Effects of Single Cortisone Injections on Brown Adipose Tissue of Developing Rats

1971 ◽  
Vol 49 (6) ◽  
pp. 501-507 ◽  
Author(s):  
Josef Skala ◽  
Peter Hahn
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Mitochondrial Protein ◽  
Mitochondrial Fraction ◽  
Brown Fat ◽  
Endogenous Respiration ◽  
Glycerophosphate Dehydrogenase ◽  
Brown Adipose ◽  
Old Rats ◽  
Brown Fat Mitochondria

An injection of a single dose of cortisone acetate (5 mg/100 g body weight) to 9-day-old rats resulted in the following changes in brown adipose tissue 24 h later: (1) the fresh weight was increased due to fat accumulation; (2) the DNA content of whole interscapular brown fat stayed unaltered, while the RNA content was increased; (3) specific activities of cytoplasmic alpha-glycerophosphate dehydrogenase and malic enzyme were increased; (4) the percentage of mitochondrial protein in the whole tissue protein was not changed, but mitochondria seemed to be more fragile, fewer were recovered by a standard isolation procedure, and more cytochrome c oxidase contaminated the microsomal fraction; (5) mitochondrial alpha-glycero-phosphate dehydrogenase and succinate dehydrogenase activities were decreased per milligram homogenate protein and (in isolated mitochondrial fraction) per milligram mitochondrial protein; (6) the endogenous respiration of brown fat mitochondria was activated much less by carnitine and CoA; and (7) CO2 formation from palmitate-14C by isolated mitochondria was considerably lower.A similar injection to 30-day-old rats had no significant effect.It is suggested that a single injection of cortisone affects the mitochondrial structure of brown adipose tissue and the ability to oxidize fatty acids and that it is effective on day 10 but not on day 30.

Brown adipose tissue activity in hypocaloric-diet fed lactating rats

1986 ◽  
Vol 6 (7) ◽  
pp. 669-675 ◽  
Author(s):  
Francesc Villarroya ◽  
Antonio Felipe ◽  
Teresa Mampel
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Mitochondrial Protein ◽  
Caloric Intake ◽  
Brown Fat ◽  
Hypocaloric Diet ◽  
Lipoprotein Lipase Activity ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Brown Adipose Tissue Activity

Hypocaloric diet feeding reduced the mitochondrial protein content and whole tissue GDP-binding in interscapular brown adipose tissue from both virgin and lactating rats. A reduction in brown fat lipoprotein lipase activity was also detected in underfed virgin and lactating animals. These results indicate that lactation in the rat, even though it produces a reduction in brown fat activity, does not impair the capacity of the tissue to respond to a diminished caloric intake by lowering its activity further.

Uncoupling protein and its mRNA in brown adipose tissue of newborn rabbits

1989 ◽  
Vol 67 (1) ◽  
pp. 54-58 ◽  
Author(s):  
D. K. Rozon ◽  
W. H. Harris ◽  
A. M. Verrinder Gibbins
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Messenger Rna ◽  
Uncoupling Protein ◽  
Mitochondrial Protein ◽  
Brown Fat ◽  
Guanosine Diphosphate ◽  
Mitochondrial Inner Membrane ◽  
Age Related ◽  
Brown Adipose

Guanosine diphosphate binding to the uncoupling protein of isolated mitochondria of brown adipose tissue in newborn rabbits was measured as an index of thermogenic activity. The binding was 0.281 ± 0.022 nmol GDP/mg mitochondrial protein at 1 day of age, 0.214 ± 0.017 at 3 days, 0.428 ± 0.038 at 5 days, and 0.208 ± 0.016 at 7 days. The increase in binding between 3 and 7 days of age suggests that the brown fat has an increased thermogenic capacity at that age. In addition, the potential for synthesis of the uncoupling protein was investigated in 1- to 5-day-old newborn rabbits by probing the total cellular ribonucleic acid for the messenger that codes for uncoupling protein. The amount of uncoupling protein messenger was highest at 1 day of age and declined at least until 5 days of age. Because the amount of uncoupling protein messenger decreased as the GDP binding increased, the results suggest that either the initially translated uncoupling protein was unmasked at about 5 days of age or there was a delay in the incorporation of uncoupling protein into the mitochondrial inner membrane, or both.Key words: brown fat, neonatal rabbit, thermogenin, messenger RNA, age-related changes.

scholarly journals UNUSUALLY HIGH MITOCHONDRIAL ALPHA GLYCEROPHOSPHATE DEHYDROGENASE ACTIVITY IN RAT BROWN ADIPOSE TISSUE

1969 ◽  
Vol 41 (2) ◽  
pp. 441-449 ◽  
Author(s):  
Kin-Ichi Ohkawa ◽  
Molly T. Vogt ◽  
Emmanuel Farber
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
High Activity ◽  
White Adipose Tissue ◽  
Histochemical Staining ◽  
Brown Fat ◽  
Staining Procedure ◽  
Mitochondrial Enzymes ◽  
Glycerophosphate Dehydrogenase ◽  
Brown Adipose

Brown adipose tissue of the rat has been found to have an unusually high activity of mitohondrial α-glycerophosphate dehydrogenase (α-GPD) when assayed both by a histochemical staining procedure and by a quantitative biochemical method with isolated mitochondria. In contrast to succinic, glutamic, and ß-hydroxybutyrate dehydrogenases, all mitochondrial enzymes, the activity of α-GPD in brown fat was 10 times that in liver, more than 20 times that in white adipose tissue, and 9 times that in kidney. The soluble NAD-linked α-GPD was also higher in brown adipose tissue than in white adipose tissue, liver, or kidney, but the differences were much less marked. The possible importance of the high activity of mitochondrial α-GPD in the regulation of synthesis of esterified lipid and in thermogenesis in brown fat is discussed.

scholarly journals Cold exposure induces different uncoupling-protein thermogenin masking/unmasking processes in brown adipose tissue depending on mitochondrial subtypes

1994 ◽  
Vol 300 (2) ◽  
pp. 463-468 ◽  
Author(s):  
M Moreno ◽  
P Puigserver ◽  
J Llull ◽  
M Gianotti ◽  
A Lanni ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Uncoupling Protein ◽  
Mitochondrial Protein ◽  
Mitochondrial Fraction ◽  
Cold Acclimatization ◽  
Molecular Events ◽  
Mitochondrial Fractions ◽  
Brown Adipose

The effect of cold exposure on thermogenic parameters such as mitochondrial protein content, GDP-binding and uncoupling protein (UCP) levels in different mitochondrial fractions from rat brown adipose tissue has been investigated. Rats were exposed from 12 h to 5 days at 4 degrees C, and three mitochondrial fractions were isolated by differential centrifugation: the M1 fraction (1000 g), the M3 fraction (3000 g) and the M15 fraction (15,000 g). Cytochrome c oxidase activity as an index of mitochondrial mass showed an increase during cold exposure. During the first 24 h of cold exposure UCP was incorporated specifically into the M3 and M15 mitochondrial fractions, and thereafter UCP appeared in the heaviest M1 fraction. However, specific GDP binding was increased during the first 24 h in the same way in all subpopulations, and this increase continued up to 72 h of cold exposure. Results suggest that different molecular events are involved during acute and chronic adaptation to cold: during the first 24 h of cold acclimatization, thermogenic activity is increased by an unmasking process of the UCP binding sites in the M1 mitochondrial fraction as UCP levels were constant and GDP binding increased, but in the M3 and M15 fraction the increase in thermogenic activity was completely due to an increase in GDP binding induced by a specific incorporation of UCP targeted to these mitochondria. Thus thermogenic parameters change in a different way in the brown-fat mitochondrial subpopulations during cold acclimatization.

Evidence that the hypothermic response of mice to Δ9-tetrahydrocannabinol is not mediated by changes in thermogenesis in brown adipose tissue

1991 ◽  
Vol 69 (6) ◽  
pp. 767-770 ◽  
Author(s):  
Roger G. Pertwee ◽  
Kevin Nash ◽  
Paul Trayhurn
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Brown Fat ◽  
Marked Rise ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Hypothermic Response ◽  
Hyperthermic Response ◽  
Brown Fat Mitochondria ◽  
Binding To Mitochondria

Δ9-Tetrahydrocannabinol (20 mg/kg i.p.) and propranolol (20 and 50 mg/kg i.p.) produced marked falls in the rectal temperatures of mice kept at an ambient temperature of 22 °C. Propranolol (50 mg/kg i.p.) also decreased the thermogenic activity of brown fat, as measured by a decrease in the level of [3H]GDP binding to mitochondria obtained from mouse interscapular brown adipose tissue. In contrast, Δ9-tetrahydrocannabinol (20 mg/kg i.p.) did not affect mitochondrial GDP binding even though the dose used was one shown previously to depress heat production. GDP binding was also unaffected by this cannabinoid in brown adipose tissue taken from mice that had been kept at 13 °C instead of 22 °C. In mice kept at 34 °C, isoprenaline (0.25 and 1.0 mg/kg s.c.) induced a marked rise in rectal temperature and increased the level of GDP binding to brown fat mitochondria. Propranolol (50 mg/kg i.p.) prevented the hyperthermic response to isoprenaline, the mice becoming hypothermic instead. Δ9-Tetrahydrocannabinol (20 mg/kg i.p.) had no effect on isoprenaline-induced hyperthermia. We conclude from these data that there is no significant involvement of brown adipose tissue in the hypothermic response of mice to Δ9-tetrahydrocannabinol.Key words: Δ9-tetrahydrocannabinol, body temperature, brown adipose tissue, GDP binding, thermogenesis.

Effect of noradrenaline chronic administration on brown fat phospholipids

1988 ◽  
Vol 8 (5) ◽  
pp. 465-469 ◽  
Author(s):  
Gérard Mory ◽  
Myriam Gawer ◽  
Jean-Claude Kader
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Brown Adipose Tissue ◽  
Acid Composition ◽  
Cold Exposure ◽  
Chronic Administration ◽  
Sympathetic Tone ◽  
Brown Fat ◽  
Brown Adipose

Chronic cold exposure of rats (9 days at 5°C) induces an alteration of the fatty acid composition of phospholipids in brown adipose tissue. The alteration is due to an increase of the unsaturation degree of these lipids. The phenomenon can be reproduced by 10−7 mole. h−1 administration of noradrenaline for 9 days in rats kept at 25°C. Thus, phospholipid alteration in brown fat of cold exposed rats is most probably a consequence of the increase of sympathetic tone which occurs in this tissue during exposure to cold.

Adrenalectomy increases brown adipose tissue metabolism in ob/ob mice housed at 35 degrees C.

1990 ◽  
Vol 259 (3) ◽  
pp. E362
Author(s):  
H K Kim ◽  
D R Romsos
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Mitochondrial Protein ◽  
Mitochondrial Mass ◽  
Warm Environment ◽  
Bat Mitochondria ◽  
Norepinephrine Turnover ◽  
Brown Adipose ◽  
Energy Retention ◽  
High Starch

Adrenalectomy arrests the development of obesity in ob/ob mice fed a high-starch diet and housed at a normal room temperature (20-25 degrees C) partly by stimulating the low thermogenic activity of brown adipose tissue (BAT). The present study was undertaken to determine if adrenalectomy would also lower energy retention and stimulate BAT metabolism in ob/ob mice housed in a warm environment (35 degrees C) where BAT thermoregulatory heat production is not needed. Adrenalectomy prevented hyperphagia and hyperinsulinemia and lowered the efficiency of energy retention in ob/ob mice housed at 35 degrees C, which is comparable to results obtained at 20-25 degrees C. Sympathetic nervous system stimulation of BAT (interscapular and subscapular depots) assessed by norepinephrine turnover was increased in adrenalectomized ob/ob mice. Thermogenic activity of BAT in adrenalectomized ob/ob mice (as assessed by GDP binding to isolated BAT mitochondria, GDP-inhibitable acetate-induced BAT mitochondrial swelling, and Mg2(/)-activated GDP binding to BAT mitochondria) was not elevated when results were expressed per milligram of mitochondrial protein but was elevated approximately 65% when expressed per interscapular and subscapular depots because adrenalectomy increased BAT mitochondrial mass. Adrenalectomy lowers the efficiency of energy retention and stimulates BAT metabolism even when ob/ob mice are housed in a warm environment.

The development of insulin resistance in brown adipose tissue may impair the acute cold-induced activation of thermogenesis in genetically obese (ob/ob) mice

1984 ◽  
Vol 4 (11) ◽  
pp. 933-940 ◽  
Author(s):  
Stewart W. Mercer ◽  
Paul Trayhurn
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Brown Fat ◽  
Acute Cold Exposure ◽  
Brown Adipose

Genetically obese (ob/ob) mice develop insulin resistance in brown adipose tissue during the fifth week of life. Prior to this, at 26 days of age, oh/oh mice show a substantial increase in GDP binding to brownadipose-tissue mitochondria during acute cold exposure. When insulin resistance in brown fat develops, by 35 days of age, the increase in GDP binding in response to cold is markedly reduced. Studies with 2-deoxyglucose suggest that insulin resistance in brown adipose tissue could impair thermogenic responsiveness during acute cold exposure by limiting the ability of the tissue to take up glucose.

OBSERVATIONS ON PEROXISOMES IN BROWN ADIPOSE TISSUE OF THE RAT

1971 ◽  
Vol 19 (11) ◽  
pp. 670-675 ◽  
Author(s):  
IRÉNE AHLABO ◽  
TUDOR BARNARD
Keyword(s):  
Hydrogen Peroxide ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Single Unit ◽  
Brown Fat ◽  
Unit Membrane ◽  
Peroxisomal Enzyme ◽  
Brown Adipose ◽  
Homogeneous Matrix ◽  
Physiologic Activity

During cytochemical studies of brown adipose tissue from rat, cytoplasmic organelles that apparently show peroxidative activity have been observed. The majority of the organelles have a diameter of 0.1-0.8 µ and a finely granular homogeneous matrix and are delimited by a single unit membrane. No sign of a "crystalloid" was seen. In order to demonstrate the peroxidative activity of the peroxisomal enzyme catalase in the organelles, brown adipose tissue was incubated in a medium containing 3,3'-diaminobenzidine tetrahydrochloride, after prefixation in 3% glutaraldehyde. The activity was blocked by 3-amino-l,2,4-triazole (an inhibitor of catalase) but not by KCN. Omission of exogenous hydrogen peroxide did not inhibit the reaction in the organelles. It is concluded that rat brown adipose tissue contains peroxisomes and, since the abundance of these organelles varies according to the physiologic activity of the tissue, peroxisomes may have a role in the thermogenic metabolism of brown fat.

Diet, lighting, and food intake affect norepinephrine turnover in dietary obesity

1987 ◽  
Vol 252 (2) ◽  
pp. R402-R408 ◽  
Author(s):  
T. Yoshida ◽  
J. S. Fisler ◽  
M. Fukushima ◽  
G. A. Bray ◽  
R. A. Schemmel
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
High Fat Diet ◽  
Brown Fat ◽  
Light Cycle ◽  
High Fat ◽  
Interscapular Brown Adipose Tissue ◽  
Norepinephrine Turnover ◽  
Brown Adipose ◽  
Dietary Obesity

The effects of dietary fat content, lighting cycle, and feeding time on norepinephrine turnover in interscapular brown adipose tissue, heart, and pancreas, and on blood 3-hydroxybutyrate, serum glucose, insulin, and corticosterone have been studied in two strains of rats that differ in their susceptibility to dietary obesity. S 5B/Pl rats, which are resistant to dietary obesity, have a more rapid turnover of norepinephrine in interscapular brown adipose tissue and heart and a greater increase in the concentration of norepinephrine in brown fat when eating a high-fat diet than do Osborne-Mendel rats, which are sensitive to fat-induced obesity. Light cycle and feeding schedule are important modulators of sympathetic activity in heart and pancreas but not in brown fat. Rats of the resistant strain also have higher blood 3-hydroxybutyrate concentrations and lower insulin and corticosterone levels than do rats of the susceptible strain. A high-fat diet increases 3-hydroxybutyrate concentrations and reduces insulin levels in both strains. These studies show, in rats eating a high-fat diet, that differences in norepinephrine turnover, particularly in brown adipose tissue, may play an important role in whether dietary obesity develops and in the manifestations of resistance to this phenomenon observed in the S 5B/Pl rat.

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