scholarly journals Pyruvate dehydrogenase activities during the fed-to-starved transition and on re-feeding after acute or prolonged starvation

1989 ◽  
Vol 258 (2) ◽  
pp. 529-533 ◽  
Author(s):  
M J Holness ◽  
M C Sugden
Keyword(s):  
Acute Phase ◽  
Pyruvate Dehydrogenase ◽  
Temporal Relationship ◽  
Pyruvate Dehydrogenase Complex ◽  
Hepatic Glycogen ◽  
Dietary Carbohydrate ◽  
Glycogen Depletion ◽  
Prolonged Starvation ◽  
Complex Activities ◽  
Dehydrogenase Complex

We investigated the temporal relationship between hepatic glycogen depletion and cardiac and hepatic PDH (pyruvate dehydrogenase complex) activities during the acute phase of starvation. There was a striking correlation between the decline in hepatic glycogen and PDH inactivation during the first 10 h of starvation. Re-feeding after 6 h starvation was associated with complete re-activation of PDH in liver and re-activation to approx. 75% of the fed value in heart, whereas in rats previously starved for 24-48 h re-activation was delayed in liver and diminished in heart. The results are discussed with reference to the fate of dietary carbohydrate after re-feeding.

scholarly journals The relationship between changes in lipid fuel availability and tissue fructose 2,6-bisphosphate concentrations and pyruvate dehydrogenase complex activities in the fed state

1988 ◽  
Vol 256 (3) ◽  
pp. 935-939 ◽  
Author(s):  
T J French ◽  
A W Goode ◽  
M J Holness ◽  
P A MacLennan ◽  
M C Sugden
Keyword(s):  
Fatty Acids ◽  
Pyruvate Dehydrogenase ◽  
Surgical Stress ◽  
Pyruvate Dehydrogenase Complex ◽  
Elevated Concentration ◽  
Fed State ◽  
Esterified Fatty Acids ◽  
The Relationship ◽  
Complex Activities ◽  
Dehydrogenase Complex

An elevated concentration of non-esterified fatty acids in the fed state elicited inhibition of cardiac, but not hepatic, pyruvate dehydrogenase complex (PDH). There was a modest decline in fructose 2,6-bisphosphate (Fru-2,6-P2) concentration in heart, and, to a lesser extent, in liver. Surgical stress decreased PDH activities and Fru-2,6-P2 concentrations in both heart and liver. Only the former response was abolished if postoperative lipolysis was inhibited. Surgery also decreased the [Fru-2,6-P2] in gastrocnemius: this response was abolished if lipolysis was inhibited.

scholarly journals Effects of administration of tri-iodothyronine on the response of cardiac and renal pyruvate dehydrogenase complex to starvation for 48 h

1985 ◽  
Vol 232 (1) ◽  
pp. 255-259 ◽  
Author(s):  
M J Holness ◽  
T N Palmer ◽  
M C Sugden
Keyword(s):  
Fatty Acids ◽  
Steady State ◽  
Fatty Acid ◽  
Pyruvate Dehydrogenase ◽  
Ketone Body ◽  
Ketone Bodies ◽  
Pyruvate Dehydrogenase Complex ◽  
Active Form ◽  
Complex Activities ◽  
Dehydrogenase Complex

Effects of administration of tri-iodothyronine (T3) on activities of cardiac and renal pyruvate dehydrogenase complex (active form, PDHa) were investigated. In fed rats, T3 treatment did not affect cardiac or renal PDHa activity, although blood non-esterified fatty acid and ketone-body concentrations were increased. Starvation (48 h) of both control and T3-treated rats resulted in similar increases in the steady-state concentrations of fatty acids and ketone bodies, but inactivation of cardiac and renal pyruvate dehydrogenase complex activities was diminished by T3 treatment. Inhibition of lipolysis increased renal and cardiac PDHa in control but not in T3-treated 48 h-starved rats, despite decreased fatty acid and ketone-body concentrations in both groups. The results suggest that hyperthyroidism influences the response of cardiac and renal PDHa activities to starvation through changes in the metabolism of lipid fuels in these tissues.

scholarly journals Hepatic carbon flux after re-feeding. Hyperthyroidism blocks glycogen synthesis and the suppression of glucose output observed in response to carbohydrate re-feeding

1987 ◽  
Vol 247 (3) ◽  
pp. 627-634 ◽  
Author(s):  
M J Holness ◽  
M C Sugden
Keyword(s):  
Pyruvate Kinase ◽  
Pyruvate Dehydrogenase ◽  
Pyruvate Dehydrogenase Complex ◽  
Glycogen Synthesis ◽  
Hepatic Glycogen ◽  
Intragastric Administration ◽  
Indirect Pathway ◽  
Glucose Flux ◽  
Glucose Output ◽  
Dehydrogenase Complex

1. The work investigated hepatic glycogen synthesis and glucose output after the intragastric administration of glucose or glycerol or the provision of chow ad libitum to 48 h-starved euthyroid or hyperthyroid rats. 2. After glucose administration, glycogen synthesis via the indirect pathway [Newgard, Hirsch, Foster & McGarry (1983) J. Biol. Chem. 258, 8046-8052] occurred concomitantly with reversal of glucose flux across the liver and re-activation of pyruvate kinase in the euthyroid controls. Glycogen synthesis was decreased and net glucose output continued in the hyperthyroid rats, but normal re-activation of pyruvate kinase was observed. 3. Use of 3-mercaptopicolinate indicated that the glucose released from liver of hyperthyroid rats was synthesized from substrates metabolized via the gluconeogenic pathway. 4. Hepatic glycogen synthesis was also impaired in hyperthyroid rats after administration of glycerol or chow. Measurement of portal-minus-hepatovenous concentration differences and arterial glucose concentrations after the administration of glycerol in combination with 3-mercaptopicolinate indicated that flux from triose phosphate to glucose 6-phosphate was not decreased. 5. Inhibited glycogen synthesis after chow re-feeding was associated with accelerated re-activation of hepatic pyruvate dehydrogenase complex in the hyperthyroid rats. 6. The results indicate three distinct and independent actions of hyperthyroidism after re-feeding: (i) it inhibits the reversal of glucose flux across the liver normally observed in response to carbohydrate; (ii) it affects glycogen deposition at a site distal to glucose 6-phosphate; (iii) it allows more rapid re-activation of liver pyruvate dehydrogenase complex in response to a mixed diet.

scholarly journals Hepatic glycogen synthesis on carbohydrate re-feeding after starvation. A regulatory role for pyruvate dehydrogenase in liver and extrahepatic tissues

1986 ◽  
Vol 235 (2) ◽  
pp. 441-445 ◽  
Author(s):  
M J Holness ◽  
T J French ◽  
M C Sugden
Keyword(s):  
Pyruvate Dehydrogenase ◽  
Pyruvate Dehydrogenase Complex ◽  
Glycogen Synthesis ◽  
Regulatory Role ◽  
Hepatic Glycogen ◽  
Glucose Administration ◽  
Hepatic Glucose ◽  
Extrahepatic Tissues ◽  
Lactate And Pyruvate ◽  
Dehydrogenase Complex

Glucose administration to 48 h-starved rats increased hepatic glucose, lactate, pyruvate and glycogen concentrations and re-activated PDH (pyruvate dehydrogenase complex) in kidney, but not in heart or liver. Dichloroacetate together with glucose re-activated PDH in all three tissues, decreased hepatic lactate and pyruvate concentrations and impaired glycogen resynthesis. Thus on re-feeding, delayed PDH re-activation is important for provision of precursors for hepatic glyconeogenesis.

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