[Use of the fatty emulsion lipomaiz in certain kidney diseases].
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The subcellular distribution and composition of endogenously synthesized lipid in isolated white adipose cells were studied to determine the nature and extent of lipid compartmentation. After brief incubation of cells with labeled glucose, acetate, or palmitic acid, over 90% of newly synthesized triglyceride was localized in the bulk-lipid phase, indicating rapid intracellular transport and storage. From 13 to 20% of the newly formed lipid was diglyceride, and over 95% of it was localized in the central lipid-storage vacuole rather than in organelle systems concerned with esterification, thus indicating intracellular segregation of newly synthesized partial glycerides. Most of the newly synthesized phosphatides partitioned with membranous organelles. Synthesis of cholesterol or cholesteryl ester was negligible. After brief incubation of cells with labeled glucose, the relative specific activity of organelle triglyceride was mitochondria >> microsomes > liposomes > soluble supernatant > bulk lipid. In pulse-chase studies the specific activity of organelle triglyceride decreased and that of the bulk fraction increased reflecting intracellular lipid transport. The data suggest that a significant proportion of newly formed lipid is transferred from mitochondrial membranes into the storage vacuole by direct lipid-lipid interaction. Liposomes, which consist of small enclosed lipid droplets resembling chylomicrons, contained triglycerides of specific activity similar to microsomal triglyceride. While the evidence that liposome triglyceride may be microsomal in origin is indirect, the results do indicate that the liposome fraction represents a phase in the transport and(or) storage of new glyceride. At least two forms of compartmentation of newly synthesized lipids occurred. The first, termed "structural," refers to localization of lipids to organelle fractions. The second type of compartmentation, termed "chemical," concerns the intracellular segregation of a specific lipid class. The accumulation and segregation of newly synthesized diglyceride in the bulk storage pool are examples of the latter form of compartmentation.
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Eight male and female students were studied during exercise to exhaustion on a bicycle ergometer at 80 and 100% of Vo2max following the ingestion of water (W), 75 g of glucose (G) or a liquid meal (M) (10 g protein, 12.5 g fat, 15 g CHO). When compared to the endurance ride (80% Vo2max) in the W treatment, endurance performance time was reduced by 19%, (p less than .05) (53.2 to 43.2 min) as a result of the preexercise glucose feeding (Trial G). No difference in performance at 80% Vo2max was found between the W and M trials. The preexercise feedings had no effect on exercise time to exhaustion at 100% Vo2max. During the G and M trials at 80% Vo2max, most of the subjects demonstrated a transient decline in serum glucose (less than 3.5 mM). After 30-40 min. of exercise, however, serum glucose returned to normal and was seldom low at the time of exhaustion. Serum free fatty acids (FFA) were depressed throughout the G trial. The results of these experiments indicate impaired lipid mobilization following CHO ingestion. The present data support our earlier findings (11) which demonstrate that glucose feedings 30-45 minutes before endurance exercise increase the rate of CHO oxidation and impede the mobilization of FFA, thereby reducing exercise time to exhaustion.
Whereas the control of cardiac function occurs through the sympathetic nervous system via the beta 1-receptors, metabolic processes are controlled via beta 1- and/or beta 2-receptors accordingly. The inhibition occurring during the use of non-selective beta-receptor blockade of the beta 2-receptors also consequently leads undesirably to possible impairment of insulin secretion and especially to glycogenolysis in the skeletal musculature. The initially more intensely inhibited lipolysis under mixed beta-receptor blockade lead among other things to more severe changes in the lipoproteins than a predominantly beta 1-selective receptor blockade through reactive compensation procedures. Generally in the treatment of arterial hypertension, as also of cardiovascular disease with beta-receptor blocker, a beta 1-receptor blocker is preferred in order to avoid as far as possible disadvantageous metabolic actions of such treatment.
The investigation (Fig. 1) clearly shows that the ability of isoprenaline in particular and, to a less extent, of noradrenaline to increase the accumulation of cyclic AMP and thus also the rate of lipolysis is enhanced in hyperthyroidism. No evidence was found of changes in the sensitivity to either beta 1- or alpha -adrenergic agonists. Although further studies are needed, the findings supported the idea that the augmented cyclic AMP accumulation is due to changes below the receptor level. Second, a significant decrease was observed in the apparent Vmax of the PDE with apparent low Km. Third, metabolic disturbances closer to the lipolytic system may exist. Some indirect evidence for this hypothesis was the finding of relatively more rapid lipolysis in relation to the cyclic AMP level in hyperthyroidism. The investigations have raised a number of questions about the nature of the metabolic changes in hyperthyroidism. The findings suggest that there are multiple abnormalities, localized at different levels of mechanisms regulating lipid mobilization. Investigations of subcutaneous tissue fragments in man seem to offer good opportunities for exploring these abnormalities.