"Prostaglandin (PG) D2 is the most potent endogenous sleep-promoting substance"

trance

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"Prostaglandin (PG) D2 is the most potent endogenous sleep-promoting substance. PGD2 is produced by lipocalin-type PGD synthase localized in the leptomeninges, choroid plexus, and oligodendrocytes in the brain, and is secreted into the cerebrospinal fluid as a sleep hormone. PGD2 stimulates DP1 receptors localized in the leptomeninges under the basal forebrain and the hypothalamus. As a consequence, adenosine is released as a paracrine sleep-promoting molecule to activate adenosine A2A receptor-expressing sleep-promoting neurons and to inhibit adenosine A1 receptor-possessing arousal neurons. PGD2 activates a center of non-rapid eye movement (NREM) sleep regulation in the ventrolateral preoptic area, probably mediated by adenosine signaling, which activation inhibits the histaminergic arousal center in the tuberomammillary nucleus via descending GABAergic and galaninergic projections. The administration of a lipocalin-type PGD synthase inhibitor (SeCl4), DP1 antagonist (ONO-4127Na) or adenosine A2A receptor antagonist (caffeine) suppresses both NREM and rapid eye movement (REM) sleep, indicating that the PGD2-adenosine system is crucial for the maintenance of physiological sleep."

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aliml

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"Nicotinic acid [not nicotinamide] and Monomethyl fumarate are potent stimuli for prostaglandin production via the activation of GPR109A receptors. Ingestion of nicotinic acid results in 400 to 800-fold increases in PGD2 plasma levels in humans."
Full agonists of GPR109A include:
 
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trance

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"Nicotinic acid [not nicotinamide] and Monomethyl fumarate are potent stimuli for prostaglandin production via the activation of GPR109A receptors. Ingestion of nicotinic acid results in 400 to 800-fold increases in PGD2 plasma levels in humans."
Full agonists of GPR109A include:
Interesting study, thank you for sharing

"In fact, metabolic heat production (VO2) was suppressed in response to nicotinic acid in our study. Consistent with our finding, 200 mg/kg nicotinic acid attenuates cold-induced increases in thermogenesis in mice52 and norepinephrine-induced53 or spontaneous54 thermogenesis in rats. A major factor contributing to decreased thermogenesis is suppressed feeding in mice. Food intake was reduced by ~75% after 250 mg/kg ip and 1 g/kg oral doses of nicotinic acid in the first 8 hours, when VO2 and sleep responses were the most pronounced"

So Niacin decreased body temp by 1-3C (dose dependent) for 6-12hrs after the dose, then was elevated slightly compared to controls after the 12 hours. Do you know why? Seems there wasn't a conclusive answer in the study. First they said it could be because of vasodilation but the decreased temp lasts well after the vasodilation:

"In mice, vasodilation induced by subcutaneous injection of 100–300 mg/kg nicotinic acid reaches a peak within 2–3 min, and by 10 min the effect is reduced by 50%. The sleep-inducing and the hypothermic actions of nicotinic acid, however, lasted for ~7–11 hours, thus it is unlikely that they are the direct consequences of the actions of nicotinic acid on cutaneous blood flow."
 
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