scholarly journals Adiponectin and Cardiovascular Risk. From Pathophysiology to Clinic: Focus on Children and Adolescents

2019 ◽  
Vol 20 (13) ◽  
pp. 3228 ◽  
Author(s):  
Antonina Orlando ◽  
Elisa Nava ◽  
Marco Giussani ◽  
Simonetta Genovesi

Adiponectin (Ad) is a cytokine produced by adipocytes that acts on specific receptors of several tissues through autocrine, paracrine, and endocrine signaling mechanisms. Ad is involved in the regulation of cell survival, cell growth, and apoptosis. Furthermore, Ad plays an important pathophysiological role in metabolic activities by acting on peripheral tissues involved in glucose and lipid metabolism such as skeletal muscle, and the liver. Adiponectin has anti-inflammatory, anti-atherogenic, and insulin-sensitizing effects. For this reason, low levels of Ad are associated with the development of cardiovascular complications of obesity in adulthood. Numerous studies have shown that, even in children and adolescents, Ad is associated with risk factors for cardiovascular diseases. In obese children, reduced levels of Ad have been reported and Ad plasma levels are inversely related with abdominal obesity. Moreover, lower Ad concentrations are associated with the development of metabolic syndrome, insulin resistance and hypertension in pediatric subjects. In addition to a higher prevalence of cardiovascular risk factors, plasma values of Ad are also inversely associated with early organ damage, such as an increase in carotid intima-media thickness. It has been suggested that low Ad levels in childhood might predict the development of atherosclerosis in adulthood, suggesting the possibility of using Ad to stratify cardiovascular risk in obese children. Some evidence suggests that lifestyle modification may increase Ad plasma levels. The aim of this review is to summarize the evidence on the relationship between Ad, obesity, metabolic alterations and hypertension in children and adolescents, and to address the possibility that Ad represents an early marker of cardiovascular risk in pediatric subjects. Furthermore, the effects of non-pharmacological treatment (weight loss and physical activity) on Ad levels are considered.

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Birgit-Christiane Zyriax ◽  
Kira Dransfeld ◽  
Eberhard Windler

Abstract Background Assessment of cardiovascular risk by scores lacks sensitivity and leaves the majority of future cardiovascular patients unidentified particularly individuals at low cardiovascular risk. The present analysis investigates into the correlation of carotid intima–media thickness (CIMT) and cardiovascular risk factors and derived scores as to the potential of improved cardiovascular risk prediction by combining the two. Methods The Stress, Atherosclerosis and ECG Study (STRATEGY) is a cross-sectional study of selectively healthy 107 women and 106 men without diagnosed and treated cardiovascular risk factors evenly distributed between 30 and 70 years. CIMT was determined by evaluating B-mode ultrasonograms offline according to a standardized protocol. The unpaired t-test was used to compare normal-distributed continuous variables, the Chi-squared test for normal-distributed categorical variables and the Mann–Whitney U test for non-normal distributed continuous variables. The association between risk prediction scores and CIMT was calculated by the Spearman rank correlation coefficient. Pearson correlation coefficient was used for the correlation between cardiovascular risk factors and CIMT. A multiple linear regression analysis was executed for the association of cardiovascular risk factors and CIMT. Results Age, systolic blood pressure, fasting glucose, total, LDL- and non-HDL-cholesterol and waist circumference were significantly associated with CIMT (each P ≤ 0.03). The Framingham Risk Score, the Prospective Cardiovascular Münster Study Score and the European Society of Cardiology Score correlated significantly but only moderately with CIMT. The Framingham Risk Score considering BMI correlated most strongly and predicted 27% of the CIMT variance in men and 20% in women. Conclusion In individuals without overt cardiovascular risk factors and thus at low cardiovascular risk, CIMT and cardiovascular risk factors correlated only partially suggesting that combining CIMT and conventional risk factors or common derived scores may improve risk prediction in individuals at low cardiovascular risk. The clinical benefit as to cardiovascular events of such combined risk prediction needs to be explored in large prospective cohorts of still healthy low-risk volunteers. DRKS ID DRKS00015209 07/02/2019 retrospectively registered https://www.drks.de/drks_web/navigate.do?navigationId=resultsExt


Author(s):  
Eliana Portilla-Fernández ◽  
Shih-Jen Hwang ◽  
Rory Wilson ◽  
Jane Maddock ◽  
W. David Hill ◽  
...  

AbstractCommon carotid intima-media thickness (cIMT) is an index of subclinical atherosclerosis that is associated with ischemic stroke and coronary artery disease (CAD). We undertook a cross-sectional epigenome-wide association study (EWAS) of measures of cIMT in 6400 individuals. Mendelian randomization analysis was applied to investigate the potential causal role of DNA methylation in the link between atherosclerotic cardiovascular risk factors and cIMT or clinical cardiovascular disease. The CpG site cg05575921 was associated with cIMT (beta = −0.0264, p value = 3.5 × 10–8) in the discovery panel and was replicated in replication panel (beta = −0.07, p value = 0.005). This CpG is located at chr5:81649347 in the intron 3 of the aryl hydrocarbon receptor repressor gene (AHRR). Our results indicate that DNA methylation at cg05575921 might be in the pathway between smoking, cIMT and stroke. Moreover, in a region-based analysis, 34 differentially methylated regions (DMRs) were identified of which a DMR upstream of ALOX12 showed the strongest association with cIMT (p value = 1.4 × 10–13). In conclusion, our study suggests that DNA methylation may play a role in the link between cardiovascular risk factors, cIMT and clinical cardiovascular disease.


2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Patrick H. Dessein ◽  
Gavin R. Norton ◽  
Margaret Badenhorst ◽  
Angela J. Woodiwiss ◽  
Ahmed Solomon

Adiponectin and leptin are likely involved in the pathophysiology of rheumatoid arthritis (RA) and therefore potential new therapeutic targets. Adiponectin inhibition could be expected to enhance cardiovascular metabolic risk. However, it is unknown whether RA changes the influence of adipokines on cardiovascular metabolic risk. We determined whether RA impacts on the independent relationships of circulating leptin and adiponectin concentrations with cardiovascular risk factors and carotid intima-media thickness (cIMT) in 277 black African subjects from a developing population; 119 had RA. RA impacted on the relationships of adiponectin concentrations with lipid concentrations and blood pressure, independent of confounders including adiposity (interactionP<0.05). This translated into an association of adiponectin concentrations with more favorable lipid variables including HDL cholesterol (P=0.0005), non-HDL cholesterol (P=0.007), and triglyceride (P=0.005) concentrations, total cholesterol-HDL cholesterol (P=0.0002) and triglycerides-HDL cholesterol (P=0.0003) ratios, and higher systolic (P=0.0006), diastolic (P=0.0004), and mean blood pressure (P=0.0007) in RA but not non-RA subjects. Leptin was not associated with metabolic risk after adjustment for adiposity. The cIMT did not differ by RA status, and adipokine concentrations were unrelated to atherosclerosis. This study suggests that leptin and adiponectin inhibition may not alter overall cardiovascular risk and disease in RA.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Rasmus S Ripa ◽  
Andreas Knudsen ◽  
Anne Mette F Hag ◽  
Annika Loft ◽  
Eric von Benzon ◽  
...  

Introduction: HIV-infected patients are at increased risk of myocardial infarction and arterial inflammation has been suggested as an explanation. Vascular inflammation can be assessed in vivo by 18F-fluorodeoxyglucose (FDG) PET. Hypothesis: Well-treated HIV-infected patients without known cardiovascular disease will have increased uptake of FDG in different arterial regions as compared to healthy controls. Methods: We prospectively included 26 HIV-infected patients on stable antiretroviral therapy and 25 healthy volunteers. All underwent whole-body PET/CT 3 hours after injection of FDG. FDG uptake was assessed (SUV) in the carotid arteries, the ascending, descending, and abdominal aorta. Carotid intima-media thickness was determined by ultrasound. Soluble biomarkers of endothelial dysfunction and inflammation were measured by ELISA. Known cardiovascular risk factors were recorded for all included. Results: The HIV-infected patients were on stable antiretroviral therapy with full viral suppression. The HIV-infected group was older (50 vs 41 yrs; p = 0.01), had higher blood pressure and total cholesterol, and accordingly a higher Framingham risk score. FDG uptake was similar in the two groups quantified as SUVmax (figure) in the carotid region (1.67 ± 0.04 vs. 1.67 ± 0.04, p = 0.98), the ascending aorta (1.84 ± 0.06 vs. 1.97 ± 0.06, p = 0.15), the descending aorta (1.89 ± 0.08 vs. 1.93 ± 0.08, p = 0.70), and the abdominal aorta (1.70 ± 0.06 vs. 1.65 ± 0.06, p = 0.56) even when adjusting for differences in risk profile. No significant correlations between SUV, carotid intima-media thickness, known cardiovascular risk factors and soluble biomarkers were found. Conclusions: We found no evidence of increased arterial inflammation among HIV-infected patients with full viral suppression compared to controls. This may challenge the idea of chronic inflammation as the cause of cardiovascular disease among optimally treated HIV-infected patients.


Sign in / Sign up

Export Citation Format

Share Document