Adiponectin and Cardiovascular Disease

Han, Seung Hwan; Quon, Michael J.; Kim, Jeong‐A; Koh, Kwang Kon

doi:10.1016/j.jacc.2006.08.061

Cited by 242 publications

(76 citation statements)

References 80 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, increased between-person variability in this scenario will make the assay CV less important and the distinction between “high” and “normal” values easier. Conversely, low levels of adiponectin are associated with higher risk of cardiovascular [13] and metabolic disease [14]. Adiponectin levels in the REGARDS cohort may be lower than in our volunteers; indeed, many of our participants had values well above the normal range suggesting better than average obesity-related risk profiles.…”

Section: Resultsmentioning

confidence: 84%

Validating laboratory results in a national observational cohort study without field centers: The Reasons for Geographic and Racial Differences in Stroke cohort

Gillett

Boyle

Zakai

et al. 2014

Clinical Biochemistry

View full text Add to dashboard Cite

Objectives The REasons for Geographic and Racial Differences in Stroke (REGARDS) study is a prospective cohort of 30,239 Americans in the contiguous United States; the first of this scale to use home visits to obtain, process, and ship biologic samples to a core laboratory. Pre-analytical factors resulting from this study design may affect the results of some laboratory assays. We investigated the impact of REGARDS processing on a variety of analytes. Design and methods In REGARDS, blood samples were processed in the field by technicians who were trained on standardized methods for phlebotomy and sample processing. Field processing included centrifugation using varying non-uniform equipment and shipping overnight on ice to the University of Vermont, where samples were re-centrifuged for 30,000 ×g-minutes and stored at −80 °C. We assessed the effects of REGARDS sample handling by processing split samples from 20 volunteers using either ideal procedures or simulated REGARDS procedures. Assays for 19 analytes for potential study in REGARDS were then run on both samples and results compared. Results Spearman correlation coefficients for analytes measured in ideal versus REGARDS processed samples ranged from 0.11 to 1.0. Thirteen of 19 analytes were highly correlated (>0.75), but platelet proteins were more variable. Conclusions Simulation of non-optimal field processing and shipment to a central laboratory showed high variability in analytes released by platelets. The majority of other analytes produced valid results, but platelet contamination in REGARDS samples makes measurement of platelet proteins unadvisable in these samples. Future analytes considered by REGARDS or similar studies should undergo similar pilot testing.

show abstract

Section: Resultsmentioning

confidence: 84%

Validating laboratory results in a national observational cohort study without field centers: The Reasons for Geographic and Racial Differences in Stroke cohort

Gillett

Boyle

Zakai

et al. 2014

Clinical Biochemistry

View full text Add to dashboard Cite

show abstract

“…Adiponectin plays the role of an antiatherogenic and anti-inflammatory modulator [18]. Several studies suggest that adiponectin inhibits many peptides and cytokines related to atherosclerosis progression [187]. Adiponectin inhibits monocyte adherence to TNF- α -stimulated endothelial cells by suppressing adhesion molecule expression [188, 189].…”

Section: Adiponectin Hypertension and Strokementioning

confidence: 99%

Association between Risk Factors for Vascular Dementia and Adiponectin

Song

Lee

Park

et al. 2014

BioMed Research International

View full text Add to dashboard Cite

Vascular dementia is caused by various factors, including increased age, diabetes, hypertension, atherosclerosis, and stroke. Adiponectin is an adipokine secreted by adipose tissue. Adiponectin is widely known as a regulating factor related to cardiovascular disease and diabetes. Adiponectin plasma levels decrease with age. Decreased adiponectin increases the risk of cardiovascular disease and diabetes. Adiponectin improves hypertension and atherosclerosis by acting as a vasodilator and antiatherogenic factor. Moreover, adiponectin is involved in cognitive dysfunction via modulation of insulin signal transduction in the brain. Case-control studies demonstrate the association between low adiponectin and increased risk of stroke, hypertension, and diabetes. This review summarizes the recent findings on the association between risk factors for vascular dementia and adiponectin. To emphasize this relationship, we will discuss the importance of research regarding the role of adiponectin in vascular dementia.

show abstract

“…Adiponectin exists in the circulation as a full-length protein and a putative proteolytic cleavage fragment consisting of the globular C-terminal domain that is pharmacologically active (Han et al 2007). In this study, globular adiponectin was used at a concentration of 5 mg/ml (Motoshima et al 2004).…”

Section: Palmitate Induces Apoptosis Through Rosmentioning

confidence: 99%

Adiponectin inhibits palmitate-induced apoptosis through suppression of reactive oxygen species in endothelial cells: involvement of cAMP/protein kinase A and AMP-activated protein kinase

Kim¹,

Song²,

Kim³

et al. 2010

Journal of Endocrinology

View full text Add to dashboard Cite

The present study examined whether adiponectin can inhibit palmitate-induced apoptosis, and also the associated mechanisms and signal transduction pathways in human umbilical vein endothelial cells. Cells treated with 500 mM palmitate for 48 h increased reactive oxygen species (ROS) generation and induced apoptosis. Treatment with antioxidant N-acetyl-L-cysteine (1 mM) and globular adiponectin (5 mg/ml) inhibited palmitate-induced ROS generation and apoptosis. The AMP-activated protein kinase (AMPK) activator 5-aminoimidazole-4-carboxamide-1-b-D-ribofuranoside (AICAR; 1 mM), and cAMP activators forskolin (10 mM) and cholera toxin (200 ng/ml) also displayed the same effects. The inhibitory effects of adiponectin on ROS generation and apoptosis were reversed by the AMPK inhibitor compound C (40 mM), cAMP inhibitor SQ22536 (50 mM), and protein kinase A (PKA) inhibitor H-89 (10 mM). The inhibitory effect of forskolin on palmitateinduced apoptosis was reversed by compound C, whereas the inhibitory effect of AICAR was not reversed by SQ22536 and H-89. AICAR and forskolin could not inhibit palmitate-induced apoptosis in cells treated with dominantnegative AMPK. Forskolin increased phosphorylated AMPK at both Thr-172 and Ser-485/491. These results suggest that adiponectin inhibits palmitate-induced apoptosis by suppression of ROS generation via both the cAMP/PKA and AMPK pathways. Interaction between cAMP/PKA and AMPK pathways may be involved.

show abstract

Adiponectin and Cardiovascular Disease

Cited by 242 publications

References 80 publications

Validating laboratory results in a national observational cohort study without field centers: The Reasons for Geographic and Racial Differences in Stroke cohort

Validating laboratory results in a national observational cohort study without field centers: The Reasons for Geographic and Racial Differences in Stroke cohort

Association between Risk Factors for Vascular Dementia and Adiponectin

Adiponectin inhibits palmitate-induced apoptosis through suppression of reactive oxygen species in endothelial cells: involvement of cAMP/protein kinase A and AMP-activated protein kinase

Contact Info

Product

Resources

About