EFFECTS OF HYPOTHYROIDISM ON THE BROWN ADIPOSE TISSUE OF ADULT RATS: COMPARISON WITH THE EFFECTS OF ADAPTATION TO COLD

1981 ◽  
Vol 91 (3) ◽  
pp. 515-524 ◽  
Author(s):  
GERARD MORY ◽  
DANIEL RICQUIER ◽  
PIERRE PESQUIÉS ◽  
PHILIPPE HÉMON
Keyword(s):  
Adipose Tissue ◽  
Thyroid Hormones ◽  
Brown Adipose Tissue ◽  
Oral Absorption ◽  
Physiological Role ◽  
Adult Rats ◽  
Adaptation To Cold ◽  
Exposure To Cold ◽  
Brown Adipose ◽  
Lipid Stores

Hypothyroidism was induced in adult rats by oral absorption of methimazole and its effects on brown adipose tissue (BAT) were studied. Hypothyroidism partially mimicked the effects of chronic exposure to cold: BAT weight and its DNA content were increased and the mitochondrial components (proteins, phospholipids) of the tissue were greatly enhanced when expressed per unit of fresh tissue weight. Moreover, hypothyroidism had the same effects as adaptation to cold on the fatty-acid composition of both total and mitochondrial phospholipids. Basal respiratory rate and total cytochrome C oxidase activity of the tissue were also increased. However, the increase in the concentration of the '32 000 mol. wt protein', a polypeptide which regulates the dissipation of heat by BAT, was smaller and non-selective in hypothyroid rats. The amount of this protein was increased per mg tissue, but not per mg mitochondrial proteins, as in rats adapted to cold. Furthermore, in contrast with the large mobilization of the lipid stores in BAT of euthyroid animals, the BAT lipid stores of hypothyroid rats were not mobilized during the first hours of exposure to cold. It may be concluded that (a) hypothyroidism induces several alterations in BAT which are characteristic of an active thermogenic state (this may be because of the response of the organism to the deficiency of thermogenesis induced by hypothyroidism), (b) this potential increase in thermogenic capacity in the BAT of hypothyroid rats has probably a limited physiological role, since thyroid hormones are necessary for the mobilization of the tissue lipids which are the fuel for production of heat and (c) these data provide evidence for a limited role of thyroid hormones in the trophic response of BAT during adaptation to cold.

Suppression of norepinephrine-induced thermogenesis in brown adipose tissue by fasting

1983 ◽  
Vol 245 (6) ◽  
pp. E582-E586 ◽  
Author(s):  
M. Hayashi ◽  
T. Nagasaka
Keyword(s):  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Thyroid Hormones ◽  
Brown Adipose Tissue ◽  
Plasma Levels ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Colonic Temperature ◽  
Induced Changes ◽  
Thermogenic Response

Fasting-induced changes in thermogenic responses to norepinephrine (NE, 4.0 micrograms X kg-1 X min-1 iv) were studied in anesthetized rats previously cold acclimated. The rats were divided into five groups at the end of 30–40 days of cold acclimation (5 degrees C). The five groups were kept for 5 days at 25 degrees C and fed (intact fed), fasted (intact fasted), fasted with daily treatment with thyroxine (T4, 2 micrograms/kg sc), thyroidectomized and fed, or thyroidectomized and fasted. In the intact fasted group, in which the weight of brown adipose tissue decreased, NE-induced increases in oxygen consumption, colonic temperature (T col), and temperature of the interscapular brown adipose tissue (TBAT) were markedly suppressed. The two thyroidectomized groups also showed a reduction in thermogenic response. In these three groups, TBAT was lower than Tcol throughout NE infusion. In the T4-treated fasted group, fasting-induced suppression of thermogenic response to NE was largely prevented. In the intact fed and the T4-treated fasted groups, TBAT attained higher values than Tcol during NE infusion. Plasma levels of thyroid hormones were significantly lower in the intact fasted group than in the intact fed or the T4-treated fasted group. These results suggest that fasting-induced suppression of the thermogenic response to NE is largely due to the reduced thermogenic response of brown adipose tissue to NE. The lowering of the levels of the thyroid hormones induced by fasting may be one of a number of causes of the reduction in the thermogenic response of brown adipose tissue.

Hypothalamic obesity, brown adipose tissue, and sympathoadrenal activity in rats

1985 ◽  
Vol 248 (5) ◽  
pp. E607-E617 ◽  
Author(s):  
J. G. Vander Tuig ◽  
J. Kerner ◽  
D. R. Romsos
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Heat Production ◽  
Adult Rats ◽  
Guanosine Diphosphate ◽  
Bat Mitochondria ◽  
Sympathoadrenal Activity ◽  
Brown Adipose ◽  
Energy Retention ◽  
Ad Libitum

Obesity-producing, hypothalamic knife cuts and ventromedial hypothalamic (VMH) lesions in ad libitum-fed adult rats increased intake of a high-fat diet (123 and 130%) and energy retention (880 and 1,099%) during the 4-wk period postsurgery; even when pair fed to control rats, energy retention of the knife-cut and lesioned rats was still elevated (105 and 155%). Thermogenic capacity of brown adipose tissue (BAT), estimated from guanosine diphosphate (GDP) binding to BAT mitochondria, was unchanged in hyperphagic knife-cut and VMH-lesioned rats and was reduced approximately 50% when these rats were pair fed to controls. Urinary excretion of norepinephrine (NE) was approximately twofold higher in ad libitum-fed, knife-cut, and lesioned rats than in control rats; restriction of energy intake decreased NE excretion to control values. Rates of NE turnover in heart paralleled urinary NE excretion, whereas NE turnover in BAT was generally not increased in the hyperphagic rats. Urinary epinephrine excretion, an index of adrenal medullary activity, was depressed in all knife-cut and VMH-lesioned rats. Hyperphagia coupled with a lack of increased heat production in BAT causes gross obesity in ad libitum-fed, knife-cut, and VMH-lesioned rats, whereas obesity in pair-fed rats develops in part at least as a result of reduced heat production by BAT.

Cinnamomum cassia extract promotes thermogenesis during exposure to cold via activation of brown adipose tissue

2021 ◽  
Vol 266 ◽  
pp. 113413 ◽  
Author(s):  
Xiang Li ◽  
Hong-Yuan Lu ◽  
Xiao-Wen Jiang ◽  
Yue Yang ◽  
Bo Xing ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cinnamomum Cassia ◽  
Exposure To Cold ◽  
Brown Adipose

Upregulation of uncoupling proteins by oral administration of capsiate, a nonpungent capsaicin analog

2003 ◽  
Vol 95 (6) ◽  
pp. 2408-2415 ◽  
Author(s):  
Yoriko Masuda ◽  
Satoshi Haramizu ◽  
Kasumi Oki ◽  
Koichiro Ohnuki ◽  
Tatsuo Watanabe ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Body Weight ◽  
Adipose Tissue ◽  
Single Dose ◽  
Thyroid Hormones ◽  
Brown Adipose Tissue ◽  
Uncoupling Proteins ◽  
Brown Adipose ◽  
Pepper Cultivar ◽  
Ucp2 Mrna

Capsiate is a nonpungent capsaicin analog, a recently identified principle of the nonpungent red pepper cultivar CH-19 Sweet. In the present study, we report that 2-wk treatment of capsiate increased metabolic rate and promoted fat oxidation at rest, suggesting that capsiate may prevent obesity. To explain these effects, at least in part, we examined uncoupling proteins (UCPs) and thyroid hormones. UCPs and thyroid hormones play important roles in energy expenditure, the maintenance of body weight, and thermoregulation. Two-week treatment of capsiate increased the levels of UCP1 protein and mRNA in brown adipose tissue and UCP2 mRNA in white adipose tissue. This dose of capsiate did not change serum triiodothyronine or thyroxine levels. A single dose of capsiate temporarily raised both UCP1 mRNA in brown adipose tissue and UCP3 mRNA in skeletal muscle. These results suggest that UCP1 and UCP2 may contribute to the promotion of energy metabolism by capsiate, but that thyroid hormones do not.

scholarly journals Activities of enzymes of glycerolipid synthesis in brown adipose tissue after treatment of rats with the adrenergic agonists BRL 26830A and phenylephrine, after exposure to cold and in streptozotocin-diabetes

1991 ◽  
Vol 277 (3) ◽  
pp. 665-669 ◽  
Author(s):  
J R D Mitchell ◽  
E D Saggerson
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Streptozotocin Diabetes ◽  
Fatty Acyl ◽  
Adrenergic Agonist ◽  
Interscapular Brown Adipose Tissue ◽  
Exposure To Cold ◽  
Brown Adipose ◽  
Glycerolipid Synthesis ◽  
Beta Adrenergic Agonist

1. Measurements were made, relative to tissue DNA, of the activities of enzymes of glycerolipid synthesis in homogenates of interscapular brown adipose tissue. These were: mitochondrial and microsomal forms of glycerolphosphate acyltransferase (GPAT), Mg(2+)-dependent phosphatidate phosphohydrolase (PPH) and fatty acyl-CoA synthetase (FAS). 2. In normal animals, 3 days of cold-exposure (4 degrees C) increased all activities. The increase in mitochondrial GPAT activity was particularly pronounced (5-fold). Administration of the beta-adrenergic agonist BRL 26830A mimicked the effect of cold on microsomal GPAT activity. Mitochondrial GPAT, PPH and FAS activities were unresponsive to BRL 26830A. The alpha-adrenergic agonist phenylephrine significantly decreased activities of GPAT and PPH. 3. Streptozotocin-diabetes decreased mitochondrial GPAT activity, but did not abolish the effect of cold to increase this activity or the activity of microsomal GPAT. Diabetes abolished the effect of cold on PPH and FAS activities. 4. The findings are relevant to signals that drive early events in mitochondriogenesis and cell proliferation in brown adipose tissue on exposure to cold.

Melatonin specifically stimulates type-II thyroxine 5′-deiodination in brown adipose tissue of Syrian hamsters

1989 ◽  
Vol 122 (2) ◽  
pp. 553-556 ◽  
Author(s):  
M. Puig-Domingo ◽  
J. M. Guerrero ◽  
A. Menéndez-Pelaez ◽  
R. J. Reiter
Keyword(s):  
Adipose Tissue ◽  
Thyroid Hormones ◽  
Brown Adipose Tissue ◽  
Harderian Gland ◽  
Control Group ◽  
Type Ii ◽  
Melatonin Treatment ◽  
Brown Adipose ◽  
Serum Thyroid Hormones ◽  
Group Serum

ABSTRACT The response of type-II thyroxine 5′-deiodinase (5′-DII)DII) to melatonin treatment was studied in the Syrian hamster. Male hamsters were treated for 15 days with a s.c. pellet containing melatonin, and 5′-DII activity in brown adipose tissue, anterior pituitary gland, Harderian gland and pineal gland was measured using a radioenzymatic technique. Melatonin-treated animals exhibited enhanced 5′-DII activity restricted to brown adipose tissue; the increase was threefold above the values measured in the control group. Serum concentrations of thyroid hormones were unaffected by melatonin treatment. We conclude that the stimulatory effect of melatonin on type-II thyroxine 5′-deiodination is specifically directed to the isoenzyme located in brown adipose tissue and is not accompanied by changes in serum thyroid hormones. Journal of Endocrinology (1989) 122, 553–556

Thyroid hormones and 5'-deiodinase in rat brown adipose tissue during fetal life

1989 ◽  
Vol 257 (5) ◽  
pp. E625-E631 ◽  
Author(s):  
M. J. Obregon ◽  
C. Ruiz de Ona ◽  
A. Hernandez ◽  
R. Calvo ◽  
F. Escobar del Rey ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Thyroid Hormones ◽  
Brown Adipose Tissue ◽  
Marked Decrease ◽  
Relative Weight ◽  
Fetal Life ◽  
Fetal Plasma ◽  
Brown Adipose ◽  
High Concentrations ◽  
Very High

Brown adipose tissue (BAT) iodothyronine 5'-deiodinase (5'D) activities are very high during fetal life but decrease 10-fold a few hours before birth. Accordingly, BAT 3,5,3'-triiodothyronine (T3) concentrations are also very high. The temporal patterns of changes in BAT 5'-D and fetal plasma insulin are similar (and differ from the pattern for catecholamines) but are not superimposable. A causal role for insulin in the activation of fetal BAT 5'-D is therefore not supported by the data. Maternal thyroidectomy leads to a decrease in the total and relative weight of fetal BAT and to a 30-50% increase in BAT 5'-D activities; BAT thyroid hormone concentrations are essentially unchanged. Fetal hypothyroidism was induced by giving methimazole and resulted in a marked decrease of BAT thyroxine (T4) and T3 concentrations. This treatment increased BAT 5'-D activity only on day 21 of gestation, but no effect was observed on day 20. The fetal 5'-D response to thyroid hormones infused into the methimazole-treated dams was studied at 21 days of gestation. The increase in BAT 5'-D induced by methimazole treatment was prevented by T4 infused into control dams but not by T3. In fetuses from thyroidectomized dams, the pattern of 5'-D regulation by thyroid hormones was impaired. It is suggested that the high concentrations of thyroid hormones present in fetal BAT might participate in the general maturation and development of fetal BAT.

Effect of maternal glucose infusion on brown adipose tissue and liver development in the neonatal lamb

1996 ◽  
Vol 8 (7) ◽  
pp. 1045 ◽  
Author(s):  
L Clarke ◽  
DC Andrews ◽  
MA Lomax ◽  
ME Symonds
Keyword(s):  
Adipose Tissue ◽  
Thyroid Hormones ◽  
Brown Adipose Tissue ◽  
Plasma Concentrations ◽  
Glucose Infusion ◽  
Late Gestation ◽  
Hepatic Glycogen ◽  
Liver Development ◽  
Brown Adipose ◽  
Maternal Glucose

The effect of maternal glucose infusion over the final 5-7 days of gestation in under-fed ewes on perirenal brown adipose tissue (BAT) and liver development in lambs over the first month of neonatal life was examined. During glucose infusion, higher maternal plasma concentrations of glucose and thyroid hormones, and lower plasma concentrations of non-esterified fatty acids and 3-hydroxybutyrate were observed, compared with saline-infused controls. These differences were not observed 1-1.5 h before parturition when plasma concentrations of glucose, lactate, cortisol and thyroid hormones all increased in control ewes. Lamb birthweight and liver and BAT weights were similar between groups, but lambs born to glucose-infused ewes had a higher hepatic glycogen content and greater iodothyronine 5'deiodinase activities in liver and BAT. The norepinephrine, epinephrine and dopamine contents were also greater in BAT sampled from lambs born to glucose infused ewes. Three lambs born to glucose-infused ewes failed to survive beyond the second week of life and exhibited abnormally low plasma triiodothyronine concentrations. It is concluded that maternal glucose infusion stimulates development of the fetal sympathetic nervous system during late gestation but this adaptation does not appear to improve postnatal survival.

scholarly journals CCAAT/enhancer-binding proteins α and β in brown adipose tissue: evidence for a tissue-specific pattern of expression during development

1994 ◽  
Vol 302 (3) ◽  
pp. 695-700 ◽  
Author(s):  
C Manchado ◽  
P Yubero ◽  
O Viñas ◽  
R Iglesias ◽  
F Villarroya ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Uncoupling Protein ◽  
Brown Fat ◽  
Brown Adipocyte ◽  
Fetal Life ◽  
Inhibitory Protein ◽  
Adult Rats ◽  
Stage Of Development ◽  
Brown Adipose

CCAAT/enhancer-binding protein (C/EBP) alpha mRNA and its protein products C/EBP alpha and 30 kDa C/EBP alpha are expressed in rat brown-adipose tissue. Results also demonstrate the expression of C/EBP beta mRNA and its protein products C/EBP beta and liver inhibitory protein (LIP) in the tissue. The abundance of C/EBP alpha and C/EBP beta proteins in adult brown fat is similar to that found in adult liver. However, the expression of C/EBP alpha and C/EBP beta is specifically regulated in brown fat during development. C/EBP alpha, 30 kDa C/EBP alpha, C/EBP beta and LIP content is several-fold higher in fetal brown fat than in the adult tissue, or liver at any stage of development. Peak values are attained in late fetal life, in concurrence with the onset of transcription of the uncoupling protein (UCP) gene, the molecular marker of terminal brown-adipocyte differentiation. When adult rats are exposed to a cold environment, which is a physiological stimulus of brown-adipose tissue hyperplasia and UCP gene expression, a specific rise in C/EBP beta expression with respect to C/EBP alpha, 30 kDa C/EBP alpha and LIP is observed. Present data suggest that the C/EBP family of transcription factors has an important role in the development and terminal differentiation of brown-adipose tissue.

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