APOLIPOPROTEIN C-III AND THE METABOLIC SYNDROME IN POSTMENOPAUSAL SEDENTARY WOMEN

Abstract

It has been shown that apolipoprotein C-III (apo C-III) inhibits the uptake of the triglyceride-rich (Tg) very low density lipoproteins (VLDL) by the liver and also inhibits lipoprotein lipase activity in vivo. These two factors may induce hypertriglyceridaemia, a biological marker of the metabolic syndrome. PURPOSE: To analyse the association between plasma triglycerides (Tg) and apolipoprotein C-III (apo C-III) and study the relationship between these measures and other cardiovascular risk factors that characterize the metabolic syndrome (high density lipoprotein cholesterol [HDL-chol], insulin, and low density lipoprotein cholesterol (LDL-chol]) in postmenopausal women. METHODS: Subjects were 123 women (age: 61.2 ± 6.3 years; weight: 66.5 ± 11.5 kg; height: 154.1 ± 5.9 cm; BMI: 27.9 ± 4.3 kg/m2), 35 of whom were on hormone replacement therapy (HRT). Tg and HDL-chol were quantified by enzymatic colorimetric methods, LDL-Chol was calculated with the Friedwald equation, insulin was determined by RIA, and apo C-III assessed with a immunoturbidimetric assay. RESULTS: Positive partial correlations, controlling for age and HRT, were observed between apo C-III and triglycerides, r = 0.31, p < 0.05. Tg was significantly (p < 0.05) associated with HDL-chol (r = −0.55), insulin (r = 0.47) and LDL-chol (r = 0.21), while apo C-III was not related (p > 0.05) with HDL-chol, insulin, and LDL-chol. CONCLUSION: In this sample of postmenopausal sedentary women with and without HRT, apo C-III was directly associated with Tg but not with any other marker of the metabolic syndrome. Triglyceride level was associated with these variables, reinforcing the current knowledge that hypertriglyceridaemia tends to cluster with high levels of LDL-chol, hyperinsulinemia, and low levels of HDL-chol. Apo C-III may have a regulatory effect that influences Tg levels, suggesting that it has an indirect role within the scope of the metabolic syndrome.