Effect of E. coli endotoxin on temperature, oxygen consumption and brown adipose tissue thermogenesis in rats and mice

1987 ◽  
Vol 7 (6) ◽  
pp. 517-523 ◽  
Author(s):  
G. Jennings ◽  
M. Elia
Keyword(s):  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Brown Adipose Tissue ◽  
Skin Temperature ◽  
Whole Body ◽  
Proton Conductance ◽  
E Coli ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis ◽  
Rats And Mice

The effects of E. coli endotoxin 0127 B8 on oxygen consumption, temperature, and on the activity of the proton conductance pathway in brown adipose tissue (BAT) were investigated in rats and mice. In rats an increase was observed in rectal and skin temperature, whole body oxygen consumption and GDP binding in BAT. In mice only the rise in rectal and skin temperature were significantly changed by endotoxin administration. These findings suggest that in some species BAT is involved in the production of endotoxin induced fever and increased energy expenditure.

Withdrawal of placental prostaglandins permits thermogenic responses in fetal sheep brown adipose tissue

1993 ◽  
Vol 74 (3) ◽  
pp. 998-1004 ◽  
Author(s):  
T. R. Gunn ◽  
K. T. Ball ◽  
P. D. Gluckman
Keyword(s):  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Brown Adipose Tissue ◽  
Umbilical Cord ◽  
Cold Water ◽  
Plasma Free Fatty Acid ◽  
Nonshivering Thermogenesis ◽  
Fetal Sheep ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis

Significant nonshivering thermogenesis cannot be demonstrated in fetal sheep cooled in utero but can be induced by supplemental oxygenation and umbilical cord occlusion, which suggests the presence of inhibitor(s) of placental origin. To test the hypothesis that an ecosanoid could be such an inhibitor, we studied eight fetal sheep at 136–141 days gestation. Thermistors were placed in the fetal esophagus, a cooling tube was placed around the trunk, a tracheal cannula and carotid catheters were inserted, and a snare was placed loosely around the umbilical cord. After indomethacin infusion for 18 h, the fetuses were cooled by 2.13 +/- 0.13 degrees C by circulating cold water through the coil. Within 60 min plasma free fatty acid levels rose threefold to 245 +/- 82 mu eq/l (P < 0.01) and glycerol levels rose to 197 +/- 17 mumol/l (P < 0.01). Ventilation caused a further rise in thermogenic indexes, and fetal oxygen consumption rose to 19.9 +/- 1.2 ml.kg-1.min-1. In four fetuses we ceased cooling, which caused thermogenic indexes to fall and oxygen consumption to fall to 6.9 +/- 1.1 ml.kg-1.min-1. We continued to cool three fetuses and infused prostaglandin E2 into the fetuses for 60 min; thermogenic indexes and oxygen consumption fell rapidly on infusion and rose rapidly when infusion ceased. We suggest that placental prostaglandins inhibit brown adipose tissue thermogenesis before birth and that withdrawal after placental separation is one factor in the initiation of nonshivering thermogenesis at birth.

scholarly journals A YY1 phosphorylation switch in brown adipose tissue orchestrates energy homeostasis.

2021 ◽  
Author(s):  
Zyanya Díaz-Hirashi ◽  
Tian Gao ◽  
Chiara Scaffidi ◽  
Monika Fey ◽  
Susan Murray ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Balance ◽  
Brown Adipose Tissue ◽  
Transcriptional Control ◽  
Energy Homeostasis ◽  
Whole Body ◽  
Regulatory Subunit ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis

Abstract Whole-body energy homeostasis is influenced by anabolic and catabolic cellular programs, which depend on environmental and nutritional cues. Adipose tissue plays a predominant role in the physiological regulation of energy balance by either storing or consuming energy through brown adipose tissue thermogenesis. It is however not clearly understood how brown adipose tissue balances catabolic and anabolic states. We show here that the transcription factor YY1 senses energetic state through a post-translational S120 phosphorylation switch. Adrenergic signaling leads to YY1 dephosphorylation which directly activates thermogenesis and a catabolic gene program while its phosphorylation maintains an anabolic program. Mechanistically, YY1 dephosphorylation increases chromatin binding at distal genomic loci respective to the transcription start site but remains constitutively bound to TSS. This mode of transcriptional control influences the activating and repressive function of YY1 and regulates catabolism/anabolism. We show that YY1 interacts with PPP1R3B, a regulatory subunit of the phosphatase PP1 and that in vivo knockdown of PPP1R3B protects against diet-induced obesity and insulin resistance. Our results uncover a novel transcriptional mechanism of metabolism orchestrated by YY1 phosphorylation switch and identifies PPP1R3B as a regulator of energy balance.

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.

A commentary on the interpretation of in vitro biochemical measures of brown adipose tissue thermogenesis

1989 ◽  
Vol 67 (8) ◽  
pp. 811-819 ◽  
Author(s):  
Paul Trayhurn ◽  
Rachel E. Milner
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Binding Sites ◽  
Protein Concentration ◽  
Uncoupling Protein ◽  
Proton Conductance ◽  
Binding Studies ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis

In this article we comment on the various in vitro biochemical measurements employed to assess the thermogenic activity and capacity of brown adipose tissue. The meaning and significance of changes in tissue weight, protein content, cell number, and mitochondrial mass are each summarized. In addition, various indices of the proton conductance pathway – mitochondrial swelling, proton conductance, uncoupling protein concentration, and GDP binding studies – are discussed. The issue of unmasking and masking of GDP binding sites is reviewed; recent reports have clearly demonstrated unmasking and masking, and it is concluded that GDP binding studies are an index of the activity of uncoupling protein, rather than a measure of its concentration. It is suggested that tissue mass, mitochondrial content, mitochondrial GDP binding, and uncoupling protein concentration represent core measurements for the biochemical assessment of the thermogenic activity and capacity of brown adipose tissue. Auxiliary measurements include Scatchard analysis of GDP binding data to distinguish changes in the number of binding sites from potential changes in Kd, and mitochondrial swelling studies, as an additional index of proton permeability. The distinction between thermogenic activity (GDP binding, proton permeability) and capacity (uncoupling protein content), both on a per unit of mitochondrial protein and per tissue basis, is emphasized.Key words: brown adipose tissue, thermogenesis, uncoupling protein, mitochondria.

Brown adipose tissue thermogenesis in women with polycystic ovary syndrome

2017 ◽  
Author(s):  
Soulmaz Shorakae ◽  
Eveline Jona ◽  
Courten Barbora de ◽  
Gavin Lambert ◽  
Elisabeth Lambert ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Polycystic Ovary Syndrome ◽  
Brown Adipose Tissue ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis
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