scholarly journals Corrigendum: Cvijic G, Lakic I, Vujovic P, Jasnic N, Djurasevic S, Dronjak-Cucakovic S, Djordjevic J. Single and combined effects of acute and chronic non-thermal stressors on rat interscapular brown adipose tissue metabolic activity. Arch biol sci. 2013;65(3):919-27 DOI:10.2298/ABS1303919C

2015 ◽  
Vol 67 (4) ◽  
pp. 1431-1431
Author(s):  
E Editorial

The Editor-in-Chief has been informed that the results in Fig. 2A in the article: Single and combined effects of acute and chronic non-thermal stressors on rat interscapular brown adipose tissue metabolic activity, published in the Archives of Biological Sciences in 2013, Vol. 65, Issue 3, partially overlap with the results in Fig. 2, published in the article: Lakic I, Drenca T, Djordjevic J, Vujovic P, Jasnic N, Djurasevic S, Dronjak-Cucakovic S, Cvijic G. Arch Biol Sci. 2011;63(3):589-96, DOI:10.2298/ABS1103589L. After inspection of these articles and illustrations, and after discussion with the corresponding author of both articles, it was revealed that this is a case of partial overlap, i.e. of the authors presenting new findings that contain a comparatively small amount of previously published information. By publishing this corrigendum the journal is providing appropriate cross-referencing to the earlier work. <br><br><font color="red"><b> Link to the corrected article <u><a href="http://dx.doi.org/10.2298/ABS1303919C">10.2298/ABS1303919C</a></b></u>

1992 ◽  
Vol 282 (1) ◽  
pp. 231-235 ◽  
Author(s):  
D M Smith ◽  
S R Bloom ◽  
M C Sugden ◽  
M J Holness

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.


1991 ◽  
Vol 277 (3) ◽  
pp. 625-629 ◽  
Author(s):  
J P Revelli ◽  
R Pescini ◽  
P Muzzin ◽  
J Seydoux ◽  
M G Fitzgerald ◽  
...  

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.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
L. Van Schaik ◽  
C. Kettle ◽  
R. Green ◽  
W. Sievers ◽  
M. W. Hale ◽  
...  

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.


Author(s):  
Clara Huesing ◽  
Rui Zhang ◽  
Sanjeev Gummadi ◽  
Nathan Lee ◽  
Emily Qualls‐Creekmore ◽  
...  

1983 ◽  
Vol 245 (6) ◽  
pp. E582-E586 ◽  
Author(s):  
M. Hayashi ◽  
T. Nagasaka

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.


1986 ◽  
Vol 251 (2) ◽  
pp. R240-R242 ◽  
Author(s):  
A. Niijima

The activity of sympathetic nerves innervating interscapular brown adipose tissue of the rat was recorded. Intravenous administrations of glucose (100-300 mg/kg) enhanced the nerve activity. However, mannose, fructose, or galactose (300 mg/kg) showed no effect, suggesting the response is related to diet-induced thermogenesis in the brown adipose tissue.


1993 ◽  
Vol 264 (1) ◽  
pp. R109-R115 ◽  
Author(s):  
M. Egawa ◽  
H. Yoshimatsu ◽  
G. A. Bray

beta-Endorphin was injected into the third cerebroventricle to investigate its effects on sympathetic nerve activity to interscapular brown adipose tissue (IBAT) in rats. Multiunit discharges of sympathetic nerves to IBAT were recorded electrophysiologically in anesthetized rats. The intracerebroventricular injection of beta-endorphin (125, 250, and 500 pmol/rat in 10 microliters) suppressed sympathetic nerve activity in a dose-related fashion (-23.9 +/- 20.4, -38.7 +/- 7.1, and -66.7 +/- 7.6% 30 min after injection) compared with preinjection baseline. N-acetyl-beta-endorphin (250 pmol) had no effect on sympathetic nerve activity to IBAT. The intraperitoneal injection of naloxone (5.0 mg/rat) did not affect sympathetic nerve activity, but preinjection of naloxone inhibited the suppressive effect of intracerebroventricular injection of beta-endorphin (250 pmol). We conclude that the intracerebroventricular administration of beta-endorphin suppressed the sympathetic nerve activity to IBAT through opioid receptors. The results of this experiment are consistent with the hypothesis that beta-endorphin has a reciprocal effect on food intake and the sympathetic nervous system.


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