DISSOCIATION OF THE CALORIGENIC ACTION OF THYROID HORMONES FROM THE DEIODINATION OF L-THYROXINE IN VIVO

1965 ◽  
Vol 48 (3) ◽  
pp. 506-512 ◽  
Author(s):  
M. Anbar ◽  
M. Inbar ◽  
J. R. Tata
Keyword(s):  
Thyroid Hormones ◽  
Metabolic Rate ◽  
Basal Metabolic Rate ◽  
Actinomycin D ◽  
Single Injection ◽  
Small Doses ◽  
Double Isotope ◽  
Stimulation Of

ABSTRACT The rate of deiodination of L-thyroxine was measured in vivo in normal and thyroidectomized rats by a technique of double isotope (125I and 131I) labelling. Small doses of Actinomycin D administered at the same time as 3,5,3′-triiodo-L-thyronine or L-thyroxine almost completely abolished the stimulatory effect of the hormones on basal metabolic rate (B. M. R.) but slightly elevated the rate of deiodination of L-thyroxine. When studied sequentially, the stimulation of B. M. R. preceded the increase in rate of deiodination of the hormone following a single injection of triiodothyronine to thyroidectomized rats. These results suggest that the rate of deiodination is not directly associated with the action of thyroid hormones.

What determines the basal metabolic rate of vertebrate cells in vivo?

Biosystems ◽  
1994 ◽  
Vol 32 (2) ◽  
pp. 83-92 ◽  
Author(s):  
Denys N. Wheatley ◽  
James S. Clegg
Keyword(s):  
Metabolic Rate ◽  
Basal Metabolic Rate

Effect of Certain Steroids on Metabolic Rate of Hyperthyroid Rats

1957 ◽  
Vol 190 (1) ◽  
pp. 142-146 ◽  
Author(s):  
R. J. Doisy ◽  
H. A. Lardy
Keyword(s):  
Thyroid Hormones ◽  
Metabolic Rate ◽  
Basal Metabolic Rate ◽  
Male Rats ◽  
Experimental Conditions ◽  
Thyroid Glands ◽  
Estrogenic Hormones

The effects of certain steroids on the elevated basal metabolic rate (BMR) associated with thyrotoxicosis were investigated. Under our experimental conditions the adrenal cortical hormones had no effect, whereas large doses of estrogenic hormones caused marked depressions of the elevated BMR of hyperthyroid male rats. This antagonism to the calorigenic action of the thyroid hormones was demonstrable also in adrenalectomized and adrenalectomized-thyroidectomized rats. It would appear that this antagonism between the estrogenic and thyroid hormones is not mediated via the pituitary, adrenal or thyroid glands.

scholarly journals ENZYME-MEMBRANE RELATIONSHIP IN PHENOBARBITAL INDUCTION OF SYNTHESIS OF DRUG-METABOLIZING ENZYME SYSTEM AND PROLIFERATION OF ENDOPLASMIC MEMBRANES

1966 ◽  
Vol 28 (2) ◽  
pp. 181-198 ◽  
Author(s):  
Sten Orrenius ◽  
Jan L. E. Ericsson
Keyword(s):  
Actinomycin D ◽  
Enzyme System ◽  
Drug Metabolizing Enzyme ◽  
Induction Process ◽  
Autophagic Activity ◽  
Metabolizing Enzyme ◽  
Parenchymal Cells ◽  
Phenobarbital Induction ◽  
Stimulation Of

The enzyme-membrane relationship in phenobarbital induction of synthesis of drug-metabolizing enzyme system and proliferation of endoplasmic membranes has been further studied. Ultrastructural observations suggest that newly formed endoplasmic membranes in rat liver parenchymal cells arise through continuous outgrowth and budding off from pre-existing cisternae and tubules of rough-surfaced endoplasmic reticulum. The membranes induced by phenobarbital treatment persist in the cytoplasm of the hepatocyte for up to 15 days after the last of a series of 5 phenobarbital injections; the phase of regression of the induced enzymes lasts for only 5 days. Disappearance of the membranes is gradual and does not seem to be associated with increased autophagic activity in the cell. A second series of injections of phenobarbital to previously induced rats—exhibiting normal drug-hydroxylating activity but an excess of liver endoplasmic membranes—is associated with a stimulation of the rate of Pi32 incorporation into microsomal phospholipid in vivo, similar to that found during the original induction process. Administration of Actinomycin D following a single phenobarbital injection delays the regression of the enhanced drug-hydroxylating activity. Finally, the effects of Actinomycin D and puromycin on the stimulated membrane formation are discussed.

A comparison of the effects of propylthiouracil and methimazol on circulating thyroid hormones and various measures of peripheral thyroid hormone effects in thyrotoxic patients

1985 ◽  
Vol 108 (1) ◽  
pp. 51-54 ◽  
Author(s):  
P. Laurberg ◽  
J. Tørring ◽  
J. Weeke
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Metabolic Rate ◽  
Treatment Period ◽  
Basal Metabolic Rate ◽  
Newly Diagnosed ◽  
Considerable Decrease ◽  
Hormone Effects

Abstract. Two groups of patients with newly diagnosed thyrotoxicosis were treated with propylthiouracil (PTU) 400 mg every 6 h for 4 days followed by methimazol (MMI) 40 mg every 6 h for 4 days or by MMI for 4 days followed by PTU for 4 days. The shift from MMI to PTU induced a considerable decrease in serum T3 while shift from PTU to MMI led to an increase in serum T3. Serum T4 decreased gradually during the whole treatment period. The opposite variations in serum T3 were accompanied by similar opposite variations in basal metabolic rate (BMR) (P < 0.001). Hence the rapid variations in serum T3 which can be induced by PTU in thyrotoxic patients, are followed by rapid alterations in the thyrotoxic state as evaluated by BMR.

Acute effects of insulin-like growth factor I and insulin on glucose metabolism in vivo

1990 ◽  
Vol 259 (4) ◽  
pp. E561-E567 ◽  
Author(s):  
R. T. Moxley ◽  
P. Arner ◽  
A. Moss ◽  
A. Skottner ◽  
M. Fox ◽  
...  
Keyword(s):  
Growth Factor ◽  
Glucose Metabolism ◽  
Metabolic Rate ◽  
Glucose Uptake ◽  
Whole Body ◽  
Hepatic Glucose ◽  
Igf I ◽  
Glucose Metabolic Rate ◽  
Stimulation Of

We have compared the actions of insulin-like growth factor (IGF-I) and insulin on glucose metabolism in vivo, using the glucose clamp technique in rats. Both hormones caused dose-dependent inhibition of hepatic glucose production, stimulation of whole body glucose disposal, and an increase in the glucose metabolic rate of specific muscles. Infusion of IGF-I also decreased the plasma concentration of insulin. An an infusion rate of 0.57 nmol.kg-1.min-1, IGF-I led to stimulation of whole body glucose uptake that was similar to the glucose uptake produced by infusion of 0.01 nmol.kg-1.min-1 insulin. The glucose metabolic rate, as measured by 2-deoxy-D-glucose uptake, was comparable in quadriceps femoris, soleus, and diaphragm muscles during the infusion of 0.57 nmol.kg-1.min-1 IGF-I and 0.01 nmol.kg-1.min-1 insulin. However, at these rates of infusion, IGF-I caused only a 38 +/- 6% inhibition of hepatic glucose output compared with 66 +/- 12% inhibition by insulin (P less than 0.05). Thus, under these conditions, muscle is more responsive than liver to IGF-I, which agrees with the complement of IGF-I receptors in the two tissues.

scholarly journals Regulation of the synthesis of lutropin-induced protein in rat testis Leydig cells

1978 ◽  
Vol 170 (1) ◽  
pp. 9-15 ◽  
Author(s):  
Felix H. A. Janszen ◽  
Brian A. Cooke ◽  
Maria J. A. Van Driel ◽  
Henk J. Van Der Molen
Keyword(s):  
Protein Synthesis ◽  
Cyclic Amp ◽  
Leydig Cells ◽  
Actinomycin D ◽  
Polyacrylamide Gel Electrophoresis ◽  
Phosphodiesterase Inhibitor ◽  
Dibutyryl Cyclic Amp ◽  
Rat Testis ◽  
Stimulation Of

The mechanism of action of lutropin on the stimulation of the synthesis of a specific lutropin-induced protein in rat testis Leydig cells was investigated. Lutropin-induced protein has a mol.wt. of approx. 21000 and is detected by labelling the Leydig-cell proteins with [35S]methionine, followed by separation by polyacrylamide-gel electrophoresis and radioautography of the dried gel. The incorporation of35S into lutropin-induced protein was used as an estimate for the synthesis of the protein. Incubation of Leydig cells with dibutyryl cyclic AMP or cholera toxin also resulted in the stimulation of synthesis of the protein. Synthesis of lutropin-induced protein, when maximally stimulated with 100ng of lutropin/ml, could not be stimulated further by addition of dibutyryl cyclic AMP. Addition of 3-isobutyl-1-methylxanthine, a phosphodiesterase inhibitor, further increased synthesis of the protein in the presence of a submaximal dose of lutropin (10ng/ml) but not in the absence of lutropin or with maximal amounts of lutropin (100 and 1000ng/ml). Actinomycin D prevented the effect of lutropin on the stimulation of lutropin-induced protein synthesis when added immediately or 1h after the start of the incubation, but not when added after 5–6h. This is interpreted as reflecting that, after induction of mRNA coding for lutropin-induced protein, lutropin had no influence on the synthesis of the protein in the presence of actinomycin D. Synthesis of the protein was also stimulated in vivo by injection of choriogonadotropin into rats 1 day after hypophysectomy, and the time course of this stimulation of lutropin-induced protein synthesis in vivo was similar to that obtained by incubating Leydig cells in vitro with lutropin. From these results it is concluded that stimulation of lutropin-induced protein synthesis by lutropin is most probably mediated by cyclic AMP and involves synthesis of mRNA.

scholarly journals THE EFFECTS OF SECRETAGOGUES ON THE INCORPORATION OF [2-3H]MYOINOSITOL INTO LIPID IN CYTOLOGICAL FRACTIONS IN THE PANCREAS OF THE GUINEA PIG IN VIVO

1973 ◽  
Vol 56 (3) ◽  
pp. 736-745 ◽  
Author(s):  
Dorothy Gerber ◽  
Margaret Davies ◽  
Lowell E. Hokin
Keyword(s):  
Endoplasmic Reticulum ◽  
Single Injection ◽  
Enzyme Secretion ◽  
Amylase Level ◽  
Membrane Flow ◽  
Secretory Cycle ◽  
Microsome Fraction ◽  
Stimulation Of ◽  
Cholinergic Drug

Stimulation of enzyme secretion in the pancreas on injection of a single dose of the cholinergic drug, pilocarpine, was associated with an increased incorporation of [2-3H]myoinositol into a lipid, which was previously characterized as phosphatidylinositol. Stimulation of enzyme secretion by hourly injection of the pancreozymin congener, caerulein, led to more increased phosphatidylinositol synthesis than with a single injection of pilocarpine. The amylase level of the pancreas remained at a low level as long as caerulein was injected, indicating continued stimulation of enzyme secretion even though increased phosphatidylinositol synthesis ceased after 6 h. Feeding gave the same stimulation of phosphatidylinositol synthesis as caerulein. The major synthesis of phosphatidylinositol in controls and the stimulation of phosphatidylinositol synthesis by pilocarpine was entirely confined to the microsome fraction throughout the experiments (up to 18 h). This shows that there is no flow of microsomal membrane (smooth- or rough-surfaced endoplasmic reticulum) to other membranous structures throughout the secretory cycle and beyond. It is concluded that the stimulation of phosphatidylinositol synthesis by pancreatic secretagogues is confined to microsomal elements and does not play any role in membrane flow.

scholarly journals Basal metabolic rate and thyroid hormones of late-middle-aged and older human subjects: the ZENITH study

2005 ◽  
Vol 59 (S2) ◽  
pp. S53-S57 ◽  
Author(s):  
N Meunier ◽  
J H Beattie ◽  
D Ciarapica ◽  
J M O'Connor ◽  
M Andriollo-Sanchez ◽  
...  
Keyword(s):  
Thyroid Hormones ◽  
Metabolic Rate ◽  
Basal Metabolic Rate ◽  
Human Subjects ◽  
Middle Aged
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