Abstract
It was shown that the energy metabolism of the heart mitochondria of experimental animals and patients is more resistant to damage at combined postinfarction cardiosclerosis and diabetes in comparison with the individual pathology. We found that the changes of free fatty acid content and conjugation of the processes of oxidation and phosphorylation in heart mitochondria are components of the metabolic stability of myocardium at the combined development of postinfarction cardiosclerosis and diabetes mellitus. Our data demonstrate a direct link between the violations of the processes of oxidative phosphorylation and accumulation of free fatty acids owing to change in activity of endogenous phospholipases, in particularly, mi- tochondrial phospholipase A2. Similar results were obtained for intraoperative biopsy specimens of patients’ hearts, and of adult Wistar rats’ hearts. We hypothesized that the preservation of energy metabolism is a manifestation of summing up of compensatory processes at de- velopment of nonspecific response of cells to damage at the early stages of pathological pro- cess.
Highlights
It is well known that many pathologies of the cardiovascular system are accompanied by increased activity of endogenous phospholipases and, as a consequence, by accumulation of free fatty acids [1] which, in turn, provokes uncoupling of the processes of oxidation and phosphorylation in mitochondria [2]
We carried out research of fatty acid content in serum, homogenates of the myocardium and in the mitochondria suspension of animals and humans in all groups studied (Table 2)
It was found that fatty acid content in blood serum of experimental animals was reliably higher in all experimental groups in relation to control, but in comparison between the experimental groups no reliable differences were observed (Table 2)
Summary
It is well known that many pathologies of the cardiovascular system are accompanied by increased activity of endogenous phospholipases and, as a consequence, by accumulation of free fatty acids [1] which, in turn, provokes uncoupling of the processes of oxidation and phosphorylation in mitochondria [2]. Lin action on adipose tissue at diabetes mellitus (DM) leads to the increased content of fatty acids in blood and their intake into the myocardial cells. Myocardial consequences of DM even in conditions of adequate oxygen supply of myocardium resemble metabolic imbalance in myocardium of patients with severe coronary heart disease (CHD) [3,4]. Animals with combined pathology are characterized by less pronounced changes in glucose levels, body weight and heart [9,10]
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