scholarly journals Regulation of glucose uptake by muscle. 9. Effects of fatty acids and ketone bodies, and of alloxan-diabetes and starvation, on pyruvate metabolism and on lactate-pyruvate and l-glycerol 3-phosphate-dihydroxyacetone phosphate concentration ratios in rat heart and rat diaphragm muscles

1964 ◽  
Vol 93 (3) ◽  
pp. 665-678 ◽  
Author(s):  
PB Garland ◽  
EA Newsholme ◽  
PJ Randle
Nature ◽  
1962 ◽  
Vol 195 (4839) ◽  
pp. 381-383 ◽  
Author(s):  
P. B. GARLAND ◽  
E. A. NEWSHOLME ◽  
P. J. RANDLE

1986 ◽  
Vol 251 (1) ◽  
pp. E42-E47 ◽  
Author(s):  
M. Bouisset ◽  
M. C. Pere ◽  
M. Gilbert

The present work performed in rabbits was designed to investigate whether changes in skeletal muscle metabolism could contribute to glucose homeostasis during late pregnancy a time at which there is a large glucose demand of the gravid uterus. We therefore studied the net substrate balance of glucose, lactate, free fatty acids, and ketone bodies across the hindlimb of pregnant animals (days 24 and 30) and virgin animals. Our data show that on day 24 the basal rate of glucose uptake is similar to that observed in virgin rabbits, but it decreases by approximately 60% on day 30 despite comparable levels of blood glucose and plasma insulin at both gestational ages. A moderate hyperglycemia (20% above basal level) and hyperinsulinemia (2- to 3-fold above basal level) sustained for 80 min failed to increase glucose uptake except in virgin animals. Estimates of the contribution of substrates to oxidative metabolism indicate that free fatty acids could represent the major fuel in all groups, whereas glucose would be of minor importance especially at term. It is concluded that in pregnancy a) under normoglycemia there is a reduced insulin effect on glucose uptake and b) under moderate hyperglycemia and hyperinsulinemia the insulin resistance results from an impaired stimulation of glucose uptake. Sparing glucose from the skeletal muscle, the mother can direct more glucose toward the uterus without marked increase in her production rate.


2001 ◽  
Vol 280 (3) ◽  
pp. H1173-H1181 ◽  
Author(s):  
Linda M. King ◽  
Robert J. Sidell ◽  
James R. Wilding ◽  
George K. Radda ◽  
Kieran Clarke

To determine whether the effects of fatty acids on the diabetic heart during ischemia involve altered glycolytic ATP and proton production, we measured energetics and intracellular pH (pHi) by using31P NMR spectroscopy plus [2-3H]glucose uptake in isolated rat hearts. Hearts from 7-wk streptozotocin diabetic and control rats, perfused with buffer containing 11 mM glucose, with or without 1.2 mM palmitate or the ketone bodies, 4 mM β-hydroxybutyrate plus 1 mM acetoacetate, were subjected to 32 min of low-flow (0.3 ml · g wet wt−1 · min−1) ischemia, followed by 32 min of reperfusion. In control rat hearts, neither palmitate nor ketone bodies altered the recovery of contractile function. Diabetic rat hearts perfused with glucose alone or with ketone bodies, had functional recoveries 50% lower than those of the control hearts, but palmitate restored recovery to control levels. In a parallel group with the functional recoveries, palmitate prevented the 54% faster loss of ATP in the diabetic, glucose-perfused rat hearts during ischemia, but had no effect on the rate of ATP depletion in control hearts. Palmitate decreased total glucose uptake in control rat hearts during low-flow ischemia, from 106 ± 17 to 52 ± 12 μmol/g wet wt, but did not alter the total glucose uptake in the diabetic rat hearts, which was 42 ± 5 μmol/g wet wt. Recovery of contractile function was unrelated to pHiduring ischemia; the glucose-perfused control and palmitate-perfused diabetic hearts had end-ischemic pHi values that were significantly different at 6.36 ± 0.04 and 6.60 ± 0.02, respectively, but had similar functional recoveries, whereas the glucose-perfused diabetic hearts had significantly lower functional recoveries, but their pHiwas 6.49 ± 0.04. We conclude that fatty acids, but not ketone bodies, protect the diabetic heart by decreasing ATP depletion, with neither having detrimental effects on the normal rat heart during low-flow ischemia.


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