Levels of adiponectin and tumor necrosis factor-alpha in members of families with familial combined hyperlipidemia
David Karasek, Helena Vaverkova, Milan Halenka, Dagmar Jackuliakova, Zdenek Frysak, Ludek Slavik & Dalibor Novotny
Introduction: The aim of this study was to evaluate the plasma levels of adiponectin and tumor necrosis factor-alpha (TNF-α) in asymptomatic, nonsmoking members of families with familial combined hyperlipidemia (FCH). We investigated the association between these cytokines and selected risk factors for atherosclerosis, markers of insulin resistance and inflammation.
Methods: Eighty-two members of 29 FCH families were divided into two groups: HL (probands and hyperlipidemic first-degree relatives, n=47) and NL (normolipidemic first-degree relatives, n=35). The control groups C-HL (n=20) and C-NL (n=20) consisted of sex- and agematched healthy individuals.
Results: Compared with healthy controls, hyperlipidemic subjects had significantly lower levels of adiponectin (13.02±4.58 vs 16.19±5.39 mg/l, P<0.05), there was not a significant difference in levels of TNF-α (24.10±28.31 vs 21.33±20.18 ng/l, NS). In normolipidemic relatives there were no significant differences in adiponectin (15.77±2.95 vs 16.53±4.26 mg/l, NS) or TNF-α (25.88±34.39 vs 23.68±17.38 ng/l, NS) levels. In members of FCH families, a significant negative correlation was found between adiponectin and trigycerides, proinsulin, C-reactive protein, body mass index, waist circumference. TNF-α did not correlate with any parameters. By using a multiple regression model in hyperlipidemic subjects, adiponectin was predicted by apolipoprotein B and C-reactive protein.
Conclusions: Clinically asymptomatic individuals with FCH showed decreased levels of adiponectin. Adiponectin was negatively associated with markers of insulin resistance, chronic inflammation and visceral obesity. In hyperlipidemic individuals decreased adiponectin levels were predicted by apolipoprotein B and C-reactive protein, independently of insulin resistance and obesity.
Supported by grant IGA MZCR NS/10284-3.