Oxygen consumption, body temperature, and brown adipose tissue in the postnatal golden hamster (Mesocricetus auratus)

1969 ◽  
Vol 170 (1) ◽  
pp. 117-123 ◽  
Author(s):  
R. D. Rink
Keyword(s):  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Body Temperature ◽  
Brown Adipose Tissue ◽  
Golden Hamster ◽  
Mesocricetus Auratus ◽  
Brown Adipose

Escherichia coli peritonitis activates thermogenesis in brown adipose tissue: relationship to fever

1991 ◽  
Vol 69 (6) ◽  
pp. 761-766 ◽  
Author(s):  
Philip J. Scarpace ◽  
Bradley S. Bender ◽  
Stephen E. Borst
Keyword(s):  
Escherichia Coli ◽  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Body Temperature ◽  
Brown Adipose Tissue ◽  
Binding Sites ◽  
Febrile Response ◽  
E Coli ◽  
Brown Adipose ◽  
Colony Forming Units

Fever is a complex and important nonspecific, host defense mechanism against infection. The generation of the heat necessary to increase body temperature may involve thermogenesis in brown adipose tissue. To investigate whether the febrile response to Escherichia coli peritonitis involves thermogenesis in brown adipose tissue, we assessed whole rat oxygen consumption and brown adipose tissue mitochondrial guanosine 5′-diphosphate binding. Non-lethal doses of E. coli, 1 × 106 to 1 × 108 colony forming units, induced a fever for greater than 8 h. In contrast, a dose of 1 × 109 colony forming units resulted in a progressive hypothermia culminating in death. A 48% increase in oxygen consumption (p < 0.05) in E. coli-infected rats occurred almost immediately, preceded the development of the fever, and was sustained throughout the fever. There was a highly significant correlation (r = 0.736, p < 0.01) between oxygen consumption and body temperature for both control and infected animals. Guanosine 5′-diphosphate binding assessed by multi-point Scatchard analysis of [3H]guanosine 5′-diphosphate binding to isolated mitochondria was increased by 45.4 ± 7.3% at 1.75 h and by 31.9 ± 9.0% at 3.5 h (p < 0.05). The greater increase was during the rising phase of the fever. Unexpectedly, a lethal dose of 5 × 109 colony forming units of E. coli also increased guanosine 5′-diphosphate binding sites by 54.4 ± 14.2% (p < 0.05) despite a hypothermia of −1.71 ± 0.29 °C. These data indicate that peritonitis induces a fever that is correlated with oxygen consumption and increased guanosine 5′-diphosphate binding sites, suggestive of brown adipose tissue thermogenesis activation. This thermogenesis appears to be contributing at least some of the heat necessary for the febrile response in rats.Key words: rat, guanosine 5′-diphosphate binding, oxygen consumption.

scholarly journals Impaired Thermogenesis and a Molecular Signature for Brown Adipose Tissue inId2Null Mice

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Peng Zhou ◽  
Maricela Robles-Murguia ◽  
Deepa Mathew ◽  
Giles E. Duffield
Keyword(s):  
Adipose Tissue ◽  
Body Temperature ◽  
Brown Adipose Tissue ◽  
Energy Homeostasis ◽  
Core Body Temperature ◽  
Specific Pattern ◽  
Molecular Signature ◽  
Brown Adipose ◽  
Core Body ◽  
The Impact

Inhibitor of DNA binding 2 (ID2) is a helix-loop-helix transcriptional repressor rhythmically expressed in many adult tissues. Our previous studies have demonstrated thatId2null mice have sex-specific elevated glucose uptake in brown adipose tissue (BAT). Here we further explored the role ofId2in the regulation of core body temperature over the circadian cycle and the impact ofId2deficiency on genes involved in insulin signaling and adipogenesis in BAT. We discovered a reduced core body temperature inId2−/− mice. Moreover, inId2−/− BAT, 30 genes includingIrs1,PPARs, andPGC-1s were identified as differentially expressed in a sex-specific pattern. These data provide valuable insights into the impact ofId2deficiency on energy homeostasis of mice in a sex-specific manner.

scholarly journals Regulatory effects of brown adipose tissue thermogenesis on maternal metabolic adaptation, placental efficiency, and fetal growth in mice

2018 ◽  
Vol 315 (6) ◽  
pp. E1224-E1231 ◽  
Author(s):  
Liping Qiao ◽  
Samuel Lee ◽  
Amanda Nguyen ◽  
William W. Hay ◽  
Jianhua Shao
Keyword(s):  
Adipose Tissue ◽  
Body Temperature ◽  
Brown Adipose Tissue ◽  
Fetal Growth ◽  
Core Body Temperature ◽  
Metabolic Adaptation ◽  
Glucose Transporter 1 ◽  
Brown Adipose ◽  
Placental Efficiency ◽  
Core Body

To determine the role of UCP1-mediated thermogenesis in controlling maternal metabolic adaptation to pregnancy, energy metabolism of C57BL/6 wild-type (WT) and Ucp1 gene knockout ( Ucp1−/−) mice was studied during pregnancy. With the progression of pregnancy, maternal energy expenditure rates (EERs), expression of UCP1, and core body temperature steadily declined in WT dams. Despite no significant alterations in core body temperature and weight gain during pregnancy, Ucp1−/− dams exhibited lower rates in EER decline. High-fat (HF) feeding not only robustly increased maternal UCP1 expression and core body temperature but also abolished gestation-suppressed EER in WT dams. However, HF-increased EERs were significantly attenuated in Ucp1−/− dams. Significantly increased fetal body weights and fetal/placental weight ratio were detected in fetuses from Ucp1−/− dams compared with fetuses from WT dams. Markedly increased expression levels of glucose transporter 1 and amino acid transporters were also observed in placentas from Ucp1−/− dams. Furthermore, blood glucose concentrations of fetuses from Ucp1−/− dams were significantly higher than those of fetuses from WT dams, indicating that maternal UCP1 has an inhibitory effect on placental efficiency and fetal growth. Taken all together, this study demonstrated that maternal brown adipose tissue plays an important role in controlling maternal metabolic adaptation and placental nutrient transport.

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.

Effects of central injection of l-carnosine on sympathetic nerve activity innervating brown adipose tissue and body temperature in rats

2007 ◽  
Vol 144 (1-3) ◽  
pp. 62-71 ◽  
Author(s):  
Mamoru Tanida ◽  
Hitoshi Gotoh ◽  
Hiroyuki Taniguchi ◽  
Hiroto Otani ◽  
Jiao Shen ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Body Temperature ◽  
Brown Adipose Tissue ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Brown Adipose

Mitochondrial respiration in muscle and liver from cold-acclimated hypothyroid rats

2003 ◽  
Vol 95 (4) ◽  
pp. 1584-1590 ◽  
Author(s):  
Angel A. Zaninovich ◽  
Inés Rebagliati ◽  
Marcela Raíces ◽  
Conrado Ricci ◽  
Karl Hagmüller
Keyword(s):  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Brown Adipose Tissue ◽  
Cold Acclimation ◽  
Cold Exposure ◽  
Mitochondrial Respiration ◽  
Mitochondrial Oxygen Consumption ◽  
Normal Body ◽  
Thyroid Ablation ◽  
Brown Adipose

The effects of long-term cold exposure on muscle and liver mitochondrial oxygen consumption in hypothyroid and normal rats were examined. Thyroid ablation was performed after 8-wk acclimation to 4°C. Hypothyroid and normal controls remained in the cold for an additional 8 wk. At the end of 16-wk cold exposure, all hypothyroid rats were alive and normothermic and had normal body weight. At ambient temperature (24°C), thyroid ablation induced a 65% fall in muscle mitochondrial oxygen consumption, which was reversed by thyroxine but not by norepinephrine administration. After cold acclimation was reached, suppression of thyroid function reduced muscle mitochondrial respiration by 30%, but the hypothyroid values remained about threefold higher than those in hypothyroid muscle in the warm. Blockade of β- and α1-adrenergic receptors in both hypothyroid and normal rats produced hypothermia in vivo and a fall in muscle, liver, and brown adipose tissue mitochondria respiration in vitro. In normal rats, cold acclimation enhanced muscle respiration by 35%, in liver 18%, and in brown adipose tissue 450% over values in the warm. The results demonstrate that thyroid hormones, in the presence of norepinephrine, are major determinants of thermogenic activity in muscle and liver of cold-acclimated rats. After thyroid ablation, cold-induced nonshivering thermogenesis replaced 3,5,3′-triiodothyronine-induced thermogenesis, and normal body temperature was maintained.

Sign in / Sign up

Export Citation Format

Share Document