0.707 vs. HOMA-IR; 0.960 vs. QUICKI). The optimal cut-off was 4.38, yielding sensitivity of 70.1% and specificity of 68.4% for diagnosing insulin resistance compared with HOMA-IR. Conclusions: The TyG index appears to be a useful, accessible, and cost-effective biomarker for early detection of insulin resistance in young Mexican adults. Its implementation could facilitate earlier diagnosis and prevention of cardiometabolic complications. Longitudinal, multicenter studies are warranted to establish population-specific reference values and to confirm its predictive value for adverse outcomes. Full article

Introduction: Polycystic ovary syndrome (PCOS) is associated with obesity, numerous metabolic complications, and an increased risk of cardiovascular disease. Adipokines, secreted by adipose tissue, may contribute to the development of these cardiometabolic disturbances. The aim of this study was to investigate the adipokine levels and their relationship with metabolic status in adolescent girls with PCOS. Patients and Methods: This cross-sectional study included 66 adolescent girls with PCOS (mean age: 16.5 ± 1.08 years; study group, SG) and 30 regularly menstruating girls (mean age: 16.2 ± 1.37 years; control group, CG) recruited between 2012 and 2017. All participants underwent physical examination, body composition assessment, liver ultrasonography, and biochemical and hormonal evaluations. Fasting venous blood samples were collected to determine the adipokine profile, and the leptin-to-adiponectin ratio (L/A) was calculated. Results: Compared with the control group, the PCOS group demonstrated significantly lower adiponectin (p = 0.019) and vaspin (p = 0.037) concentrations, and higher RBP-4 levels (p = 0.048). Positive correlations were observed between adiponectin, apelin, and omentin, while negative correlations were found between leptin and L/A and HDL cholesterol levels in the SG. Omentin showed a negative association, and leptin and L/A a positive association, with triglyceride concentration. In the SG, resistin and visfatin levels were negatively correlated with total cholesterol, and resistin also showed a negative correlation with LDL cholesterol. In patients with PCOS, adverse associations were observed between carbohydrate metabolism parameters and insulin resistance indices, while insulin sensitivity indices correlated positively with adiponectin and omentin concentrations. Visfatin levels in the SG correlated negatively with QUICKI. Conclusions: The adipokine profile of adolescent girls with PCOS differs from that of regularly menstruating peers, particularly in adiponectin, RBP-4, and vaspin concentrations. However, the absence of significant correlations between RBP-4 and vaspin and lipid or carbohydrate metabolism parameters suggests that these adipokines are not reliable markers of metabolic disturbances in adolescent girls with PCOS. Full article