The effect of amino acids, monoamines and polyamines on pyruvate dehydrogenase activity in mitochondria from rat adipocytes

1990 ◽  
Vol 93 (2) ◽  
Author(s):  
FrederickL. Kiechle ◽  
Halina Malinski ◽  
DianeM. Dandurand ◽  
JanetB. McGill
Keyword(s):  
Amino Acids ◽  
Dehydrogenase Activity ◽  
Pyruvate Dehydrogenase ◽  
Rat Adipocytes

scholarly journals Inactivation of rat adipocyte pyruvate dehydrogenase by palmitate. Protection against this effect by insulin in the presence of glucose

1979 ◽  
Vol 184 (1) ◽  
pp. 59-62 ◽  
Author(s):  
S R Sooranna ◽  
E D Saggerson
Keyword(s):  
Amino Acids ◽  
Fatty Acids ◽  
Dehydrogenase Activity ◽  
Pyruvate Dehydrogenase ◽  
Protective Action ◽  
Active Form ◽  
Rat Plasma ◽  
Epididymal Fat ◽  
Fat Pads

1. Adipocytes from rat epididymal fat-pads were incubated for 30 min with 5 mM-glucose and concentrations of lactate, pyruvate and amino acids typical of those found in rat plasma. 2. PDHa (active form of pyruvate dehydrogenase) activity was significantly increased after incubation of the cells with insulin (200 micro-i.u./ml), and decreased by incubation with palmitate (0.5–2 mM). 3. In the presence of insulin, palmitate did not decrease PDHa activity. 4. Dichloroacetate (1 mM) increased PDHa activity in the absence of palmitate to the same extent as did insulin. In the presence of dichloroacetate but the absence of insulin, palmitate decreased PDHa activity. In the presence of dichloroacetate and insulin, palmitate again did not decrease PDHa activity. 5. It is concluded that, in the presence of glucose, insulin has a strong protective action against inactivation of adipocyte PDHa by fatty acids.

Stimulation of Pyruvate Dehydrogenase Activity in Intact Rat Adipocytes by Insulin Mediator from Rat Skeletal Muscle*

Endocrinology ◽  
1985 ◽  
Vol 116 (3) ◽  
pp. 1011-1016 ◽  
Author(s):  
LEONARD JARETT ◽  
ELLEN H. A. WONG ◽  
JUDITH A. SMITH ◽  
S. LANCE MACAULAY
Keyword(s):  
Skeletal Muscle ◽  
Dehydrogenase Activity ◽  
Pyruvate Dehydrogenase ◽  
Rat Skeletal Muscle ◽  
Rat Adipocytes ◽  
Stimulation Of

Pyruvate dehydrogenase activity in cardiac mitochondria from genetically diabetic mice

Diabetes ◽  
1985 ◽  
Vol 34 (11) ◽  
pp. 1075-1081 ◽  
Author(s):  
T. H. Kuo ◽  
F. Giacomelli ◽  
J. Wiener ◽  
K. Lapanowski-Netzel
Keyword(s):  
Dehydrogenase Activity ◽  
Pyruvate Dehydrogenase ◽  
Diabetic Mice ◽  
Cardiac Mitochondria ◽  
Genetically Diabetic Mice

scholarly journals FoxO1 inhibition alleviates type 2 diabetes-related diastolic dysfunction by increasing myocardial pyruvate dehydrogenase activity

Cell Reports ◽  
2021 ◽  
Vol 35 (1) ◽  
pp. 108935
Author(s):  
Keshav Gopal ◽  
Rami Al Batran ◽  
Tariq R. Altamimi ◽  
Amanda A. Greenwell ◽  
Christina T. Saed ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Diastolic Dysfunction ◽  
Dehydrogenase Activity ◽  
Pyruvate Dehydrogenase

Regulation by Insulin and Free Fatty Acids of Pyruvate Dehydrogenase Activity in Perfused Rat Liver

1977 ◽  
Vol 5 (4) ◽  
pp. 1000-1001 ◽  
Author(s):  
DAVID L. TOPPING ◽  
M. ANWAR GOHEER ◽  
HALDANE G. COORE ◽  
PETER A. MAYES
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Dehydrogenase Activity ◽  
Rat Liver ◽  
Pyruvate Dehydrogenase ◽  
Perfused Rat Liver

scholarly journals The glucagon-induced activation of pyruvate dehydrogenase in hepatocytes is diminished by 4β-phorbol 12-myristate 13-acetate. A role for cytoplasmic Ca2+ in dehydrogenase regulation

1987 ◽  
Vol 241 (3) ◽  
pp. 729-735 ◽  
Author(s):  
J M Staddon ◽  
R G Hansford
Keyword(s):  
Dehydrogenase Activity ◽  
Phorbol Ester ◽  
Pyruvate Dehydrogenase ◽  
Kinase Activity ◽  
Rat Hepatocytes ◽  
Pyruvate Kinase Activity ◽  
Isolated Rat Hepatocytes ◽  
Intact Cells ◽  
Subsequent Addition ◽  
Isolated Rat

Phenylephrine, vasopressin and glucagon each increased the amount of active (dephospho) pyruvate dehydrogenase (PDHa) in isolated rat hepatocytes. Treatment with 4 beta-phorbol 12-myristate 13-acetate (PMA) opposed the increase in PDHa caused by both phenylephrine and glucagon, but had no effect on the response to vasopressin: PMA alone had no effect on PDHa. As PMA is known to prevent the phenylephrine-induced increase in cytoplasmic free Ca2+ concentration ([Ca2+]c) and to diminish the increase [Ca2+]c caused by glucagon, while having no effect on the ability of vasopressin to increase [Ca2+]c, these data are consistent with the notion that in intact cells an increase in [Ca2+]c results in an increase in the mitochondrial free Ca2+ concentration, which in turn leads to the activation of PDH. In the presence of 2.5 mM-Ca2+, glucagon caused an increase in NAD(P)H fluorescence in hepatocytes. This increase is taken to reflect an enhanced activity of mitochondrial dehydrogenases. PMA alone had no effect on NAD(P)H fluorescence; it did, however, compromise the increase produced by glucagon. When the extracellular free [Ca2+] was decreased to 0.2 microM, glucagon could still increase NAD(P)H fluorescence. Vasopressin also increased fluorescence under these conditions; however, if vasopressin was added after glucagon, no further increase in fluorescence was observed. Treatment of the cells with PMA resulted in a smaller increase in NAD(P)H fluorescence on addition of glucagon: the subsequent addition of vasopressin now caused a further increase in fluorescence. Changes in [Ca2+]c corresponding to the changes in NAD(P)H fluorescence were observed, again supporting the idea that [Ca2+]c indirectly regulates intramitochondrial dehydrogenase activity in intact cells. PMA alone had no effect on pyruvate kinase activity, and the phorbol ester did not prevent the inactivation caused by glucagon. The latter emphasizes the different mechanisms by which the hormone influences mitochondrial and cytoplasmic metabolism.

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