J. Karlsson

Coenzyme Q10, Alpha-Tocopherol and Free Cholesterol in HDL and LDL Fractions

Twenty-three randomly selected plasma samples from apparently healthy, middle aged men were analysed for coenzyme Q10 (CoQ10), alpha-tocopherol (AT) and free cholesterol (FC) in: 1) whole plasma, 2) the HDL lipoprotein fraction after LDL precipitation (VLDL + LDL). CoQ10, AT and FC in plasma averaged 0.69 +/- .11, 6.74 +/- 1.78 micrograms x ml-1 and 0.59 +/- .11 mg x ml-1 and in HDL 0.17, 3.24 micrograms x ml-1 and 0.17 mg x ml-1 or 29, 48 and 29% of plasma values. Amounts of CoQ10 and AT were correlated to that of FC in all pools. The amount of HDL-CoQ10 but not of HDL-AT fell, with the HDL-FC expressed as the fraction of plasma FC. In all pools, N-AT versus AT initially increased and then levelled off, indicating saturation like conditions in contrast to CoQ10. Thus, CoQ10 and AT are differently allocated in HDL and LDL. This might have a bearing both on the suggested lipoprotein protection against peroxidation by these two antioxidants, but also on the distribution and allocation in different organs of CoQ10 and AT by HDL and LDL transportation.

Ubiquinone and α-tocopherol in plasma; means of translocation or depot

SummaryUbiquinone (UQ) and α-tocopherol (AT) are two highly lipophilic antioxidants which can be dissolved only in lipid layers or attached to protein structures. Analyses of both UQ and AT in whole blood and plasma demonstrate identical values, which excludes any significant allocation to blood cells. The lipoidic plasma structures constitute the plasma lipoprotein fractions of high (HDL), low (LDL), and very low (VLDL) density in addition to chylomicrons. This means by definition that blood and plasma UQ and AT values are limited if not related to the lipoidic deposit volume. UQ and AT increase linearly with free cholesterol (FC). FC has therefore been suggested to be a good marker for the deposit volume. The ratios UQ and AT over FC - normalized UQ (N-UQ) and normalized AT (N-AT) - have been computed for inter-and intraindividual comparisons. With a plasma UQ content of 1 μg/ml (≈ 1 μmol/l) and a plasma volume of 41, UQ makes up about 15% of the total heart content or under 1% of UQ in skeletal muscle. The corresponding value for the total extracellular UQ content is less than 2%. This means that extracellular UQ has no or a very minor role as a UQ depot. The same is true for AT. However, for transportation and allocation determinations of N-UQ and N-AT are relevant. Assuming only a lipoprotein-related transportation, healthy persons have saturated plasma UQ and AT values in only 25% and 10% of the population, respectively. All patient categories studied have been found nonsaturated. VLDL plus LDL constitute some 90% of the UQ deposit volume. VLDL and LDL are released from the liver to transport fat, for example, to muscle tissue. HDL has a corresponding cholesterol-transporting function. Uptake depends on the local lipoprotein lipase activity. Do these transports also function as means for UQ and AT transport? Per unit of FC, UQ content in VLDL+LDL is about five times that in HDL. The corresponding AT value is about unity. This difference between UQ and AT storage does not exclude the possibility that VLDL+LDL particles possess the ability to transport UQ between different compartments when so necessary.

Carbohydrate and fat metabolism in contracting canine skeletal muscle

SummaryIsolated canine gracilis muscles were perfused in situ with a free flow (systemic blood flow; FF) or a constant flow (blood from a reservoir; CF). The nervous supply was stimulated electrically for 60 min. A-V-concentration differences for glucose, pyruvate, lactate, glycerol, FFA and O2 were obtained as well as the concentrations of ATP, CP, glycogen and lactate in the muscle.Resting O2 uptake ranged from 4 to 11 μmoles×100 g−1×min−1 (FF; CF). A 30- and 5-fold increase in O2 uptake occurred during stimulation in the FF and CF-experiments, respectively. The release of lactate was, however, the same (20–40 μmoles×100 g×min−1) although the muscle lactate concentration was much higher in the CF experiments. In the CF experiment stimulation did not significantly increase glucose uptake which ranged from 0.3 to 3.3 μmoles×100 g−1 ×min−1 at rest. Conversely, stimulation resulted in a 6-fold increase in glucose uptake in the FF experiments. No definite tendency for a FFA uptake or a glycerol release was found in either experiment (FF, CF). Glycogen depletion during the stimulation period amounted to 20–30 μmoles×g−1. Thus the glucose uptake could account for only 12% of the carbohydrate utilized during the stimulation period.