Regulation of prostaglandin E2 and Fα productions by rat brown fat during the perinatal period ; effects of ambient temperature

Portet, R; Marco, F. De; Zizine, L; Senault, Claude; Bertin, R

doi:10.1016/s0300-9084(82)80168-5

Biochimie

1982

DOI: 10.1016/s0300-9084(82)80168-5

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Regulation of prostaglandin E2 and Fα productions by rat brown fat during the perinatal period ; effects of ambient temperature

R Portet

F. De Marco

L Zizine

et al.

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Cited by 4 publications

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“…For example, PGE 2 has been shown to be produced in the brown adipose tissue (BAT) (61) and to increase the calcium concentration and O 2 consumption (V O 2 ) in rat brown adipocytes via a direct action (43). Furthermore, PGE 2 and other pyrogens (LPS) can induce expression of uncoupling proteins in brown adipocytes and hepatocytes, also via direct actions (2,10).…”

mentioning

confidence: 99%

Fever response to intravenous prostaglandin E₂ is mediated by the brain but does not require afferent vagal signaling

Ootsuka¹,

Blessing²,

Steiner³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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PGE2 produced in the periphery triggers the early phase of the febrile response to infection and may contribute to later phases. It can be hypothesized that peripherally synthesized PGE2 transmits febrigenic signals to the brain via vagal afferent nerves. Before testing this hypothesis, we investigated whether the febrigenic effect of intravenously administered PGE2 is mediated by the brain and is not the result of a direct action of PGE2 on thermoeffectors. In anesthetized rats, intravenously injected PGE2 (100 microg/kg) caused an increase in sympathetic discharge to interscapular brown adipose tissue (iBAT), as well as increases in iBAT thermogenesis, end-expired CO2, and colonic temperature (Tc). All these effects were prevented by inhibition of neuronal function in the raphe region of the medulla oblongata using an intra-raphe microinjection of muscimol. We then asked whether the brain-mediated PGE2 fever requires vagal signaling and answered this question by conducting two independent studies in rats. In a study in anesthetized rats, acute bilateral cervical vagotomy did not affect the effects of intravenously injected PGE2 (100 microg/kg) on iBAT sympathetic discharge and Tc. In a study in conscious rats, administration of PGE2 (280 microg/kg) via an indwelling jugular catheter caused tail skin vasoconstriction, tended to increase oxygen consumption, and increased Tc; none of these responses was affected by total truncal subdiaphragmatic vagotomy performed 2 wk before the experiment. We conclude that the febrile response to circulating PGE2 is mediated by the brain, but that it does not require vagal afferent signaling.

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mentioning

confidence: 99%

Fever response to intravenous prostaglandin E₂ is mediated by the brain but does not require afferent vagal signaling

Ootsuka¹,

Blessing²,

Steiner³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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In vitro study of adrenergic stimulation of 32p incorporation into phospholipids of brown adipose tissue of control and cold-acclimated rats

Senault

Meister

Portet

1988

Comparative Biochemistry and Physiology Part A: Physiology

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Rare fatty acids in brown fat are substrates for thermogenesis during arousal from hibernation

Carneheim

Cannon

Nedergaard

1989

American Journal of Physiology-Regulatory, Integrative and Comp

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Because brown adipose tissue lipids are the preferred substrate for thermogenesis during arousal from hibernation, the fatty acid composition of brown fat lipids was followed during cold acclimation and during a hibernation bout. In control golden hamsters (living at 22 degrees C), the fatty acid composition of the white adipose tissue closely resembled that of the food, but brown adipose tissue contained more animal-derived fatty acids. As an effect of acclimation to cold, the fatty acid composition of brown adipose tissue changed to resemble that of the food, and no marked differences between white and brown adipose tissue were then evident. During a hibernation bout, a major part of the fatty acids accumulated in brown fat during entry into hibernation consisted of "rare" acids, such as homo-gamma-linoleic acid. Homo-gamma-linoleic, together with eicosadienoic acid and lignoceric acid, was preferentially utilized during the early phase of arousal. During this phase, "bulk" fatty acids, such as linoleic acid, were spared, whereas in late arousal, linoleic acid was the preferred substrate. It was concluded that rare fatty acids are of quantitative significance in brown adipose tissue during hibernation and arousal.

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Regulation of prostaglandin E2 and Fα productions by rat brown fat during the perinatal period ; effects of ambient temperature

Cited by 4 publications

References 7 publications

Fever response to intravenous prostaglandin E₂ is mediated by the brain but does not require afferent vagal signaling

Fever response to intravenous prostaglandin E₂ is mediated by the brain but does not require afferent vagal signaling

In vitro study of adrenergic stimulation of 32p incorporation into phospholipids of brown adipose tissue of control and cold-acclimated rats

Rare fatty acids in brown fat are substrates for thermogenesis during arousal from hibernation

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Regulation of prostaglandin E2 and Fα productions by rat brown fat during the perinatal period ; effects of ambient temperature

Cited by 4 publications

References 7 publications

Fever response to intravenous prostaglandin E2 is mediated by the brain but does not require afferent vagal signaling

Fever response to intravenous prostaglandin E2 is mediated by the brain but does not require afferent vagal signaling

In vitro study of adrenergic stimulation of 32p incorporation into phospholipids of brown adipose tissue of control and cold-acclimated rats

Rare fatty acids in brown fat are substrates for thermogenesis during arousal from hibernation

Contact Info

Product

Resources

About

Fever response to intravenous prostaglandin E₂ is mediated by the brain but does not require afferent vagal signaling

Fever response to intravenous prostaglandin E₂ is mediated by the brain but does not require afferent vagal signaling