By Stephen W. Schaffer, M. Saadeh Suleiman
This booklet covers the $64000 position that Mitochondria play in metabolic pathways, legislation of cytosolic ingredients, beginning sign pathways, legislation of apoptosis, and modulating mobile hypertrophy and proliferation.
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Extra resources for Mitochondria: The Dynamic Organelle (Advances in Biochemistry in Health and Disease)
This increase in flux could be a result of either an increase in sarcolemmal abundance of CD36 or an increase in intrinsic transport activity (Luiken et al. 2004a). In similar studies performed in skeletal muscle, the apparent maximum velocity of transport is increased independent of changes in Km. This finding suggests that the increase in fatty acid uptake is dependent on an increase in total transporter in the sarcolemma (Bonen et al. 2000). Subsequent fractionation of cardiac myocytes showed that under basal conditions CD36 is localized at both the sarcolemma membrane and in intracellular stores (Luiken et al.
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1993). These long-chain fatty acylCoAs can then either be esterified to TGs by glycerolphosphate acyltransferase 2. Regulation of Fatty Acid Oxidation of the Heart 35 (Coleman et al. 2000) or transported into the mitochondria for subsequent -oxidation (Lopaschuk et al. 1994a). 5. Triacylglycerol as a Source of Fatty Acids TG stores in the myocardium can be very important endogenous sources of fatty acids for fatty acid oxidation (Crass 1977; Paulson and Crass 1982; Saddik and Lopaschuk 1992). In the unphysiological condition of an isolated heart being perfused in the absence of exogenous fatty acids, the heart can meet 50% of its energy requirements by mobilizing its TG stores.