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Lower adiponectin is associated with subclinical cardiovascular disease among HIV-infected men.
Ketlogetswe, KS, Post, WS, Li, X, Palella, FJ, Jacobson, LP, Margolick, JB, Kingsley, LA, Witt, MD, Dobs, AS, Budoff, MJ, et al
AIDS (London, England). 2014;(6):901-9
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Abstract
OBJECTIVE To examine whether altered levels of adipokines, adipose-derived peptides associated with myocardial infarction in the general population, may contribute to subclinical coronary atherosclerosis in HIV-infected persons. DESIGN Nested cohort study. METHODS We studied HIV-infected (HIV+) and HIV-uninfected (HIV-) men in the Multicenter AIDS Cohort Study with noncontrast computed tomography (CT) to measure coronary artery calcium and regional adiposity; 75% additionally underwent coronary CT angiography to measure plaque composition and stenosis. Adiponectin and leptin levels were assessed. Multiple regression models were used to assess associations between adipokine levels and HIV disease parameters, regional adiposity, and plaque adjusted for age, race, HIV serostatus, and cardiovascular disease (CVD) risk factors. RESULTS Significant findings were limited to adiponectin. HIV-positive men (n=493) had lower adiponectin levels than HIV-negative men (n=250) after adjusting for CVD risk factors (P<0.0001), which became nonsignificant after adjustment for abdominal visceral and thigh subcutaneous adipose tissue. Among HIV-positive men, lower adiponectin levels were associated with higher CD4 T-cell counts (P=0.004), longer duration of antiretroviral therapy (P=0.006), and undetectable HIV RNA levels (P=0.04) after adjusting for age, race, and CVD risk factors; only CD4 cell count remained significant after further adjustment for adipose tissue. In both groups, lower adiponectin levels were associated with increased odds of coronary stenosis more than 50% (P<0.007). Lower adiponectin levels were associated with increased extent of plaque in HIV-positive and of mixed plaque in HIV-negative men. CONCLUSION Adiponectin levels were lower in HIV-infected men and related to the severity of subclinical atherosclerosis, independent of traditional CVD risk factors.
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Adiponectin levels in circulation and breast milk and mRNA expression in adipose tissue of preeclampsia women.
Liu, Y, Zhu, L, Pan, Y, Sun, L, Chen, D, Li, X
Hypertension in pregnancy. 2012;(1):40-9
Abstract
OBJECTIVE Physiological insulin resistance occurs in normal pregnancy and is exaggerated in women with preeclampsia (PE). Adiponectin is a hormone with insulin-sensitizing, anti-atherogenic, and anti-inflammatory properties. Reports published on association between adiponectin levels and PE risk have been conflicting. This study sought to better determine the circulating adiponectin levels and its mRNA expression in adipose tissue in women with PE. METHODS This report includes a cross-sectional study at a Chinese clinical research center and meta-analysis. The cross-sectional study included normal pregnancy women (n = 28) and PE women (n = 20) who underwent cesarean operation. Adiponectin concentrations in maternal serum, cord blood, and colostrums were determined by ELISA. Adiponectin mRNA expression levels in adipose tissue were measured by quantitative real-time PCR. Meta-analysis was done on 13 studies, including 302 PE women and 385 normal pregnancy women. RESULTS In comparison with controls, PE women had higher serum adiponectin concentrations in maternal blood and breast milk, but lower adiponectin concentration in cord blood. Adiponectin mRNA expression in the subcutaneous (Sc) and omental adipose tissues (OM) did not differ between the two groups of women. Meta-analysis confirms that the circulating adiponectin levels were elevated in PE women (p < 0.01). CONCLUSIONS PE women had a higher adiponectin concentration in the maternal blood as well as breast milk but lower adiponectin concentration in umbilical cord blood when compared to women with normal pregnancy. The elevated circulating adiponectin levels in PE women are probably because of a reduced degradation/elimination rather than an increased synthesis of this hormone.