Nonshivering thermogenesis without interscapular brown adipose tissue involvement during conditioned fear in the rat

2009 ◽  
Vol 296 (4) ◽  
pp. R1239-R1247 ◽  
Author(s):  
Andrew Marks ◽  
Daniel M. L. Vianna ◽  
Pascal Carrive
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Conditioned Fear ◽  
Nonshivering Thermogenesis ◽  
Interscapular Brown Adipose Tissue ◽  
Warm Up ◽  
Induced Hyperthermia ◽  
Adrenoceptor Antagonist ◽  
Brown Adipose ◽  
The Difference

As with other forms of psychological stress, conditioned fear causes an increase in body temperature. The mechanisms underlying this stress-induced hyperthermia are not well understood, but previous research suggests that nonshivering thermogenesis might contribute, as it does during cold exposure. The major source of nonshivering thermogenesis in the rat is brown adipose tissue (BAT), and the largest BAT deposit in that species is in the interscapular area just below the skin. BAT is also under sympathetic control via β-adrenoceptors. If BAT contributes to fear-induced hyperthermia, then the interscapular skin should warm up faster than other skin areas, and this response should be suppressed by the β-adrenoceptor antagonist, propranolol. We tested this noninvasively by infrared thermography. In conscious rats, 30 min of contextual fear caused hyperthermia (as indicated by a +1.5°C increase in lumbar back skin temperature) and increased the difference in temperature between interscapular and lumbar back skin (TiScap − TBack) by +1°C. Propranolol (10 mg/kg ip) completely abolished this hyperthermia; however, the TiScap-TBack increase was not reduced. In contrast, exposure to cold air (4°C) induced a +2.7°C increase in TiScap-TBack, which was reduced to +1°C after propranolol. The results show that conditioned fear-induced hyperthermia is of nonshivering origin and mediated by β-adrenoceptors, but interscapular BAT does not contribute to it and does not appear to be activated, either.

Interscapular Location of Brown Adipose Tissue: Role in Noradrenaline-Induced Calorigenesis in Cold-Acclimated Rats

1974 ◽  
Vol 52 (2) ◽  
pp. 225-229 ◽  
Author(s):  
Jean Himms-Hagen
Keyword(s):  
Spinal Cord ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Metabolic Response ◽  
Complete Removal ◽  
Nonshivering Thermogenesis ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Local Direction ◽  
The Difference

Tying Sulzer's vein does not alter the enhanced metabolic response to noradrenaline of cold-acclimated rats, neither immediately after the operation nor 1, 2, or 5 days later. In contrast, removal of the interscapular brown adipose tissue, while having no marked immediate effect upon the enhanced metabolic response to noradrenaline, causes a delayed loss of the enhancement during the subsequent 2 days. These findings argue against the hypothesis that the local direction of heat from the interscapular brown adipose tissue via Sulzer's vein to the spinal cord has importance in determining the capacity of the rat to respond to noradrenaline or to use nonshivering thermogenesis. The difference between the effect of complete removal of the interscapular brown adipose tissue and the effect of tying Sulzer's vein would suggest that the reduced circulation through the interscapular brown adipose tissue when Sulzer's vein is tied is still sufficient for it to exert its influence upon other tissues. The results are compatible with the endocrine hypothesis for the function of the interscapular brown adipose tissue during acclimation to cold.

Nesfatin-1 Acts Centrally to Induce Sympathetic Activation of Brown Adipose Tissue and Non-Shivering Thermogenesis

2019 ◽  
Vol 51 (10) ◽  
pp. 678-685 ◽  
Author(s):  
Luka Levata ◽  
Riccardo Dore ◽  
Olaf Jöhren ◽  
Markus Schwaninger ◽  
Carla Schulz ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
Body Weight Loss ◽  
Whole Body ◽  
Central Administration ◽  
Adrenergic Stimulation ◽  
Interscapular Brown Adipose Tissue ◽  
Adrenoceptor Antagonist ◽  
Brown Adipose

AbstractNesfatin-1 has originally been established as a bioactive peptide interacting with key hypothalamic nuclei and neural circuitries in control of feeding behavior, while its effect on energy expenditure has only recently been investigated. Hence, the aim of this study was to examine whether centrally acting nesfatin-1 can induce β3-adrenergic stimulation, which is a prerequisite for the activation of thermogenic genes and heat release from interscapular brown adipose tissue, key physiological features that underlie increased energy expenditure. This question was addressed in non-fasted mice stereotactically cannulated to receive nesfatin-1 intracerebroventricularly together with peripheral injection of the β3-adrenoceptor antagonist SR 59230 A, to assess whole-body energy metabolism. Using a minimally invasive thermography technique, we now demonstrate that the thermogenic effect of an anorectic nesfatin-1 dose critically depends on β3 adrenergic stimulation, as the co-administration with SR 59230 A completely abolished heat production from interscapular brown adipose tissue and rise in ocular surface temperature, thus preventing body weight loss. Moreover, through indirect calorimetry it could be shown that the anorectic concentration of nesfatin-1 augments overall caloric expenditure. Plausibly, central administration of nesfatin-1 also enhanced the expression of DIO2 and CIDEA mRNA in brown adipose tissue critically involved in the regulation of thermogenesis.

The effect of age and cold acclimation on the metabolism of brown adipose tissue in cold-exposed rats

1969 ◽  
Vol 47 (3) ◽  
pp. 251-256 ◽  
Author(s):  
Jean Himms-Hagen
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Total Lipids ◽  
Nonshivering Thermogenesis ◽  
Interscapular Brown Adipose Tissue ◽  
Adipose Tissue Metabolism ◽  
Glucose Carbon ◽  
Exposure To Cold ◽  
Brown Adipose ◽  
Effect Of Age

The effect of exposure to cold (4°) on the incorporation of glucose carbon into total lipids of interscapular brown adipose tissue was studied in warm-acclimated and cold-acclimated rats of different ages. Exposure to cold had little effect on the very low incorporation in warm-acclimated rats regardless of their ages. Incorporation was always greater in cold-acclimated rats in the cold than in warm-acclimated rats in the cold, but the increase due to cold exposure was smaller in young cold-acclimated rats than in older cold-acclimated rats. The concentration of glucose in the blood was highest in the youngest rats and was increased further after exposure to cold; older rats did not become hyperglycemic in the cold. The relation between brown adipose tissue metabolism and nonshivering thermogenesis is discussed.

Nonshivering thermogenesis and the thermogenic capacity of brown fat in fasted and/or refed mice

1988 ◽  
Vol 254 (1) ◽  
pp. R11-R16 ◽  
Author(s):  
P. Trayhurn ◽  
G. Jennings
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cytochrome Oxidase ◽  
Oxidase Activity ◽  
Uncoupling Protein ◽  
Nonshivering Thermogenesis ◽  
Interscapular Brown Adipose Tissue ◽  
Cytochrome Oxidase Activity ◽  
Brown Adipose ◽  
Thermogenic Capacity

The effects of fasting and refeeding on nonshivering thermogenesis and the properties of brown adipose tissue have been investigated in mice. Fasting for 48 h led to a substantial reduction in the capacity for nonshivering thermogenesis, and there was no recovery of thermogenic capacity during the first 5 days of refeeding. A period of 10-15 days of refeeding was required for full restoration of thermogenic capacity. The mice were hyperphagic during the first 6 days of refeeding, but body weight was recovered after 24 h. The amount of interscapular brown adipose tissue decreased substantially on fasting, but it recovered 24 h after the initiation of refeeding. Cytochrome oxidase activity, the level of mitochondrial GDP binding, and the specific mitochondrial concentration of uncoupling protein in brown adipose tissue were each reduced by fasting. Although both GDP binding and the specific concentration of uncoupling protein rapidly returned to normal on refeeding, the activity of cytochrome oxidase was not normalized until 10 days after the end of the fast. These results indicate that a prolonged period of refeeding is required for the recovery in the capacity for nonshivering thermogenesis following a fast, a similar time course being evident for the recovery of cytochrome oxidase activity in brown adipose tissue. It is suggested that the fasting-induced reduction in the capacity for nonshivering thermogenesis is linked primarily to a loss of mitochondria from brown adipose tissue and that the normalization of thermogenic capacity is dependent on the restoration of mitochondrial mass.

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.

Sign in / Sign up

Export Citation Format

Share Document