There are limited studies on the epidemiology of chronic kidney disease (CKD) burden among adolescents and emerging adults. We aimed to assess the global, regional, and national trends in CKD burden among adolescents and emerging adults.

The Global Burden of Disease 2021 study was utilized to evaluate the incidence, prevalence, mortality, disability-adjusted life years (DALYs) and average annual percentage changes (AAPC) in CKD among populations aged 15 to 29 years from 1990 to 2021.

From 1990 to 2021, age-standardized incidence (AAPC: 0.85%, 95% uncertainty interval [95% UI]: 0.81%-0.88%), prevalence (AAPC: 0.22%, 95% UI: 0.19%-0.25%), and mortality (AAPC: 0.18%, 95% UI: 0.04%-0.32%) rates of CKD have risen globally among adolescents and emerging adults. In 2021, Southeast Asia had the highest age-standardized prevalence (5370.39 [95% UI: 4060.97-6929.79] per 100,000 population), while Central sub-Saharan Africa had the highest mortality rate (5.05 [95% UI: 3.49-7] per 100,000 population). In 2021, glomerulonephritis and 'other and unspecified causes' accounted for 94% of new cases, 83% of prevalent cases, and 92% of mortality cases. Frontier analyses suggest that regions at varying stages of development still hold substantial potential for further improvements in addressing CKD.

Globally, the burden of CKD among adolescents and emerging adults continues to rise, with Southeast Asia and sub-Saharan Africa bearing a disproportionate burden. Nevertheless, there remain substantial opportunities across all levels of the development spectrum to alleviate the CKD burden through enhanced health interventions and resource allocation.

Hypertension is the most common cardiovascular disease in Africa, with a 19.3% prevalence in Nigeria. Its incidence, along with prehypertension, is rising among young adults, including undergraduate clinical students, due to risk factors like stress, poor sleep, unhealthy eating, inactivity, and substance use. However, data on prehypertension among young adults in Africa, including Nigeria, is limited. This study aims to determine the prevalence of hypertension and prehypertension among clinical undergraduate students and examine the relationship between risk factors and these conditions.

A descriptive cross-sectional study of clinical students in the College of Medicine, University of Ibadan, Nigeria. These are students in the Clinical Science department who had crossed from the pre-clinical arm into the clinical arm of their training. They are Physiotherapy and Biomedical Laboratory Sciences students in 400-500 level, as well as Dentistry and Medicine and Surgery students in 300-600 level. 346 participants were selected from the study population through a random probability sampling technique, and data were collected using a self-administered structured questionnaire. Participants' blood pressure, weight, height, Body Mass Index (BMI), and waist-to-hip ratio were measured. Data were analyzed using SPSS, with descriptive statistics and chi-square test used to determine relationships between sociodemographic factors and hypertension/pre-hypertension. Stress was self-reported. The level of statistical significance was set at 0.05.

Of the 346 participants, 57% were male, while 43% female. The mean age was 23.9 ± 0.2 years. The prevalence of hypertension was 8%, and that of prehypertension was significantly higher at 33%. The prevalence of hypertension was significantly higher in males than in females. Approximately 6 out of every 50 male students were hypertensive. Hypertension was found to be associated with gender, level of study and marital status. 77% reported a moderate-to-high perceived stress levels, which could be contributing to developing hypertension.

This study found a high prevalence of prehypertension and hypertension among clinical students, with smoking, poor sleep, and perceived stress as common risk factors. Most affected students were unaware of their condition and received no treatment. The findings underscore the need for institutions to implement cost-effective hypertension awareness and screening programs for undergraduate clinical students, emphasizing early identification, lifestyle modification, and appropriate treatment to reduce future cardiovascular risks.

Clinical trial number not applicable.

Hypertension and obesity are common in systemic lupus erythematosus (SLE) patients, with obesity-related changes potentially driving hypertension. However, the specific adiposity measures associated with hypertension in SLE patients remain unclear. This study assessed the association between myosteatosis and sarcopenia detected on abdominal CT and hypertension in SLE patients. Mediators of the association between myosteatosis and hypertension were also investigated.

This was a retrospective study involving SLE patients enrolled from January 2017 to August 2023 and who underwent abdominal CT at the L3 level to track myosteatosis and sarcopenia based on the skeletal muscle mean radiodensity (SMD) and skeletal muscle index considered as binary and continuous variables. The association between these body composition measures and hypertension was tested using logistic regression analyses, while mediation modeling was used to assess the mediators.

A total of 279 adult SLE patients (median age, 41.00 [30.00, 51.00] years; 245 women) were included in this study. Hypertension was associated with myosteatosis (adjusted OR: 3.54; 95% CI: 1.18-10.61 for the binary variable and 1.31; 95% CI: 1.02-1.68 for the continuous variable). No statistically significant association was observed between hypertension and sarcopenia (adjusted OR: 0.48; 95%CI: 0.23-1.01 for the binary variable and 0.95; 95%CI: 0.78-1.16 for the continuous variable). Mediation analyses revealed eGFR could mediate the association between myosteatosis (considered as a continuous variable) and hypertension in SLE patients when taken alone (95% CI: 0.0177-0.2765) or in combination with the TyG index (95% CI: 0.0032-0.0614).

Myosteatosis was associated with hypertension in SLE patients. eGFR alone or in combination with the TyG index may mediate this association.

The global prevalence of obesity has more than doubled over the past four decades, currently affecting more than a billion individuals. Beyond its recognition as a high-risk condition that is causally linked to many chronic illnesses, obesity has been declared a disease per se that results in impaired quality of life and reduced life expectancy. Notably, two-thirds of obesity-related excess mortality is attributable to cardiovascular disease. Despite the increasingly appreciated link between obesity and a broad range of cardiovascular disease manifestations including atherosclerotic disease, heart failure, thromboembolic disease, arrhythmias, and sudden cardiac death, obesity has been underrecognized and sub-optimally addressed compared with other modifiable cardiovascular risk factors. In the view of major repercussions of the obesity epidemic on public health, attention has focused on population-based and personalized approaches to prevent excess weight gain and maintain a healthy body weight from early childhood and throughout adult life, as well as on comprehensive weight loss interventions for persons with established obesity. This clinical consensus statement by the European Society of Cardiology discusses current evidence on the epidemiology and aetiology of obesity; the interplay between obesity, cardiovascular risk factors and cardiac conditions; the clinical management of patients with cardiac disease and obesity; and weight loss strategies including lifestyle changes, interventional procedures, and anti-obesity medications with particular focus on their impact on cardiometabolic risk and cardiac outcomes. The document aims to raise awareness on obesity as a major risk factor and provide guidance for implementing evidence-based practices for its prevention and optimal management within the context of primary and secondary cardiovascular disease prevention.

This meta-analysis aims to evaluate the effects of blood flow restriction (BFR) training on cardiometabolic health and body composition in adults with overweight and obesity.

Following PRISMA guidelines, a systematic search of PubMed (MEDLINE), EMBASE, Web of Science, Cochrane, and Scopus databases was conducted on 15 March 2024. Pooled effects for each outcome were summarized using Hedge's g (g) through meta-analysis-based random effects models, and subgroup analyses were used to explore moderators.

A total of 11 studies with 242 participants (Age:32.6 ± 3.6, BMI:27.2 ± 3.5) were included. Regarding cardiometabolic health, BFR training significantly reduced systolic blood pressure (g = 0.62 [0.08, 1.16], p = 0.02), while no significant differences were observed in maximal oxygen uptake (g = 0.48 [-0.21, 1.17], p = 0.17) or diastolic blood pressure (g = 0.31 [-0.22, 0.84], p = 0.25). Regarding body composition, BFR training significantly reduced body fat percentage (g = 0.30 [0.01, 0.58]; p = 0.04), while no significant differences (p > 0.05) were observed in body weight (g = 0.14 [-0.14, 0.42]), body mass index (g = 0.08 [-0.21, 0.38]), waist circumference (g = 0.13 [-0.28, 0.53]), or waist-to-hip ratio (g = 0.48 [-0.19, 1.15]). Subgroup analysis revealed no significant difference in improving systolic blood pressure (g = 0.57 [-0.10, 1.24] vs. g = 0.70 [-0.18, 1.59]) and body fat percentage (g = 0.20 [-0.20, 0.61] vs. g = 0.45 [-0.05, 0.95]) between BFR resistance training and BFR aerobic training. In all selected studies, the overall risk of bias was categorized as "some concern". The certainty of evidence for the BFR outcomes was low.

BFR training shows promise in improving cardiometabolic health and body composition, indicating that it may serve as a beneficial, individualized exercise prescription for improving cardiovascular disease risk and fat loss in adults with excess body weight and obesity.

https://archive.org/details/osf-registrations-uv6jx-v1.

Previous studies on the correlation between serum selenium and hypertension have yielded inconsistent results. Our previous analysis of participants from the National Health and Nutrition Examination Survey (NHANES) 2011-2018 indicated that elevated serum selenium concentrations were associated with an increased risk of metabolic abnormalities in obese individuals, with the primary effect being on blood pressure in males. The aim of this study was to further elucidate the relationship between serum selenium and the risk of hypertension in obese males. In this study, we examined the correlation between serum selenium concentrations and hypertension in 2,585 male participants with a body mass index (BMI) ≥ 30 kg/m2 aged between 20 and 80 years from the 2011-2018 NHANES database. The associations between serum selenium levels and hypertension were evaluated through weighted generalized linear regression analyses. To examine the saturation threshold effect between serum selenium and hypertension, a generalized additive model (GAM) and a two-piecewise linear regression model were employed. Furthermore, the saturation threshold effect was evaluated separately in subgroups stratified by BMI and age. The weighted prevalence of hypertension (51.84%) was slightly higher than that of nonhypertension (48.16%) in the participants included in this study. After rigorous adjustment for sociodemographic, physical, and laboratory test covariates, the weighted odds ratio (OR) of hypertension increased by 103% for every 1 standard deviation (SD) increase (approximately 24.41 µg) in the serum selenium concentration in participants assigned to the highest serum selenium group (weighted OR = 2.03; 95% CI = 1.24-3.32; P = 0.013). A calculation was subsequently performed to determine the saturation threshold effect of selenium on hypertension among participants in the medium and highest selenium concentration subgroups. The findings indicated that participants with serum selenium concentrations exceeding the saturation threshold (2.56 µM) demonstrated an elevated risk of developing hypertension (weighted OR = 9.58; 95% CI = 2.74-33.46; P = 0.000) in comparison to those with serum selenium concentrations below the threshold. Subgroup analyses demonstrated that serum selenium concentrations exceeding the saturation threshold were associated with an increased risk of hypertension in participants with a BMI ≤ 35 kg/m2 (weighted OR = 9.11; 95% CI = 1.43-58.24; P = 0.030) or those aged less than 55 years or younger (weighted OR = 8.37; 95% CI = 1.71-40.94; P = 0.014). For obese adult males who require additional selenium supplementation to enhancing their overall health and well-being, it is strongly recommended that the serum selenium concentrations be monitored throughout the course of supplementation to ensure that they remain within the relatively safe range (approximately less than 215.75 µg/L).

Background: Essential hypertension, a prevalent cardiovascular condition, poses a significant health burden worldwide. Based on the latest American clinical guidelines, half of adults in the United States have hypertension. Of these, only about a half are treated and about a quarter are adequately controlled for hypertension. Given its impact on morbidity and mortality, ensuring effective management of high blood pressure is crucial to reduce associated risks and improve patient outcomes.Objective: This review aims to provide a comprehensive and up-to-date summary of the latest cardiology guidelines and evidence-based research on essential hypertension, with a focus on guiding outpatient clinical practice.Methods: The review evaluates both non-pharmacological approaches and pharmacological interventions to offer clinicians practical insights. Notably, it emphasizes the importance of individualized treatment plans tailored to patients' specific risk profiles and comorbidities.Results: By consolidating the latest advancements in hypertension management, this review provides clinicians with an up-to-date reference, offering a nuanced understanding of treatment goals and strategies.Conclusion: Through the incorporation of evidence-based recommendations, healthcare practitioners can optimize patient care, mitigate potential complications, and improve overall outcomes in essential hypertension.

Chronic kidney disease (CKD) and hypertension share a complex relationship, each exacerbating the progression of the other. CKD contributes to hypertension by decreasing renal function, leading to fluid retention and increased plasma volume, whereas hypertension exacerbates CKD by increasing glomerular pressure and causing renal damage. This review examines the intertwined nature of CKD and hypertension, exploring the factors driving hypertension in CKD and how hypertension accelerates CKD progression. It discusses the role of the renin-angiotensin system and inflammatory cytokines in this relationship, as well as the potential of blood pressure management to slow renal decline. While studies suggest that meticulous blood pressure control can help attenuate CKD progression, optimal management strategies remain unclear and require further investigation. This review also evaluates the evidence surrounding strict antihypertensive therapy in patients with CKD, considering both diabetic and non-diabetic cases. It recommends blood pressure targets based on CKD stage and presence of diabetes, emphasizing the importance of individualized treatment approaches. Renin-angiotensin system inhibitors are highlighted as a key pharmacological intervention due to their renal protective effects, particularly in patients with CKD with proteinuria. However, evidence regarding their efficacy in patients with CKD but without proteinuria is inconclusive. This review underscores the need for comprehensive approaches to effectively address the intertwined nature of CKD and hypertension and calls for further research to optimize clinical management strategies in this complex interplay.

This study was conducted to investigate the association between alcohol consumption in adolescence and the risk of hypertension or prehypertension development in early adulthood. This cohort study included adolescent participants aged 12-18 years from the 2000-2011 China Health and Nutrition Survey. Cox proportional risk regression models were used to analyze the associations of the frequency of alcohol consumption, alcohol intake, and type of alcohol with the risk of developing hypertension or prehypertension. Restricted cubic spline analysis was used to assess the dose-response relationships for alcohol intake and their hazard ratios (HRs). A total of 1556 participants were included in the final analysis. Among the overall population, 448 (30.81%) and 35 (34.31%) participants developed hypertension or prehypertension, respectively. Compared with no alcohol consumption, alcohol consumption ≥ 2 times/week and consumption of ≥2 types of alcohol were associated with an increased risk of hypertension and prehypertension, with HRs of 1.97 (95% confidence interval [CI] 1.17-3.34; p = 0.011) and 1.77 (95% CI 1.01-3.09; p = 0.046), respectively. Alcohol intake of > 96 mL/week was associated with an increased risk of hypertension and prehypertension, with HRs of 2.09 (95% CI 1.12-3.90; p = 0.020) and 2.07 (95% CI 1.11-3.84; p = 0.021), respectively. The restricted cubic spline analysis showed that the risk of developing high blood pressure or prehypertension tends to increase with increasing alcohol consumption. Heavy alcohol consumption in adolescence increased the risk of developing hypertension and prehypertension in early adulthood.

This study aimed to investigate the association of combination of birth weight and current body mass index (BMI) with the risk of hypertension in adulthood. This cross-sectional study used data from the Tohoku Medical Megabank Community-based Cohort Study conducted in Japan. A total of 10,688 subjects aged ≥20 years were eligible. We calculated the least square (LS) means of systolic blood pressure (SBP) and trend tests were performed to evaluate the linear relationships between birth weight categories and SBP. We also used a multivariate logistic regression analysis to assess the risk of hypertension associated with the combination of birth weight and current BMI. There was a statistically inverse association between birth weight and SBP in the 20-64 age group, but no significant association in the ≥65 age group. Low birth weight (LBW) with normal BMI group had a higher risk of hypertension than the normal or high birth weight groups with normal BMI. Furthermore, the group with LBW and BMI ≥25.0 kg/m2 was the highest risk for hypertension (adjusted odds ratio: 2.73; 95% CI, 2.04-3.65) compared to the reference group (birth weight 2500-3499 g and BMI 18.5-24.9 kg/m2). There was a significant association between LBW and subsequent risk of hypertension. In addition, participants with lower birth weights had a higher risk of hypertension than those with higher birth weights. However, even in participants with a lower birth weight, the risk of hypertension could be reduced when they maintained an optimal BMI.

Diet and lifestyle modifications remain the foundation of obesity treatment, but they have historically proven insufficient for significant, long-term weight loss. As a result, there is a high demand for new pharmacologic treatments to promote weight loss and prevent life-threatening diseases associated with obesity. Researchers are particularly interested in 1 type of drug, glucagon-like peptide 1 receptor agonists (GLP-1 RAs), because of its promising potential in addressing the limitations of non-pharmacologic treatments. In addition to their role in weight loss, these drugs have shown promising early evidence of cardiovascular benefits in obese patients, further enhancing their clinical relevance. Semaglutide and liraglutide, which were initially approved for the treatment of type 2 diabetes, have since been approved by the Food and Drug Administration as weight loss medications due to their effectiveness in promoting significant and sustained weight loss. In this narrative review, we will explore the mechanism of GLP-1 RAs, their effects on weight loss, cardiovascular risk factors and outcomes, common adverse effects, and strategies for managing these effects.

The global prevalence of obesity has more than doubled over the past four decades, currently affecting more than a billion individuals. Beyond its recognition as a high-risk condition that is causally linked to many chronic illnesses, obesity has been declared a disease per se that results in impaired quality of life and reduced life expectancy. Notably, two-thirds of obesity-related excess mortality is attributable to cardiovascular disease. Despite the increasingly appreciated link between obesity and a broad range of cardiovascular disease manifestations including atherosclerotic disease, heart failure, thromboembolic disease, arrhythmias, and sudden cardiac death, obesity has been underrecognized and sub-optimally addressed compared with other modifiable cardiovascular risk factors. In the view of major repercussions of the obesity epidemic on public health, attention has focused on population-based and personalized approaches to prevent excess weight gain and maintain a healthy body weight from early childhood and throughout adult life, as well as on comprehensive weight loss interventions for persons with established obesity. This clinical consensus statement by the European Society of Cardiology discusses current evidence on the epidemiology and aetiology of obesity; the interplay between obesity, cardiovascular risk factors and cardiac conditions; the clinical management of patients with cardiac disease and obesity; and weight loss strategies including lifestyle changes, interventional procedures, and anti-obesity medications with particular focus on their impact on cardiometabolic risk and cardiac outcomes. The document aims to raise awareness on obesity as a major risk factor and provide guidance for implementing evidence-based practices for its prevention and optimal management within the context of primary and secondary cardiovascular disease prevention.

The prevalence of diabetes and hypertension according to body mass index (BMI) status in Brazilian adults has not been described yet. Herein, we aimed to identify the time trends in hypertension and diabetes, individually and combined (multimorbidity), by BMI in Brazilian adults.

In this time series cross-sectional study, we retrieved self-reported data from 806 169 adults between 2006 and 2023, using the Surveillance System of Risk and Protective Factors from Chronic Diseases by Telephone Survey (Vigitel). Weight and height were used to classify participants into normal/underweight (<25 kg/m2), pre-obesity (25 to 29.9 kg/m2), and obesity (≥ 30 kg/m2). We calculated the prevalence of medical diagnoses of hypertension and diabetes, individually and combined, by BMI categories, and by sociodemographic characteristics (sex, age group, educational attainment) for participants with obesity. We performed Prais-Winsten linear regression models to identify temporal trends.

The prevalence of hypertension and diabetes increased between 2006 and 2023. Among adults with obesity, we observed a slight decrease in the prevalence of hypertension (from 44.5% in 2006 to 41.7% in 2023) and the prevalence of either hypertension or diabetes (47.1% to 45.5%); an increase in the prevalence of diabetes (12.8% to 15.13) and both conditions combined (10.2% to 11.2%). Participants with obesity had more than twice the prevalence of hypertension and diabetes compared with those who were normal/underweight. We observed a differential time trend by sex, age group, and educational attainment.

Our findings indicate the need for differentiated approaches for interventions for hypertension and diabetes, considering variations over time by sociodemographic characteristics.

Obesity has known to be a modifiable risk factor associated with worse outcomes in chronic kidney disease (CKD), but few studies have examined the impact of obesity on CKD incidence in the general population. The purpose of this study was to investigate the role of body mass index (BMI) and waist-to-hip ratio (WHR) as predictors of incident CKD and to evaluate the impact of weight reduction on CKD prevention.

A total of 2,711 participants from a community-based cohort with normal renal function were prospectively analyzed. Among participants with obesity, we analyzed the change in WHR to evaluate the association of obesity reduction with CKD development.

During a mean follow-up of 11.03 ± 4.22 years, incident CKD occurred in 190 (7.0%) participants. In the fully adjusted multivariable Cox proportional hazard models, the risk of incident CKD increased with higher BMI (hazard ratio, 1.06; 95% confidence interval, 1.00-1.11; p = 0.033) and higher WHR (hazard ratio, 1.33; 95% confidence interval, 1.07-1.66; p = 0.009). In the Kaplan-Meier analysis, cumulative adverse renal events were significantly more common in the maintained obesity group than in the reduced obesity group (p = 0.001).

Both higher BMI and WHR were associated with development of CKD, but the magnitude of the effect of WHR was higher than that of BMI. Moreover, reducing obesity would be beneficial for renal prognosis.

Several randomized controlled trials (RCTs) have explored the impact of melatonin on body composition and blood pressure (BP). However, the findings from these studies remain a topic of debate. This systematic review and meta-analysis of RCTs sought to evaluate the effects of melatonin consumption on body composition (body weight (BW), body mass index (BMI), waist circumference (WC), hip circumference (HC)) and asleep/daytime BP (systolic blood pressure (SBP) and diastolic blood pressure (DBP)) in adults.

In order to identify eligible RCTs, a systematic literature search was carried out up to June 2024 in PubMed, Embase, Scopus, and Web of Science without any language restrictions. The I2 statistic was used to perform heterogeneity tests on the selected studies. After evaluating random effects models based on heterogeneity tests, the weighted mean differences (WMD) with a 95 % confidence interval (CI) were calculated using pooled data.

Overall, 28 studies (n = 1,543 participants) met our inclusion criteria. A pooled analysis of studies demonstrated that melatonin consumption led to a significant reduction in HC (WMD: 1.21 cm; 95 % CI: 1.94 to -0.49; P = 0.001), and daytime DBP (WMD: 1.40 mmHg; 95 % CI: 2.46 to -0.34; P = 0.009) in comparison with the control group. However, no substantial effects were observed on BW, BMI, WC, and SBP compared to the control group. Conclusion: The current meta-analysis of RCTs shows that treatment with melatonin reduces HC and daytime DBP levels in adults. However, further well-designed RCTs with large sample sizes and long durations are necessary to determine the effect of this supplement on body composition and BP.

Disorders in energy homeostasis can lead to various metabolic diseases, particularly obesity. The obesity epidemic has led to an increased incidence of obesity-related nephropathy (ORN), a distinct entity characterized by proteinuria, glomerulomegaly, progressive glomerulosclerosis, and renal function decline. Obesity and its associated renal damage are common in clinical practice, and their incidence is increasing and attracting great attention. There is a great need to identify safe and effective therapeutic modalities, and therapeutics using chemical compounds and natural products are receiving increasing attention. However, the summary is lacking about the specific effects and mechanisms of action of compounds in the treatment of ORN. In this review, we summarize the important clinical features and compound treatment strategies for obesity and obesity-induced kidney injury. We also summarize the pathologic and clinical features of ORN as well as its pathogenesis and potential therapeutics targeting renal inflammation, oxidative stress, insulin resistance, fibrosis, kidney lipid accumulation, and dysregulated autophagy. In addition, detailed information on natural and synthetic compounds used for the treatment of obesity-related kidney disease is summarized. The synthesis of detailed information aims to contribute to a deeper understanding of the clinical treatment modalities for obesity-related kidney diseases, fostering the anticipation of novel insights in this domain.

Obesity is associated with a higher risk of cardiovascular disease. Understanding the associations between comprehensive health parameters and body mass index (BMI) may lead to targeted prevention efforts.

Project Baseline Health Study (PBHS) participants were divided into six BMI categories: underweight (BMI <18.5 kg/m2), normal weight (BMI 18.5-24.9 kg/m2), overweight (BMI 25-29.9 kg/m2), class I obesity (30-34.9 kg/m2), class II obesity (35-39.9 kg/m2), and class III obesity (BMI ≥40 kg/m2). Demographic, cardiometabolic, mental health, and physical health parameters were compared across BMI categories, and multivariable logistic regression models were fit to evaluate associations.

A total of 2,493 PBHS participants were evaluated. The mean age was 50±17.2 years; 55 % were female, 12 % Hispanic, 16 % Black, and 10 % Asian. The average BMI was 28.4 kg/m2±6.9. The distribution of BMI by age group was comparable to the 2017-2018 National Health and Nutrition Examination Survey (NHANES) dataset. The obesity categories had higher proportions of participants with CAC scores >0, hypertension, diabetes, lower HDL-C, lower vitamin D, higher triglycerides, higher hsCRP, lower mean step counts, higher mean PHQ-9 scores, and higher mean GAD-7 scores.

We identified associations of cardiometabolic and mental health characteristics with BMI, thereby providing a deeper understanding of cardiovascular health across BMI.

Obesity upsurges the risk of developing cardiovascular disease, primarily heart failure and coronary heart disease. Chia seeds have a high concentration of dietary fiber and increased concentrations of anti-inflammatoryand antioxidant compounds. They are used for weight loss plus enhancing blood glucose and lipid profile. The current perspective was commenced to examine the protective influence of chia seeds ingestion on cardiovascular disease risk factors in high-fat diet-fed rats. Forty male albino rats (with an initial body weight of 180-200 g) were used in this study. Rats were randomly and equally divided into 4 groups: Group I was the control group and group II was a control group with chia seeds supplementation. Group III was a high-fat diet group (HFD) that received HFD for 10 weeks and group IV was fed on HFD plus chia seeds for 10 weeks. In all groups Echocardiographic measurements were performed, initial and final BMI, serum glucose, AC/TC ratio, lipid profile, insulin (with a computed HOMA-IR), creatinine phosphokinase-muscle/brain (CPK-MB), CRP, and cardiac troponin I (cTnI) and MAP were estimated. Whole heart weight (WHW) was calculated, and then WHW/body weight (BW) ratio was estimated. Eventually, a histopathological picture of cardiac tissues was performed to assess the changes in the structure of the heart under Haematoxylin and Eosin and Crossmon's trichrome stain. Ingestion of a high diet for 10 weeks induced a clear elevation in BMI, AC/ TC, insulin resistance, hyperlipidemia, CRP, CPK-MB, and cTnI in all HFD groups. Moreover, there was a significant increase in MAP, left ventricular end diastolic diameter (LVEDD), and left ventricular end systolic diameter (LVESD). Furthermore, histological cardiac examination showed structural alteration of the normal structure of the heart tissue with an increase in collagen deposition. Also, the Bcl-2 expression in the heart muscle was significantly lower, but Bax expression was significantly higher. Chia seeds ingestion combined with HFD noticeably ameliorated the previously-recorded biochemical biomarkers, hemodynamic and echocardiography measures, and histopathological changes. Outcomes of this report reveal that obesity is a hazard factor for cardiovascular disease and chia seeds could be a good candidate for cardiovascular system protection.

To explore the topology of the white matter network in individuals with essential hypertension by graph theory.

T1-weighted image and diffusion tensor imaging (DTI) data from 43 patients diagnosed with essential hypertension (EHT) and 33 individuals with normotension (healthy controls, HCs) were incorporated in this cross-sectional study. Furthermore, structural networks were constructed by graph theory to calculate whole brain network characteristics and intracerebral node characteristics.

Both EHT and HC groups displayed small-worldness in their structural networks. The area under the curve (AUC) of the small-worldness coefficient (σ) was higher in the EHT group compared to the HC group, whereas the AUC of assortativity was lower in the EHT group in contrast to the HC group. The nodal clustering coefficient (CP) and local efficiency (Eloc) of the EHT group decreased in the right dorsolateral superior frontal gyrus and the left medial superior frontal gyrus. These values increased in the left anterior cingulate and paracingulate gyrus. Furthermore, weight and body mass index (BMI) were positively correlated with σ.

The EHT group showed brain network separation and integration dysfunction. Weight and BMI were positively correlated with σ. The data acquired in this investigation implied that altered structural connectivity in the prefrontal region may be a potential neuroimaging marker in EHT patients.

We examined potential sex differences in appetite and blood pressure (BP) responses to melanocortin-4 receptor (MC4R) blockade in offspring from lean and obese parents. Offspring from normal (N) diet-fed parents were fed N (NN) or high-fat (H) diets (NH) from weaning until adulthood. Offspring from obese H diet-fed parents were also fed N (HN) or H diets (HH). Adult male and female offspring were implanted with BP telemetry probes and intracerebroventricular cannulas to infuse MC4R antagonist or vehicle. Infusion of the MC4R antagonist SHU-9119 (1 nmol/h) for 7 days caused larger increases in calorie intake and body weight in obese compared with lean offspring. In male offspring, HH and HN groups exhibited higher baseline BP compared with NN and NH, and HH showed a greater reduction in BP during SHU-9119 infusion. In female offspring, HH also showed higher baseline BP and greater reduction in BP during MC4R blockade. SHU-9119 reduced heart rate in all groups, but reductions were more pronounced in offspring from lean parents. Combined α and β-adrenergic blockade reduced BP more in male HH offspring compared with NN controls. Losartan reduced BP more in male NH, HN, and HH offspring compared with NN controls. Losartan and α- and β-adrenergic blockade reduced BP similarly in all female groups. These results suggest that endogenous MC4R activity contributes to elevated BP in obese offspring from obese parents. Our findings also indicate important sex differences in the mechanisms of BP control in male and female offspring of obese parents.

The success of sodium-glucose cotransporter 2 inhibitors and bariatric surgery in patients with chronic kidney disease has highlighted the importance of glomerular hyperfiltration and hypertrophy in the progression of kidney disease. Sustained glomerular hyperfiltration and hypertrophy can lead to glomerular injury and progressive kidney damage. This article explores the relationship between obesity and chronic kidney disease, focusing on the roles of glomerular hyperfiltration and hypertrophy as hallmarks of obesity-related kidney disease. The pathological mechanisms underlying this association include adipose tissue inflammation, dyslipidemia, insulin resistance, chronic systemic inflammation, oxidative stress, and overactivation of the sympathetic nervous system, as well as the renin-angiotensin aldosterone system. This article explains how glomerular hyperfiltration results from increased renal blood flow and intraglomerular hypertension, inducing mechanical stress on the filtration barrier and post-filtration structures. Injured glomeruli increase in size before sclerosing and collapsing. Therefore, using extreme values, such as the maximal glomerular diameter, could improve the understanding of the data distribution and allow for better kidney failure predictions. This review provides important insights into the mechanisms underlying glomerular hyperfiltration and hypertrophy and highlights the need for further research using glomerular size, including maximum glomerular profile, calculated using needle biopsy specimens.

The lifetime occurrence rate of kidney stones is 14%, making it one of the most prevalent urological conditions. Other contributing elements, such as obesity, diabetes, diet, and heredity, are also taken into account. Our research sought to explore the potential link between high visceral fat scores (METS-VF) and the occurrence of kidney stones, as a means of understanding how to prevent them.

This research utilized data from the National Health and Nutrition Examination Survey (NHANES), mirroring the demographics of the United States. We carried out an in-depth analysis of the connection between METS-VF and kidney stones, based on data from 29,246 participants in the National Health and Nutrition Examination Survey spanning 2007 to 2018, involving logistic regression, segmentation, and dose-response curve analysis.

Our study of 29,246 potential participants found that METS-VF was positively associated with the prevalence and progression of kidney stones. After subgroup analysis by gender, race, blood pressure, and blood glucose, our results showed that the ORs for METS-VF and kidney stones were (1.49, 1.44) in males and females, respectively; while in Mexicans, whites, blacks, and In other populations, the OR values were (1.33, 1.43, 1.54, 1.86); in hypertensive and normal populations, the OR values were (1.23, 1.48); in diabetic patients and normoglycemic patients were (1.36,1.43). This proves that it works for all groups of people.

Our studies demonstrate a strong connection between METS-FV and the emergence of kidney stones. It would be beneficial to investigate METS-VF as a marker for kidney stone development and progression in light of these findings.

To study differences in cardiovascular risk factors and diseases between patients with and without genetic variants in the leptin-melanocortin pathway.

A cross-sectional study of patients with a history of severe obesity genotyped in June 2019 as participants of the Mayo Clinic Biobank was conducted in March 2022 to assess differences in cardiovascular risk and diseases between carriers of a heterozygous variant in the leptin-melanocortin pathway and noncarriers. Cardiovascular risk factors included hypertension, diabetes, dyslipidemia, and smoking. Cardiovascular disease includes coronary artery disease, peripheral artery disease, and cerebrovascular accidents. Patients with a history of bariatric surgery were excluded. We used logistic regression models to estimate the odds ratio and 95% CI, adjusting for age, body mass index (BMI), and sex.

Among a total of 168 carriers (8%; 121 [72%] female; mean [SD] age, 65.1 [14.9] years; BMI, 44.0 [7.4] kg/m2) and 2039 noncarriers (92%; 1446 [71%] female; mean [SD] age, 64.9 [14.4] years; BMI, 42.9 [6.6] kg/m2), carriers had higher prevalence odds of hypertension (odds ratio, 3.26; 95% CI, 2.31 to 4.61; P<.001) and reported higher number of cardiovascular risk factors compared with noncarriers (2.4 [1.1] vs 2.0 [1.1]; P<.001). There were no significant differences in the adjusted odds associated with diabetes, dyslipidemia, smoking, or cardiovascular disease.

Despite having similar body weight and BMI, carriers of heterozygous variants in the leptin-melanocortin pathway had higher rates of hypertension than noncarriers. These findings point to an association between hypertension and leptin-melanocortin pathway variants.

Maternal obesity is a key predictor of childhood obesity and a determining factor for a child's body composition. Thus, any form of maternal nutrition during the gestational period plays a vital role in influencing the growth of the fetus. Elateriospermum tapos (E. tapos) yogurt has been found to comprise many bioactive compounds such as tannins, saponins, α-linolenic acid, and 5'-methoxy-bilobate with apocynoside I that could cross the placenta and exhibit an anti-obesity effect. As such, this study aimed to investigate the role of maternal E. tapos yogurt supplementation on offspring body composition. In this study, 48 female Sprague Dawley (SD) rats were induced with obesity using a high-fat diet (HFD) and were allowed to breed. Upon confirmation of pregnancy, treatment was initiated with E. tapos yogurt on the obese dams up to postnatal day 21. The weaning offspring were then designated into six groups according to their dam's group (n = 8) as follows; normal food and saline (NS), HFD and saline (HS), HFD and yogurt (HY), HFD and 5 mg/kg of E. tapos yogurt (HYT5), HFD and 50 mg/kg of E. tapos yogurt (HYT50), and HFD and 500 mg/kg of E. tapos yogurt (HYT500). The body weight of the offspring was accessed every 3 days up to PND 21. All the offspring were euthanized on PND 21 for tissue harvesting and blood sample collection. The results showed that both male and female offspring of obese dams treated with E. tapos yogurt showed growth patterns similar to NS and reduced levels of triglycerides (TG), cholesterol, LDL, non-HDL, and leptin. Liver enzymes such as ALT, ALP, AST, GGT, and globulin, and renal markers such as sodium, potassium, chloride, urea, and creatinine levels significantly reduced (p < 0.05) in the offspring of E. tapos yogurt-treated obese dams with the normal histological architecture of the liver, kidney, colon, RpWAT, and visceral tissue that is comparable to NS. In toto, E. tapos yogurt supplementation of obese dams exerted an anti-obesity effect by preventing intergenerational obesity by reversing HFD-induced damage in the fat tissue of the offspring.

Increasing evidence suggests excess skin Na+ accumulation in hypertension; however, the role of skin-specific mechanisms of local Na+/water regulation remains unclear. We investigated the association between measures of sweat and trans-epidermal water loss (TEWL) with Na+ content in the skin ([Na+]skin) and clinical characteristics in consecutive hypertensive patients. We obtained an iontophoretic pilocarpine-induced sweat sample, a skin punch biopsy for chemical analysis, and measures of TEWL from the upper limbs. Serum vascular endothelial growth factor-c (VEGF-c) and a reflectance measure of haemoglobin skin content served as surrogates of skin microvasculature. In our cohort (n = 90; age 21-86 years; females = 49%), sweat composition was independent of sex and BMI. Sweat Na+ concentration ([Na+]sweat) inversely correlated with [K+]sweat and was higher in patients on ACEIs/ARBs (P < 0.05). A positive association was found between [Na+]sweat and [Na+]skin, independent of sex, BMI, estimated Na+ intake and use of ACEi/ARBs (Padjusted = 0.025); both closely correlated with age (P < 0.01). Office DBP, but not SBP, inversely correlated with [Na+]sweat independent of other confounders (Padjusted = 0.03). Total sweat volume and Na+ loss were lower in patients with uncontrolled office BP (Padjusted < 0.005 for both); sweat volume also positively correlated with serum VEGF-c and TEWL. Lower TEWL was paralleled by lower skin haemoglobin content, which increased less after vasodilatory pilocarpine stimulation when BMI was higher (P = 0.010). In conclusion, measures of Na+ and water handling/regulation in the skin were associated with relevant clinical characteristics, systemic Na+ status and blood pressure values, suggesting a potential role of the skin in body-fluid homeostasis and therapeutic targeting of hypertension.

Accumulating evidence suggests that maternal overnutrition can result in a higher development risk of obesity and renal disease in the offspring's adulthood. The present study tested different lipid levels in the maternal diet during pregnancy and lactation and its repercussions on the offspring of Wistar rats. Offspring of 1, 7, 30 and 90-d-old were divided into the following groups: Control (CNT) - offspring of dams that consumed a standard chow diet (3.5% of lipids); Experimental 1 (EXP1) - offspring of dams exposed to a high-fat diet (HFD) (28% of lipids); and Experimental 2 (EXP2) - offspring of dams exposed to a HFD (40% of lipids). Regarding maternal data, there was a decrease in the amount of diet ingested by EXP2. Daily caloric intake was higher in EXP1, while protein and carbohydrate intakes were lower in EXP2. While lipid intake was higher in the experimental groups, EXP1 consumed more lipids than EXP2, despite the body weight gain being higher in EXP2. Adult offspring from EXP1 presented higher blood glucose. Regarding morphometric analysis, in both experimental groups, there was an increase in the glomerular tuft and renal corpuscle areas, but an increase in the capsular space area only in EXP1. There was a decrease in the glomerular filtration rate (GFR) in EXP1, in contrast to an increase in GFR of EXP2, along with an increase in urinary protein excretion. In conclusion, the maternal HFDs caused significant kidney damage in offspring, but had different repercussions on the type and magnitude of recorded change.

We studied the predictive and prognostic influences of hypertension (HT), type 2 diabetes (T2D), weight, and p53 mutations in metastatic colorectal cancer (CRC) patients.

T2D was diagnosed according to the ADA criteria. HT was classified according to the ACC/AHA guidelines. BMI (body-mass index) was calculated and classified according to the WHO criteria. TruSigt™Oncology 500 kit was applied to construct the genomic libraries for Next Generation Sequencing (NGS) analysis. The Illumina NovaSeq 6000 technological platform and the Illumina TruSight Oncology 500 bioinformatics pipeline were applied to analyze results. Overall survival (OS) was calculated through Kaplan-Meier curves. Univariate and multivariate analyses were performed to assess the relationships between clinical and/or molecular covariates. Associations between HT, T2D, BMI, p53, and clinical variables were evaluated by the χ2 test. P < 0.05 were considered statistically significant.

Two-hundred-forty-four patients were enrolled. One-hundred-twenty (49.2%), 110 (45.1%), and 50 (20.5%) patients were affected by overweight, HT, and T2D, respectively. DC (disease control) was achieved more frequently in patients without T2D (83.1%) compared to the diabetic ones (16.9%) (P = 0.0246). DC, KRAS mutational status, T2D, BMI, and concomitant presence of T2D, BMI, and HT associated with survival (P < 0.05). At multivariate analysis, age (≥65 vs. <65 years), response to first-line chemotherapy (DC vs. no DC), and concomitant presence of T2D, BMI, and HT (HR: 4.56; 95% CI: 2.40-8.67; P = 0.0217) emerged as independent prognostic variables. P53 was mutated in 31/53 analyzed cases (60.4%). The most frequent gene variants were p.Arg175His and p.Cys135Tyr. High BMI (>25 kg/m2) associated with occurrence of p53 mutations (P < 0.0001). P53 mutated patients presented a worse prognosis compared to the wild-type ones (HR: 3.21; 95% CI: 1.43-7.23; P = 0.0047).

Diabetic, hypertensive and overweight metastatic CRC patients are a negative prognostic subgroup deserving specific therapeutic strategies. P53 mutations associate with prognosis and BMI unrevealing complex and unexplored connections between metabolism and cancer occurrence.

Body sodium (Na) levels must be maintained within a narrow range for the correct functioning of the organism (Na homeostasis). Na disorders include not only elevated levels of this solute (hypernatremia), as in diabetes insipidus, but also reduced levels (hyponatremia), as in cerebral salt wasting syndrome. The balance in body Na levels therefore requires a delicate equilibrium to be maintained between the ingestion and excretion of Na. Salt (NaCl) intake is processed by receptors in the tongue and digestive system, which transmit the information to the nucleus of the solitary tract via a neural pathway (chorda tympani/vagus nerves) and to circumventricular organs, including the subfornical organ and area postrema, via a humoral pathway (blood/cerebrospinal fluid). Circuits are formed that stimulate or inhibit homeostatic Na intake involving participation of the parabrachial nucleus, pre-locus coeruleus, medial tuberomammillary nuclei, median eminence, paraventricular and supraoptic nuclei, and other structures with reward properties such as the bed nucleus of the stria terminalis, central amygdala, and ventral tegmental area. Finally, the kidney uses neural signals (e.g., renal sympathetic nerves) and vascular (e.g., renal perfusion pressure) and humoral (e.g., renin-angiotensin-aldosterone system, cardiac natriuretic peptides, antidiuretic hormone, and oxytocin) factors to promote Na excretion or retention and thereby maintain extracellular fluid volume. All these intake and excretion processes are modulated by chemical messengers, many of which (e.g., aldosterone, angiotensin II, and oxytocin) have effects that are coordinated at peripheral and central level to ensure Na homeostasis.

Pulmonary arterial pressure (PAP) can be used as an indicator of susceptibility to pulmonary hypertension and subsequent potential to develop right-sided heart failure (RHF). Previously reported heritability estimates of PAP have been moderate to high. Based on these estimates, selection for the indicator trait, PAP, could reduce the incidence of RHF due to hypoxia. Previous studies have also speculated that increased growth rates and body fat accumulation contribute to increased PAP and RHF. Research evaluating the genetic relationships between PAP and performance traits (e.g., yearling weight and postweaning gain) has yielded conflicting results, leading to ambiguity and uncertainty regarding the underlying genetic relationships. Additionally, no previous research has evaluated the relationship between PAP and ultrasound carcass traits. Therefore, the objective of this study was to estimate trait heritabilities and genetic correlations between PAP, post-weaning growth traits, and ultrasound carcass traits in Angus cattle, using data (n = 4,511) from the American Angus Association. We hypothesized that traits associated with increased growth and muscle would have a positive genetic (i.e., unfavorable) relationship with PAP. Estimates for heritability and genetic correlations were obtained using a multi-trait animal model. Heritability estimates for PAP (0.21 ± 0.04), post-weaning gain (PWG; 0.31 ± 0.04), and yearling weight (YWT; 0.37 ± 0.04) were within the range of estimates previously reported. Genetic correlations were weak (< 0.20) between PAP, PWG, and YWT. A low-to-moderate genetic correlation between PAP and ultrasound ribeye area (UREA) was found (0.25 ± 0.12). Genetic correlations between PAP, ultrasound back fat (UBF), ultrasound intramuscular fat (IMF), and ultrasound rump fat (RUMP) were weak (ranging in magnitude from -0.05 to 0.10) and therefore, do not provide strong support for the hypothesis of an antagonistic relationship between PAP and carcass ultrasound traits, while heritability estimates for UBF (0.43 ± 0.05), UREA (0.31 ± 0.04), IMF (0.35 ± 0.04), and RUMP (0.47 ± 0.05) were in the range of previously reported values.

Visceral adipose tissue plays a central role in obesity and metabolic syndrome and is an independent risk factor for both cardiovascular and metabolic disorders. Increased visceral adipose tissue promotes adipokine dysregulation and insulin resistance, leading to several health issues, including systemic inflammation, oxidative stress, and activation of the renin-angiotensin-aldosterone system. Moreover, an increase in adipose tissue directly and indirectly affects the kidneys by increasing renal sodium reabsorption, causing glomerular hyperfiltration and hypertrophy, which leads to increased proteinuria and kidney fibrosis/dysfunction. Although the interest in the adverse effects of obesity on renal diseases has grown exponentially in recent years, the relationship between obesity and renal prognosis remains controversial. This may be attributed to the long clinical course of obesity, numerous obesity-related metabolic complications, and patients' attributes. Multiple individual attributes influencing the pathophysiology of fat accumulation make it difficult to understand obesity. In such cases, it may be effective to elucidate the pathophysiology by conducting research tailored to individual attributes from the perspective of attribute-based medicine/personalized medicine. We consider the appropriate use of clinical indicators necessary, according to attributes such as chronic kidney disease stage, level of visceral adipose tissue accumulation, age, and sex. Selecting treatments and clinical indicators based on individual attributes will allow for advancements in the clinical management of patients with obesity and chronic kidney disease. In the clinical setting of obesity-related nephropathy, it is first necessary to accumulate attribute-based studies resulting from the accurate evaluation of visceral fat accumulation to establish evidence for promoting personalized medicine.

Recent technological developments enable big data-driven insights on diurnal changes. This study aimed to describe the trajectory of multiple and advanced parameters using a medical-grade wearable remote patient monitor.

Parameters were monitored for 24 h in 256 ambulatory participants who kept living their normal life. Parameters included heart rate, blood pressure, stroke volume, cardiac index, systemic vascular resistance, blood oxygen saturation, and respiratory rate. Diurnal variations were evaluated, and analyses were stratified based on sex, age, and body mass index.

All parameters showed diurnal changes (p < 0.001). Females demonstrated higher heart rate and cardiac index with lower systemic vascular resistance. Obese participants had a higher blood pressure, and lower stroke volume and cardiac index. Systemic vascular resistance was higher among the elderly. Diurnal changes corresponded with awake-sleep hours and differed between sex, age, and body mass index groups.

Wearable monitoring platforms could decipher hemodynamic changes in subgroups of individuals, and might help with efforts to provide personalized medicine, pre-symptomatic diagnosis and prevention, and drug development.

The prevalence of obesity has increased dramatically during the past decades, which has been a major health problem. Since 1975, the number of people with obesity worldwide has nearly tripled. An increasing number of studies find obesity as a driver of chronic kidney disease (CKD) progression, and the mechanisms are complex and include hemodynamic changes, inflammation, oxidative stress, and activation of the renin-angiotensin-aldosterone system (RAAS). Obesity-related kidney disease is characterized by glomerulomegaly, which is often accompanied by localized and segmental glomerulosclerosis lesions. In these patients, the early symptoms are atypical, with microproteinuria being the main clinical manifestation and nephrotic syndrome being rare. Weight loss and RAAS blockers have a protective effect on obesity-related CKD, but even so, a significant proportion of patients eventually progress to end-stage renal disease despite treatment. Thus, it is critical to comprehend the mechanisms underlying obesity-related CKD to create new tactics for slowing or stopping disease progression. In this review, we summarize current knowledge on the mechanisms of obesity-related kidney disease, its pathological changes, and future perspectives on its treatment.

We review a collection of published renal epithelial transport models, from which we build a consistent and reusable mathematical model able to reproduce many observations and predictions from the literature. The flexible modular model we present here can be adapted to specific configurations of epithelial transport, and in this work we focus on transport in the proximal convoluted tubule of the renal nephron. Our mathematical model of the epithelial proximal convoluted tubule describes the cellular and subcellular mechanisms of the transporters, intracellular buffering, solute fluxes, and other processes. We provide free and open access to the Python implementation to ensure our multiscale proximal tubule model is accessible; enabling the reader to explore the model through setting their own simulations, reproducibility tests, and sensitivity analyses.

Aortic diseases (ADs), including aortic dissection, aortic aneurysm, and aortic rupture, are fatal, with extremely high mortality rates. A body shape index (ABSI), an anthropometric measure calculated as waist circumference adjusted by height and weight, improves the predictive capacity for mortality. However, whether ABSI is a risk factor for AD-related mortality in the general population remains unclear.

We used a nationwide database of 630,842 individuals (aged 40-75 years) who participated in the annual "Specific Health Check and Guidance in Japan" between 2008 and 2010.

During the follow-up period of 3.8 years, 159 AD-related deaths occurred, including 105 aortic dissections and 54 aortic aneurysm ruptures. The subjects were divided into three groups based on ABSI tertiles. Kaplan-Meier analysis demonstrated that the 3^rd tertile (with the highest ABSI) had the greatest risk among the three groups. Multivariate Cox proportional hazard regression analysis demonstrated that ABSI was significantly associated with AD-related death after adjusting for confounding risk factors. Neither waist circumference nor body mass index consistently predicted AD-related death in the multivariate model. The prediction capacity was significantly improved by the addition of ABSI to the confounding risk factors.

We demonstrated for the first time that ABSI, a surrogate marker for abdominal visceral fat tissue, was associated with AD-related deaths in the general population, suggesting the importance of central adiposity in the development of AD.

Systemic arterial hypertension is one of the leading causes of morbidity and mortality in the general population, being a risk factor for many cardiovascular diseases. Although its pathogenesis is complex and still poorly understood, some systems appear to play major roles in its development. This review aims to update the current knowledge on the interaction of the intrarenal renin-angiotensin system (RAS) and dopaminergic system in the development of hypertension, focusing on recent scientific hallmarks in the field. The intrarenal RAS, composed of several peptides and receptors, has a critical role in the regulation of blood pressure (BP) and, consequently, the development of hypertension. The RAS is divided into two main intercommunicating axes: the classical axis, composed of angiotensin-converting enzyme, angiotensin II, and angiotensin type 1 receptor, and the ACE2/angiotensin-(1-7)/Mas axis, which appears to modulate the effects of the classical axis. Dopamine and its receptors are also increasingly showing an important role in the pathogenesis of hypertension, as abnormalities in the intrarenal dopaminergic system impair the regulation of renal sodium transport, regardless of the affected dopamine receptor subtype. There are five dopamine receptors, which are divided into two major subtypes: the D1-like (D1R and D5R) and D2-like (D2R, D3R, and D4R) receptors. Mice deficient in any of the five dopamine receptor subtypes have increased BP. Intrarenal RAS and the dopaminergic system have complex interactions. The balance between both systems is essential to regulate the BP homeostasis, as alterations in the control of both can lead to hypertension.

Binge drinking (BD) is the most common alcohol consumption model among adolescents. BD exposure during adolescence disrupts the nervous system function, being involved in the major mortality causes at this age: motor vehicle accidents, homicides and suicides. Recent studies have also shown that BD consumption during adolescence affects liver, renal and cardiovascular physiology, predisposing adolescents to future adult cardiometabolic damage. BD is a particularly pro-oxidant alcohol consumption pattern, because it leads to the production of a great source of reactive oxygen species (ROS) via the microsomal ethanol oxidizing system, also decreasing the antioxidant activity of glutathione peroxidase (GPx). Selenium (Se) is a mineral which plays a pivotal role against oxidation; it forms part of the catalytic center of different antioxidant selenoproteins such as GPxs (GPx1, GPx4, GPx3) and selenoprotein P (SelP). Specifically, GPx4 has an essential role in mitochondria, preventing their oxidation, apoptosis and NFkB-inflamative response, being this function even more relevant in heart's tissue. Se serum levels are decreased in acute and chronic alcoholic adult patients, being correlated to the severity of oxidation, liver damage and metabolic profile. Experimental studies have described that Se supplementation to alcohol exposed mice clearly decreases oxidative and liver damage. However, clinical BD effects on Se homeostasis and selenoproteins' tissue distribution related to oxidation during adolescence are not yet studied. In this narrative review we will describe the use of sodium selenite supplementation as an antioxidant therapy in adolescent BD rats in order to analyze Se homeostasis implication during BD exposure, oxidative balance, apoptosis and inflammation, mainly in liver, kidney, and heart. These biomolecular changes and the cardiovascular function will be analyzed. Se supplementation therapies could be a good strategy to prevent the oxidation, inflammation and apoptosis generated in tissues by BD during adolescence, such as liver, kidney and heart, improving cardiovascular functioning.

Obesity poses significant challenges to healthcare globally, particularly through its bi-directional relationship with co-morbid metabolic conditions such as type 2 diabetes and hypertension. There is also emerging evidence of an association between obesity and chronic kidney disease (CKD) which is less well characterized.

A literature search of electronic libraries was conducted to identify and present a narrative review of the interplay between obesity and CKD.

Obesity may predispose to CKD directly as it is linked to the histopathological finding of obesity-related glomerulopathy and indirectly through its widely recognized complications such as atherosclerosis, hypertension, and type 2 diabetes. The biochemical and endocrine products of adipose tissue contribute to pathophysiological processes such as inflammation, oxidative stress, endothelial dysfunction, and proteinuria. The prevention and management of obesity may prove critical in counteracting both the development and advancement of CKD. Moreover, measures of abdominal adiposity such as waist circumference, are generally associated with worse morbidity and mortality in individuals receiving maintenance hemodialysis.

Obesity is a risk factor for the onset and progression of CKD and should be recognized as a potential target for a preventative public health approach to reduce CKD rates within the general population. Future research should focus on the use of glucagon-like peptide-1 receptor agonists and sodium-glucose cotransporter 2 inhibitors in patients with CKD and obesity due to their multi-faceted actions on major outcomes.