Carnitine modulates crucial myocardial adenosine triphosphatases and acetylcholinesterase enzyme activities in choline-deprived rats

Abstract

Choline is an essential nutrient, and choline deficiency has been associated with cardiovascular morbidity. Choline is also the precursor of acetylcholine (cholinergic component of the heart's autonomic nervous system), whose levels are regulated by acetylcholinesterase (AChE). Cardiac contraction-relaxation cycles depend on ion gradients established by pumps like the adenosine triphosphatases (ATPases) Na(+)/K(+)-ATPase and Mg(2+)-ATPase. This study aimed to investigate the impact of dietary choline deprivation on the activity of rat myocardial AChE (cholinergic marker), Na(+)/K(+)-ATPase, and Mg(2+)-ATPase, and the possible effects of carnitine supplementation (carnitine, structurally relevant to choline, is used as an adjunct in treating cardiac diseases). Adult male albino Wistar rats were distributed among 4 groups, and were fed a standard or choline-deficient diet for one month with or without carnitine in their drinking water (0.15% w/v). The enzyme activities were determined spectrophotometrically in the myocardium homogenate. Choline deficiency seems to affect the activity of the aforementioned parameters, but only the combination of choline deprivation and carnitine supplementation increased myocardial Na(+)/K(+)-ATPase activity along with a concomitant decrease in the activities of Mg(2+)-ATPase and AChE. The results suggest that carnitine, in the setting of choline deficiency, modulates cholinergic myocardial neurotransmission and the ATPase activity in favour of cardiac work efficiency.

Immunohistochemical determination of the extracellular matrix modulation in a rat model of choline‐deprived myocardium: the effects of carnitine

“…Furthermore, recent evidence has shown that choline dietary deprivation could potentially evoke changes in ion gradients during the cardiac cycle . These data, along with the intriguing question raised by the present study regarding the possible silent interference of the nutritional status with the cardiac ECM homeostasis, suggest that the efficacy of commonly prescribed drugs used in cardiac failure management could be affected .…”

“…Except for their effect on the regulation of ECM homeostasis, MMPs interfere with cell survival, differentiation, inflammation and angiogenesis triggering the expression of vascular endothelial growth factor (VEGF) [61,62]. It is already known that choline deficiency has been associated with upregulation of VEGF [63][64][65], but the causative contribution of which in the pathogenesis of choline deficiency-mediated heart dysfunction [3] could be difficult to assume in this setting as on the other hand, the concurrent established carnitine deficiency [66] might induce downregulation of VEGF [67,68], (Figure 7). Up to date, the patterns of expression of MMPs and TIMPs in the current experimental conditions, and especially as far as the heart tissue is concerned, have not been investigated.…”