Growth of interscapular brown adipose tissue in cold-acclimated hypophysectomized rats maintained on thyroxine and corticosterone

1982 ◽  
Vol 60 (8) ◽  
pp. 838-842 ◽  
Author(s):  
Mathias Fellenz ◽  
Joan Triandafillou ◽  
Cynthia Gwilliam ◽  
Jean Himms-Hagen
Keyword(s):  
Molecular Weight ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Relative Proportion ◽  
Pituitary Hormones ◽  
Proton Conductance ◽  
Polypeptide Composition ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Hypophysectomized Rats

Brown adipose tissue (BAT) of rats is known to grow in response to acclimation to cold. The growth is accompanied by changes in mitochondrial polypeptide composition (an increase in the relative proportion of a polypeptide of molecular weight 32 000, known to be associated with the thermogenic proton conductance pathway). The mediator of the change in mitochondrial polypeptide composition is unknown. The objective of these experiments was to find out whether any of the pituitary hormones might be the mediator. Treatment of rats with growth hormone failed to alter BAT size or mitochondrial polypeptide composition. BAT grew and the change in BAT mitochondrial polypeptide composition occurred in cold-acclimated hypophysectomized rats, maintained on thyroxine and corticosterone to ensure their survival in the cold. It is concluded that none of the pituitary hormones is the mediator for the cold-induced change in BAT mitochondrial polypeptide composition or is required to exert a direct effect on BAT for cold-induced BAT growth to occur. It also seems unlikely that more than a maintenance amount of glucocorticoids is required for normal cold-induced growth of BAT; these hormones are thus also unlikely to mediate the change in BAT mitochondrial polypeptide composition. The requirement for no more than a maintenance amount of thyroxine for BAT growth and for the cold-induced change in BAT mitochondrial polypeptide composition confirms previous conclusions drawn from studies on cold-acclimated thyroidectomized rats.

Polypeptide turnover in brown adipose tissue mitochondria during acclimation of rats to cold

1980 ◽  
Vol 58 (4) ◽  
pp. 336-344 ◽  
Author(s):  
Jean Himms-Hagen ◽  
Elizabeth Dittmar ◽  
Gloria Zaror-Behrens
Keyword(s):  
Molecular Weight ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Initial Phase ◽  
Mitochondrial Membrane ◽  
High Capacity ◽  
Proton Conductance ◽  
General Increase ◽  
Brown Adipose ◽  
Selective Increase

During the initial phase of cold-induced growth of brown adipose tissue in rats there is a selective increase in the incorporation of infused [3H]phenylalanine into mitochondrial membrane polypeptides of molecular weight 25 000–35 000. This is interpreted as a selective increase in the synthesis of a 32 000 polypeptide, of which the proportion is known to increase in brown adipose tissue mitochondria when the tissue has a high capacity for thermogenesis, as in the cold-acclimated rat. This polypeptide is known to be associated with the thermogenic proton conductance pathway. A simultaneous selective decrease in degradation or the formation from larger mitochondrial membrane polypeptides may also occur. In fully cold-acclimated rats, in which a new steady state is reached, there is a general increase in turnover of all mitochondrial membrane polypeptides but no marked selective changes in pattern of incorporation of radioactive amino acid or in rates of disappearance of radioactivity from groups of polypeptides. Isolated brown adipose tissue mitochondria incorporate [3H]phenylalanine principally into polypeptides of molecular weight 25 000–35 000. No change in the pattern of incorporation occurred in mitochondria isolated from brown adipose tissue of cold-exposed (2 weeks) rats. On the basis of these and preceding results it is concluded that the cold-induced change in mitochondrial composition in brown adipose tissue, which occurs at the same time as tissue and mitochondrial growth, is brought about by selective changes in cytosolic protein synthesis and possibly also by selectively altered degradation or conversion of mitochondrial polypeptides.

Mitochondrial proton leak in obesity-resistant and obesity-prone mice

2007 ◽  
Vol 293 (5) ◽  
pp. R1773-R1780 ◽  
Author(s):  
Brian D. Fink ◽  
Judy A. Herlein ◽  
Katrine Almind ◽  
Saverio Cinti ◽  
C. Ronald Kahn ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Muscle Tissue ◽  
Proton Conductance ◽  
High Fat ◽  
Interscapular Brown Adipose Tissue ◽  
Hindlimb Muscle ◽  
Brown Adipose ◽  
Ucp1 Expression ◽  
Ucp3 Expression

We quantified uncoupling proteins (UCPs) in molar amounts and assessed proton conductance in mitochondria isolated from interscapular brown adipose tissue (IBAT) and hindlimb muscle [known from prior work to contain ectopic brown adipose tissue (BAT) interspersed between muscle fibers] of obesity-resistant 129S6/SvEvTac (129) and obesity-prone C57BL/6 (B6) mice under conditions of low (LF) and high-fat (HF) feeding. With usual feeding, IBAT mitochondrial UCP1 content and proton conductance were greater in 129 mice than B6. However, with HF feeding, UCP1 and proton conductance increased more in B6 mice. Moreover, with HF feeding GDP-inhibitable proton conductance, specific for UCP1, equaled that seen in the 129 strain. UCP1 expression was substantial in mitochondria from hindlimb muscle tissue (ectopic BAT) of 129 mice as opposed to B6 but did not increase with HF feeding in either strain. As expected, muscle UCP3 expression increased with HF feeding in both strains but did not differ by strain. Moreover, the proton conductance of mitochondria isolated from hindlimb muscle tissue did not differ by strain or diet. Our data uncover a response to weight gain in obesity-prone (compared to resistant) mice unrecognized in prior studies that examined only UCP1 mRNA. Obesity-prone mice have the capacity to increase both IBAT UCP1 protein and mitochondrial proton conductance as much or more than obesity-resistant mice. But, this is only achieved only at a higher body mass and, therefore, may be adaptive rather than preventative. Neither obesity-prone nor resistant mice respond to HF feeding by expressing more UCP1 in ectopic BAT within muscle tissue.

Role of thyroid hormone in cold-induced changes in rat brown adipose tissue mitochondria

1982 ◽  
Vol 60 (5) ◽  
pp. 530-537 ◽  
Author(s):  
Joan Triandafillou ◽  
Cynthia Gwilliam ◽  
Jean Himms-Hagen
Keyword(s):  
Adipose Tissue ◽  
Thyroid Hormone ◽  
Brown Adipose Tissue ◽  
Cytochrome Oxidase ◽  
Polypeptide Composition ◽  
Inner Mitochondrial Membrane ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Intact Rats

The role of thyroid gland in cold-induced growth of brown adipose tissue and in cold-induced adaptive changes in brown adipose tissue mitochondria was investigated. Interscapular brown adipose tissue of thyroidectomized rats maintained at 28 °C was of normal size (protein, cytochrome oxidase content) and its mitochondria were normal, as judged from the level of GDP binding and the polypeptide composition. (GDP binds to a 32 000 dalton polypeptide component of the inner mitochondrial membrane. This component is part of the thermogenic proton conductance pathway. The level of GDP binding is a sensitive indicator of the thermogenic state of the tissue.) Brown adipose tissue mitochondria of thyroidectomized rats exposed to 4 °C for 15 h did not show the usual increase in GDP binding, an indication of a lack of a thermogenic response; the response was restored in thyroxine-treated thyroidectomized animals. In thyroidectomized rats treated with a low maintenance dose of thyroxine (25 μg/kg, s.c., three times per week) and acclimated to cold (4 °C) for 2 weeks, a normal growth of brown adipose (increase in protein and cytochrome oxidase) and normal changes in mitochondria (increase in GDP binding and an increase in the proportion of polypeptides of molecular weight 31 200 – 34 400) occurred. Treatment of intact rats with a large dose of thyroxine (1000 μg/kg, s. c., per day) resulted in a large increase in wet weight, mainly due to lipid accumulation since only small increases in protein and cytochrome oxidase and no change in DNA content occurred; mitochondrial GDP binding was decreased and polypeptide composition unchanged. It is concluded that thyroid hormone exerts a permissive effect on the cold-induced, noradrenaline-mediated, unmasking of GDP-binding sites in brown adipose tissue. The failure of the thyroidectomized rat to survive at 4 °C is probably primarily due to its inability to activate thermogenesis in its brown adipose tissue. Thyroid hormone does not appear to be involved, other than in a permissive way, in long-term cold-induced growth and mitochondrial changes in brown adipose tissue, since these occur normally in the presence of only small amounts of thyroxine in thyroidectomized rats and do not occur in intact rats treated with large amounts of thyroxine.

Increased purine nucleotide binding, altered polypeptide composition, and thermogenesis in brown adipose tissue mitochondria of cold-acclimated rats

1978 ◽  
Vol 56 (6) ◽  
pp. 378-383 ◽  
Author(s):  
M. Desautels ◽  
G. Zaror-Behrens ◽  
J. Himms-Hagen
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Nucleotide Binding ◽  
Proton Conductance ◽  
Purine Nucleotide ◽  
Polypeptide Composition ◽  
Purine Nucleotides ◽  
Brown Adipose ◽  
Simultaneous Decrease ◽  
Thermogenic Capacity

Rapid increases in atractyloside-insensitive binding of purine nucleotides (ADP or GDP) and in a polypeptide of 32 000 occur in brown adipose tissue mitochondria of the rat during acclimation to cold. The increased binding is apparent within 1 h and reaches a maximum after 3–7 days of exposure to 4 °C. The increase in the 32 000 peptide occurs more slowly and reaches a maximum after 2–3 weeks. There is a simultaneous decrease in a polypeptide of 96 000, apparent after 1 day and reaching a maximum after 1–2 weeks. Results are interpreted in terms of the appearance of an increased amount of the purine nucleotide-sensitive proton conductance pathway in association with the development of an enhanced thermogenic capacity of brown adipose tissue mitochondria during acclimation of the rat to cold.

scholarly journals Glucose transporter expression and glucose utilization in skeletal muscle and brown adipose tissue during starvation and re-feeding

1992 ◽  
Vol 282 (1) ◽  
pp. 231-235 ◽  
Author(s):  
D M Smith ◽  
S R Bloom ◽  
M C Sugden ◽  
M J Holness
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Tibialis Anterior ◽  
Glucose Transporter ◽  
Glucose Utilization ◽  
Interscapular Brown Adipose Tissue ◽  
Glut 4 ◽  
Mrna Concentration ◽  
Brown Adipose ◽  
Transporter Expression

Starvation (48 h) decreased the concentration of mRNA of the insulin-responsive glucose transporter isoform (GLUT 4) in interscapular brown adipose tissue (IBAT) (56%) and tibialis anterior (10%). Despite dramatic [7-fold (tibialis anterior) and 40-fold (IBAT)] increases in glucose utilization after 2 and 4 h of chow re-feeding, no significant changes in GLUT 4 mRNA concentration were observed in these tissues over this re-feeding period. The results exclude changes in GLUT 4 mRNA concentration in mediating the responses of glucose transport in these tissues to acute re-feeding after prolonged starvation.

scholarly journals Changes in β1- and β2-adrenergic receptor mRNA levels in brown adipose tissue and heart of hypothyroid rats

1991 ◽  
Vol 277 (3) ◽  
pp. 625-629 ◽  
Author(s):  
J P Revelli ◽  
R Pescini ◽  
P Muzzin ◽  
J Seydoux ◽  
M G Fitzgerald ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Adrenergic Receptor ◽  
State Level ◽  
Total Density ◽  
Mrna Levels ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Displacement Experiments ◽  
Beta 2

The aim of the present work was to study the effect of hypothyroidism on the expression of the beta-adrenergic receptor (beta-AR) in interscapular brown adipose tissue and heart. The total density of plasma membrane beta-AR per tissue is decreased by 44% in hypothyroid rat interscapular brown adipose tissue and by 55% in hypothyroid rat heart compared with euthyroid controls. The effects of hypothyroidism on the density of both beta 1- and beta 2-AR subtypes were also determined in competition displacement experiments. The densities of beta 1- and beta 2-AR per tissue are decreased by 50% and 48% respectively in interscapular brown adipose tissue and by 52% and 54% in the heart. Northern blot analysis of poly(A)+ RNA from hypothyroid rat interscapular brown adipose tissue demonstrated that the levels of beta 1- and beta 2-AR mRNA per tissue are decreased by 73% and 58% respectively, whereas in hypothyroid heart, only the beta 1-AR mRNA is decreased, by 43%. The effect of hypothyroidism on the beta 1-AR mRNA is significantly more marked in the interscapular brown adipose tissue than in the heart. These results indicate that beta-AR mRNA levels are differentially regulated in rat interscapular brown adipose tissue and heart, and suggest that the decrease in beta-AR number in interscapular brown adipose tissue and heart of hypothyroid animals may in part be explained by a decreased steady-state level of beta-AR mRNA.

scholarly journals Stimulatory, but not anxiogenic, doses of caffeine act centrally to activate interscapular brown adipose tissue thermogenesis in anesthetized male rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
L. Van Schaik ◽  
C. Kettle ◽  
R. Green ◽  
W. Sievers ◽  
M. W. Hale ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Basolateral Amygdala ◽  
Free Breathing ◽  
Male Rats ◽  
Central Administration ◽  
Hypothalamic Area ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis

AbstractThe role of central orexin in the sympathetic control of interscapular brown adipose tissue (iBAT) thermogenesis has been established in rodents. Stimulatory doses of caffeine activate orexin positive neurons in the lateral hypothalamus, a region of the brain implicated in stimulating BAT thermogenesis. This study tests the hypothesis that central administration of caffeine is sufficient to activate BAT. Low doses of caffeine administered either systemically (intravenous [IV]; 10 mg/kg) and centrally (intracerebroventricular [ICV]; 5–10 μg) increases BAT thermogenesis, in anaesthetised (1.5 g/kg urethane, IV) free breathing male rats. Cardiovascular function was monitored via an indwelling intra-arterial cannula and exhibited no response to the caffeine. Core temperature did not significantly differ after administration of caffeine via either route of administration. Caffeine administered both IV and ICV increased neuronal activity, as measured by c-Fos-immunoreactivity within subregions of the hypothalamic area, previously implicated in regulating BAT thermogenesis. Significantly, there appears to be no neural anxiety response to the low dose of caffeine as indicated by no change in activity in the basolateral amygdala. Having measured the physiological correlate of thermogenesis (heat production) we have not measured indirect molecular correlates of BAT activation. Nevertheless, our results demonstrate that caffeine, at stimulatory doses, acting via the central nervous system can increase thermogenesis, without adverse cardio-dynamic impact.

Organization of sympathetic innervation of interscapular brown adipose tissue in the mouse

2021 ◽  
Author(s):  
Clara Huesing ◽  
Rui Zhang ◽  
Sanjeev Gummadi ◽  
Nathan Lee ◽  
Emily Qualls‐Creekmore ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Sympathetic Innervation ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose
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