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Associations of Serum Uric Acid with Endogenous Cholesterol Synthesis Indices in Men with High Cardiometabolic Risk

Publikace na 1. lékařská fakulta |
2020

Tento text není v aktuálním jazyce dostupný. Zobrazuje se verze "en".Abstrakt

Background: Patients with metabolic syndrome (MetS) have increased endogenous synthesis of cholesterol, together with lower level of intestinal cholesterol absorption. However, less is known about how individual metabolic disturbances linked to MetS correlate with dysregulated cholesterol homeostasis.

Methods: We consecutively examined 178 probands (91 women/87 men) characterized by the presence of one or two components of MetS (group with an increased cardiometabolic risk [CMR]) and 42 healthy controls (24 men/18 women) of similar age, as well. In all probands, the surrogate markers for cholesterol biosynthesis (lathosterol) and absorption (campesterol and beta-sitosterol) were measured by capillary gas chromatography.

In CMR group, we performed multivariate regression analysis to assess the dependence of the parameters of cholesterol biosynthesis/absorption on components of MetS including serum uric acid (SUA), apolipoprotein B (apoB), and age. Results: In CMR group, higher lathosterol to total plasma cholesterol (TC) ratio (LCR) was influenced by gender (P = 0.05, analysis of covariance [ANCOVA] for age), whereas ratios of campesterol (beta-sitosterol, respectively) to TC were lower in CMR group (P < 0.001 and P = 0.002, ANCOVA for age).

In men, LCR was positively associated with SUA, apoB, and hypertension (all P < 0.05). Lathosterol to campesterol or beta-sitosterol ratios were highly dependent on SUA (both P < 0.01), the former being dependent also on apoB (P < 0.01).

In women, these parameters were only weakly dependent on SUA. Conclusions: These results show that the concentration of SUA in men of CMR group is associated with the indices of de novo cholesterol biosynthesis.

This association is probably influenced by interaction of arterial hypertension and apoB levels with cholesterol homeostasis.