CONICET | Buscador de Institutos y Recursos Humanos

Experimental works in animals or in human populations have demonstrated that the manipulation of mineral components of the diet exerts a significant influence on the ethiopathogenesis of different illnesses including cardiovascular diseases. In relation to calcium ion (Ca2+) it was demonstrated that it is crucial for numerous biological functions. It is involved in the regulation of several enzyme systems, cytoskeleton structure and cellular motility. In this review we summarized the most important contributions carried out about the relationship between calcium level and lipid metabolism. We found that feeding rats a calcium-deficient diet evoked changes in the quality and proportion of fatty acid (FA) chains acylated to neutral and polar lipids from several tissues. These changes, characterized by an increment of saturated FA and a depletion of polyunsaturated FA were associated with alterations in various enzyme activities involved in lipid metabolism. We found a decrease in phospholipase A2 and in desaturase (delta 5, delta 6 y delta 9) activities with a reduction in the transcription rate for mRNA that encodes for liver delta 6 desaturase. Calcium-deficient diet also produced an increase in microsomal acyl-CoA synthetase activity for different fatty acids without any alteration in substrate selectivity. Some enzyme activities involved in glycerolipid metabolism were also modified. These changes produced modifications in the interlipid and lipid/protein relationships, and in the pattern of incorporation of labeled precursors into each glycerolipid classes. All these findings, together with our recent study dealing with the direct correlation between NO availability and [Ca2+] in liver, suggest that a decreased intake of calcium should be considered as a harmful- non conventional- risk factor for the development of cardiovascular diseases.