Stimulation of oxidative metabolism by thyroid hormones in an apodan amphibian, Gegenophis carnosus (Beddome)

1990 ◽  
Vol 79 (2) ◽  
pp. 246-252 ◽  
Author(s):  
K.K. Sutharam ◽  
M.C.Subash Peter ◽  
Oommen V. Oommen
Keyword(s):  
Thyroid Hormones ◽  
Oxidative Metabolism ◽  
Stimulation Of

Adrenal hormones and oxidative metabolism of the garden lizard (Calotes versicolor)

1983 ◽  
Vol 99 (2) ◽  
pp. 211-216 ◽  
Author(s):  
B. B. Pd. Gupta ◽  
J. P. Thapliyal
Keyword(s):  
Oxygen Consumption ◽  
Thyroid Hormones ◽  
Oxidative Metabolism ◽  
Whole Body ◽  
Endocrine Glands ◽  
Adrenal Hormones ◽  
Calotes Versicolor ◽  
Specific Tissue ◽  
Almost All ◽  
Stimulation Of

Daily administration of adrenaline over a 10-day period invariably induced significant increases in the metabolic rate of the whole body and of specific tissue (liver, muscle, kidney and brain) of both intact and thyroidectomized lizards except during June (breeding season) when the presence of thyroid hormones was a prerequisite for the stimulation of oxygen consumption by the whole body, muscle, kidney and brain but not by the liver. Corticosterone had no effect on whole body oxygen consumption but stimulated, inhibited or was without influence on the oxygen consumption of individual tissues, depending on the season and the presence or absence of thyroid hormones. It is suggested that adrenaline, due to its temperature-independent calorigenic effect, acts as the emergency hormone for energy release and helps the animal to survive during hibernation (winter months) when almost all the endocrine glands are inactive.

Mechanism of increase of myocardial oxygen uptake produced by catecholamines1

1965 ◽  
Vol 209 (5) ◽  
pp. 913-918 ◽  
Author(s):  
Francis J. Klocke ◽  
Gerard A. Kaiser ◽  
John Ross ◽  
Eugene Braunwald
Keyword(s):  
Cardiac Arrest ◽  
Oxygen Uptake ◽  
Oxidative Metabolism ◽  
Beating Heart ◽  
Canine Heart ◽  
Direct Stimulation ◽  
Before And After ◽  
Heart Preparation ◽  
Hemodynamic Performance ◽  
Stimulation Of

The relative roles of augmented hemodynamic performance and direct stimulation of oxidative metabolism in mediating the increase of myocardial oxygen uptake (MVo2) produced by catecholamines have been examined in an isolated canine heart preparation. The responses of MVo2 to graded doses of isoproterenol, norepinephrine, or epinephrine were determined before and after the induction of cardiac arrest with potassium. Although increases of MVo2 occurred in the arrested state with the larger doses of the amines, they constituted only a small fraction, generally between 5 and 20%, of the increases produced by the same doses of amines when the hearts were beating. It is concluded that while large doses of catecholamines can increase oxidative metabolism of the nonbeating heart by a small amount, the increases of MVo2 produced by catecholamines in the beating heart are due in large part to the hemodynamic alterations which the amines induce.

Imatinib Mesylate Induced Reversal of Leukemic Gene Phenotype in HL60 Cells Coincides with Stimulation of Oxidative Metabolism.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4190-4190
Author(s):  
Michael Pfeilstocker ◽  
Peter Wihlidal ◽  
Franz Varga ◽  
Elisabeth Pittermann ◽  
Heidrun Karlic
Keyword(s):  
Type 2 Diabetes ◽  
Transcription Factors ◽  
Cell Line ◽  
Imatinib Mesylate ◽  
Oxidative Metabolism ◽  
Myeloid Leukemia ◽  
Fat Metabolism ◽  
Fold Stimulation ◽  
Stimulation Of

Abstract Besides blockade of tyrosine kinases such as c-kit, Imatinib mesylate (IM) regulates glucose flux through downregulation of GLUT-1 transporters in human leukemia cells. This mechanism has the potential to induce regression of type 2 diabetes and hyperlipidemia as observed in patients with chronic myeloid leukemia or hypereosinophilic syndrome. In addition, there is a stimulatory effect of IM on differentiation of human mesenchymal stem cells. Its synergism with retinoic acid or low dose Ara-C is applied in treatment of acute myeloid leukemia (AML). Thus, the AML-derived c-kit positive cell line HL60 was chosen for studying the effect of IM on expression of genes associated with differentiation and metabolism. We analysed the possible feedback on transcription factors (AML1 and AML3) and consequences regarding differentiation and metabolism - associated genes. Quantitative reverse transcriptase PCR analyses revealed that IM treatment of HL60 cells downregulates mRNA synthesis of AML1 and AML3 by 70% without affecting transcription of the c-abl tyrosine kinase. IM reduces expression of CD34 mRNA from 20% to 6% of the housekeeping gene G6PD. The appearance of differentiated cells was accompanied by a remarkable stimulation of mRNAs from CD11b and CD14 (monocyte markers) reaching 4-fold higher expression levels relative to G6PD. This was associated with an increased proportion of osteocalcin (OCN), which has recently been shown to enhance mitochondrial activity. A 2-fold stimulation of a fat-metabolism associated mitochondrial palmitoyltransferase (CPT1B) and 10-fold stimulation of microsomal carnitine palmitoyltransferase and the carnitine transporter OCTN2 supports previous data indicating an IM-associated stimulation of oxidative metabolism resulting in a regression of type-2 diabetes and hyperlipidemia. Our current investigations show that IM-associated attenuation of cell proliferation inhibited transcription factors AML1 and AML3 and triggered differentiation in the leukemic cell line HL60, as reflected by altered mRNA expression of surface marker genes. The IM - induced stimulation of lipid metabolism in HL60 confirms previous data indicating a reversal of the Warburg effect in K562 cells without cytocidal activity. This indicates a similar mechanism as known for other drugs and strategies targeting glucose or fat metabolism, which are discussed in the context of cancer prevention and treatment.

Prolactin and Growth Hormone Stimulation of Lactation in Mice Requires Thyroid Hormones

1999 ◽  
Vol 221 (4) ◽  
pp. 345-351 ◽  
Author(s):  
A. V. Capuco ◽  
S. Kahl ◽  
L. J. W. Jack ◽  
J. O. Bishop ◽  
H. Wallace
Keyword(s):  
Growth Hormone ◽  
Thyroid Hormones ◽  
Hormone Stimulation ◽  
Stimulation Of

scholarly journals Stimulation of the respiration rate of rat liver mitochondria by sub-micromolar concentrations of extramitochondrial Ca2+

1987 ◽  
Vol 245 (1) ◽  
pp. 217-222 ◽  
Author(s):  
J D Johnston ◽  
M D Brand
Keyword(s):  
Respiration Rate ◽  
Rat Liver ◽  
Oxidative Metabolism ◽  
Mitochondrial Respiration ◽  
Liver Mitochondria ◽  
Ruthenium Red ◽  
Rat Liver Mitochondria ◽  
Mitochondrial Matrix ◽  
Stimulation Of

1. The respiration rate of rat liver mitochondria was stimulated by up to 70% when the extramitochondrial Ca2+ concentration was raised from 103 to 820 nM. This occurred when pyruvate, 2-oxoglutarate, or threo-(Ds)-isocitrate was employed as substrate, but not when succinate was used. 2. Ruthenium Red prevented the stimulation of mitochondrial respiration by extramitochondrial Ca2+, showing that the effect required Ca2+ uptake into the mitochondrial matrix. 3. Starvation of rats for 48 h abolished the stimulation of mitochondrial respiration by extramitochondrial Ca2+ when pyruvate was used as substrate, but did not affect the stimulation of 2-oxoglutarate oxidation by extramitochondrial Ca2+. 4. Our findings are in accord with proposals that oxidative metabolism in liver mitochondria may be stimulated by Ca2+ activation of intramitochondrial dehydrogenases.

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