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Randle cycle

Randle PJ The glucose-fatty acid cycle—biochemical aspects. Atherosclerosis Rev 1991 22 183-... [Pg.236]

Figure 16.1 The glucose/fatty add cycle. The dotted Lines represent regulation. Glucose in adipose tissue produces glycerol 3-phosphate which enhances esterification of fatty acids, so that less are available for release. The effect is, therefore, tantamount to inhibition of lipolysis. Fatty acid oxidation inhibits pyruvate dehydrogenase, phosphofructokinase and glucose transport in muscle (Chapters 6 and 7) (Randle et al. 1963). Figure 16.1 The glucose/fatty add cycle. The dotted Lines represent regulation. Glucose in adipose tissue produces glycerol 3-phosphate which enhances esterification of fatty acids, so that less are available for release. The effect is, therefore, tantamount to inhibition of lipolysis. Fatty acid oxidation inhibits pyruvate dehydrogenase, phosphofructokinase and glucose transport in muscle (Chapters 6 and 7) (Randle et al. 1963).
P. J. Randle, P. B. Garland, C. N. Hales, and E. A. Newsholme, The glucose fatty-acid cycle. Its role in insulin sensitivity and the metabolic disturbances of diabetes mellitus, Lancet 1, 785-789 (1963). [Pg.9]

Whereas most studies have focused on fhe effects of NA on lipid metabohsm, the action of NA on carbohydrate metabohsm is less well understood. After acute NA administration, glucose concentrations have been reported to decrease [435], rise [436] or remain unaltered [437] in rats and humans. Results of glucose tolerance tests after acute NA intake have also been inconsistent [438, 439]. Chronic administration of NA has consistenfly resulted in deterioration of glucose tolerance and elevation of fasting blood glucose concentrations in normal humans [439-441] and impairment of glycemic control in NIDDM patients [440]. These effects are contrary to expectations based on the glucose-FA cycle of Randle and coworkers [38, 39]. If reduction of hpolysis and NEFA availability reduces oxidation... [Pg.286]

Randle has reviewed his concept of a glucose-fatty acid cycle, with some new experimental material. 5 There has been a recent review of gluconeogenesis, with good current references.The control of phospho-fructokinase, one of the important rate limiting enzymes of glycolysis, is still not fully understood. The activity of the enzyme in mammalian muscle is influenced by substrate concentration and by wiiich can acti-... [Pg.181]

The term "caloric homeostasis" was coined by Fredickson and Gordon (1958) to express the joint and complementary roles which free fatty acids and glucose play in the blood in supplying the respiration fuel. The interconversion of carbohydrate and fat has been described by Randle et al. (1963) as the glucose-fatty acid cycle (see Figure 2) Reactions 1 and 2 occurs when there is a surplus of carbohydrate (or of ingested fat). Reaction 3 occurs on fasting. The plasma non-esterified fatty acid... [Pg.56]

Fig. 2 The "glucose fatty acid cycle" according to Randle et al., 1963. Fig. 2 The "glucose fatty acid cycle" according to Randle et al., 1963.
Peuhkurinen KJ (1982)Accumulation and disposal of tricarboxylic acid cycle intermediates during propionate oxidation in the isolated perfused rat heart. Biochem. Biophys. Acta 721 124-134 Randle PJ, Tubbs PK (1979) Carbohydrate and fatty acid metabolism. In Berne, RM, Spherelakis N, Geiger SR (eds) Handbook of Physiology, The Cardiovascular System. Bethesda pp 804-844... [Pg.410]

Bevilacqua, S., Buzzigoli, G., Bonadonna, R., Brandi, L. S., Oleggini, M., Boni, C., Geloni, M., and Ferrannini, E., 1990, Operation of Randle s cycle in patients with NIDDM, Diabetes 39 383-389. [Pg.399]

For a reversible redox couple, the number of electrons transferred in the electrode reaction can be determined by the Randles-Sevcik equation for the forward sweep of the first cycle... [Pg.56]

Phosphorylation - Dephosphorylation Cycles and the Regulation of Fuel Selection in Mammals Philip J. Randle... [Pg.178]

Wieland (1961) proposed a theory which attributes the defect in lipogenesis to an altered NADH NAD ratio in diabetes. The increased rate of fatty acid oxidation leads to a raised NADH NAD within the diabetic liver cell. This causes the NADH-dependent ox-aloacetate-malate equilibrium to shift in favor of malate and, therefore, a lowering of the limiting component of the citric acid cycle, viz. oxaloacetate. This would result in extreme intracellular deficiency of citrate. While this theory might have some pertinence for the liver, the same changes apparently do not take place in heart. The citrate concentration is elevated in hearts from diabetic or fasted rats (Parmeggiani and Bowman, 1963 Garland and Randle, 1964). [Pg.135]

R.L. Larson, and R.F. Randle, The bovine estrous cycle and synchronization of estrus. College of Veterinary Medicine, Kansas State University, USA, 2006. [Pg.238]


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See also in sourсe #XX -- [ Pg.49 ]




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