Lp(a) is a cardiovascular risk factor influenced by the LPA gene and apo(a) isoforms. Their relationship is not always linear and there are discordant phenotypes, for this reason in our work we evalua Show more
Lp(a) is a cardiovascular risk factor influenced by the LPA gene and apo(a) isoforms. Their relationship is not always linear and there are discordant phenotypes, for this reason in our work we evaluated the association between apo(a) isoforms and Lp(a) levels in patients with acute coronary syndrome (ACS). To this end, 43 patients with ACS and Lp(a) >50mg/dL were studied. The isoforms were characterized in 12bands by Western blotting. The association between bands and Lp(a) concentrations was evaluated by statistical analysis. It was observed that the intermediate molecular weight bands (b5-b8) were the most frequent, with band 8 predominating. No significant association was found between isoform size and Lp(a) levels (P>.05). We conclude that in this cohort no correlation was observed between apo(a) and Lp(a) isoforms. Other genetic or regulatory mechanisms could explain the observed variability, supporting the need for larger studies. Show less
Hormone-sensitive lipase (HSL) is a key enzyme in the mobilization of fatty acids from intracellular stores. In mice, HSL deficiency results in male sterility caused by a major defect in spermatogenes Show more
Hormone-sensitive lipase (HSL) is a key enzyme in the mobilization of fatty acids from intracellular stores. In mice, HSL deficiency results in male sterility caused by a major defect in spermatogenesis. The testes contain high concentrations of PUFA and specific PUFA are essential for spermatogenesis. We investigated the fatty acid composition and the mRNA levels of key enzymes involved in fatty acid metabolism in testis of HSL-knockout mice. HSL deficiency altered fatty acid composition in the testis but not in plasma. The most important changes were decreases in the essential n-6 PUFA LNA and the n-3 PUFA ALA, and an increase in the corresponding synthesis intermediates C22:4n-6 and C22:5n-3 without changes in DPAn-6 or DHA acids. Mead acid, which has been associated with an essential fatty acid deficit leading to male infertility, was increased in the testis from HSL-knockout mice. Moreover, the expression of SCD-1, FADS1, and FADS2 was increased while expression of ELOVL2, an essential enzyme for the formation of very-long PUFA in testis, was decreased. Given the indispensability of these fatty acids for spermatogenesis, the changes in fatty acid metabolism observed in testes from HSL-knockout male mice may underlie the infertility of these animals. Show less