Adiponectin Regulation in Cardiovascular Disease

Ruijter, Hester M. den; Pasterkamp, Gérard; Jager, Saskia C.A. de

doi:10.1161/atvbaha.114.304380

Cited by 7 publications

(5 citation statements)

References 17 publications

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“…It was recently proposed as a crucial modulator of HDL functionality 32 . The role of adiponectin in CVD is not clear since low levels in asymptomatic individuals have been associated with decreased CVD risk, and low level of adiponectin was shown to be a predictor of poor prognosis in patients with established CVD 33 . While Marsche et al showed plasma adiponectin levels to be strongly associated with efflux in healthy obese adults, we could not confirm these findings but observed an inverse association between CEC and serum adiponectin levels in our study.…”

Section: Discussionmentioning

confidence: 99%

HDL cholesterol efflux capacity is inversely associated with subclinical cardiovascular risk markers in young adults: The cardiovascular risk in Young Finns study

Hunjadi

Lamina

Kahler

et al. 2020

Sci Rep

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The atherogenic process begins already in childhood and progresses to symptomatic condition with age. We investigated the association of cholesterol efflux capacity (CEC) and vascular markers of subclinical atherosclerosis in healthy, young adults. CEC was determined in 2282 participants of the Young Finns study using cAMP treated 3H-cholesterol-labeled J774 cells. The CEC was correlated to baseline and 6-year follow-up data of cardiovascular risk factors and ultrasound measurements of arterial structure and function. CEC was higher in women, correlated with total cholesterol, HDL-C, and apolipoprotein A-I, but not with LDL-C or apolipoprotein B. Compared to the lowest CEC quartile, the highest CEC quartile was significantly associated with high CRP levels and inversely associated with adiponectin. At baseline, high CEC was associated with decreased flow-mediated dilation (FMD) and carotid artery distensibility, as well as an increased Young's modulus of elasticity, indicating adverse changes in arterial structure, and function. The association reversed with follow-up FMD data, indicating the interaction of preclinical parameters over time. A higher CEC was directly associated with a lower risk of subclinical atherosclerosis at follow-up. In young and healthy subjects, CEC was associated with important lipid risk parameters at baseline, as in older patients and CAD patients, but inversely with early risk markers for subclinical atherosclerosis.

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Section: Discussionmentioning

confidence: 99%

HDL cholesterol efflux capacity is inversely associated with subclinical cardiovascular risk markers in young adults: The cardiovascular risk in Young Finns study

Hunjadi

Lamina

Kahler

et al. 2020

Sci Rep

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“…Increased cumulative inflammation in deficient mice resulted in increased systemic insulin resistance. Changes in adipocyte size and ectopic lipid deposition in liver were minimal; however, Ctnnb1 −/− mice exhibited reduced VAT and circulating adiponectin, which has anti-inflammatory and cardioprotective functions ( den Ruijter et al., 2014 ). A link between β-catenin signaling and insulin resistance has been previously described.…”

Section: Discussionmentioning

confidence: 99%

Visceral Adipose Tissue Immune Homeostasis Is Regulated by the Crosstalk between Adipocytes and Dendritic Cell Subsets

et al. 2018

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SummaryVisceral adipose tissue (VAT) has multiple roles in orchestrating whole-body energy homeostasis. In addition, VAT is now considered an immune site harboring an array of innate and adaptive immune cells with a direct role in immune surveillance and host defense. We report that conventional dendritic cells (cDCs) in VAT acquire a tolerogenic phenotype through upregulation of pathways involved in adipocyte differentiation. While activation of the Wnt/β-catenin pathway in cDC1 DCs induces IL-10 production, upregulation of the PPARγ pathway in cDC2 DCs directly suppresses their activation. Combined, they promote an anti-inflammatory milieu in vivo delaying the onset of obesity-induced chronic inflammation and insulin resistance. Under long-term over-nutrition, changes in adipocyte biology curtail β-catenin and PPARγ activation, contributing to VAT inflammation.

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“…Neonatal hyperoxia reduced the expression of 8 genes involved in fatty acid metabolism including the core enzymes in the de novo fatty acid synthesis pathway such as fatty acid synthase (Fasn), the enzyme that synthesizes the 16-carbon saturated fatty acid palmitate from acetyl-CoA and malonyl-CoA (34); elongation of very long chain fatty acids 6 (Elovl6), the enzyme that extends palmitate to produce the 18 carbon saturated fatty acid stearate (35); and stearoyl-CoA desaturase 1 (Scd1), which convert palmitate and stearate to the mono-unsaturated fatty acids palmitoleate and oleate (36), and thyroid hormone-inducible hepatic protein (Thrsp), which binds FASN and increases its activity (37). Neonatal hyperoxia also downregulated cell death inducing DFFA like effector c (Cidec), a protein required for the storage of triglycerides as lipid droplets (38), and adiponectin (Adipoq), an adipokine that protects cardiomyocytes from oxidative stress and apoptosis following ischemic injury (39).…”

Section: Neonatal Hyperoxia Inhibits the De Novo Fatty Acid Synthesismentioning

confidence: 99%

Neonatal hyperoxia inhibits proliferation of atrial cardiomyocytes by suppressing fatty acid synthesis

Cohen

Yee

Porter

et al. 2020

Preprint

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Preterm birth increases the risk for pulmonary hypertension and heart failure in adulthood.Oxygen therapy can damage the immature cardiopulmonary system and may be partially responsible for the cardiovascular disease in adults born preterm. We previously showed that exposing newborn mice to hyperoxia causes pulmonary hypertension by 1 year of age that is preceded by a poorly understood loss of pulmonary vein cardiomyocyte proliferation. We now show that hyperoxia also inhibits the proliferation of left atrial cardiomyocytes and causes diastolic heart failure by thinning the walls of the left atrium and disrupting its ability to pump effectively. Transcriptomic profiling showed that neonatal hyperoxia permanently suppressed fatty acid synthase (Fasn), stearoyl-CoA desaturase 1 (Scd1) and other fatty acid synthesis genes in the atria of mice, the HL-1 line of mouse atrial cardiomyocytes and left atrial tissue explanted from human infants. Suppressing Fasn or Scd1 reduced HL-1 cell proliferation while overexpressing these genes maintained their expansion in hyperoxic conditions, suggesting hyperoxia directly inhibits atrial cardiomyocyte proliferation by repressing Fasn and Scd1. Pharmacologic interventions that restore Fasn, Scd1 and other fatty acid synthesis genes in atrial cardiomyocytes may thus provide a way of ameliorating the adverse effects of supplemental oxygen on preterm infants.

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Adiponectin Regulation in Cardiovascular Disease

Cited by 7 publications

References 17 publications

HDL cholesterol efflux capacity is inversely associated with subclinical cardiovascular risk markers in young adults: The cardiovascular risk in Young Finns study

HDL cholesterol efflux capacity is inversely associated with subclinical cardiovascular risk markers in young adults: The cardiovascular risk in Young Finns study

Visceral Adipose Tissue Immune Homeostasis Is Regulated by the Crosstalk between Adipocytes and Dendritic Cell Subsets

Neonatal hyperoxia inhibits proliferation of atrial cardiomyocytes by suppressing fatty acid synthesis

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