Disease relevance of Armoslip CP

• In contrast, oleamide was equally effective in inducing hypothermia in mice lacking the 5-HT(7) receptors as in wild-type mice [1].
• Here we show that daily intraperitoneal (i.p.) injections of oleamide, a sleep-inducing lipid hormone, weakly inhibited the spontaneous metastasis of BL6 cells [2].
• Mouse neuroblastoma N(18)TG(2) cells are an excellent model system for the study of oleamide biosynthesis because these cells convert [(14)C]-oleic acid to [(14)C]-oleamide and express PAM in a regulated fashion [3].
• Oleamide produced equivalent apnea suppression [4].
• A derivative of oleamide potently inhibits the spontaneous metastasis of mouse melanoma BL6 cells [2].

Psychiatry related information on Armoslip CP

• The inhibitors may serve as useful tools to clarify the role of endogenous oleamide and anandamide and may prove to be useful therapeutic agents for the treatment of sleep disorders or pain [5].
• Oleamide is an endogenous lipid that accumulates during sleep deprivation and has hypothermic effects when administered to rodents [6].
• MEASUREMENTS AND RESULTS: Our data show that delta9THC and oleamide each stabilized respiration during all sleep stages [4].
• In addition, oleamide decreased body temperature and locomotor activity in a dose-dependent manner [7].
• Here we show that systemic administration of oleamide (10 and 20 mg/kg) in rats increased slow-wave sleep 2, without affecting blood pressure and heart rate [7].

High impact information on Armoslip CP

• Previously, we reported the structure and sleep-inducing properties of cis-9-octadecenamide, a lipid isolated from the cerebrospinal fluid of sleep-deprived cats. cis-9-Octadecenamide, or oleamide, has since been shown to affect serotonergic systems and block gap-junction communication in glial cells (our unpublished results) [8].
• BACKGROUND & AIMS: Fatty acid amide hydrolase (FAAH) catalyzes the hydrolysis both of the endocannabinoids (which are known to inhibit intestinal motility) and other bioactive amides (palmitoylethanolamide, oleamide, and oleoylethanolamide), which might affect intestinal motility [9].
• Further analysis using oleamide to downregulate gap junction communication in nontransgenic outgrowth cultures showed that this independent method of reducing gap junction communication in cardiac crest cells also resulted in a reduction in the rate of crest migration [10].
• Oleamide is a sleep-inducing lipid originally isolated from the cerebrospinal fluid of sleep-deprived cats [11].
• In contrast, oleamide had no effect on mechanically stimulated calcium wave transmission in this same cell type [11].

Chemical compound and disease context of Armoslip CP

• Taken together, the results show that 5-HT-induced hypothermia is mediated by the 5-HT(7) receptor, and that oleamide may act through an independent mechanism as well as at an allosteric 5-HT(7) receptor site to regulate body temperature [1].
• In both genotypes, oleamide produced hypomotility, hypothermia, and ptosis, all of which were enhanced in FAAH(-/-) mice, were unaffected by the CB1 antagonist N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-di-chlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide hydrochloride (SR141716A) and occurred in CB1(-/-) mice [12].
• Palmitoleic and oleic acid seem to be especially important for sleep disorders, may be due to their function as precursors of the sleep inducing oleamide [13].
• Oleamide and oleoylglycine both induced profound hypothermia and decreased locomotion, over equivalent dose ranges and time courses, whereas, closely related compounds, stearamide and oleic acid, were essentially without effect [14].

Biological context of Armoslip CP

• When administered together, 5-HT and oleamide showed additive or greater than additive effects in reducing body temperature [1].
• Additionally, our data indicate that oleamide acts at an apparent allosteric site on the 5HT7 receptor and elicits functional responses via activation of this site [15].
• These results indicate that oleamide can modulate 5HT-mediated signal transduction at different subtypes of mammalian 5HT receptors [15].
• We used several human osteoblastic cell lines, as well as bone-derived primary osteoblastic cells, to show that confluent cultures of human osteoblastic cells grown under osteogenic conditions developed an adipocytic phenotype after 3 days of complete inhibition of GJC using AGRA or oleamide, two dissimilar nontoxic reversible inhibitors [16].
• The biosynthesis and tissue distribution of oleamide remain to be assessed in order to both substantiate its role as a sleep-inducing factor and investigate its participation in other physiopathological situations [17].

Anatomical context of Armoslip CP

• In HeLa cells expressing the 5HT7 receptor subtype, oleamide caused a concentration-dependent increase in cAMP accumulation but with lower efficacy than that observed by 5HT [15].
• The presence of functional gap junctions in CHO cells was confirmed through oleamide inhibition of lucifer yellow transfer [18].
• In the thalamus and hypothalamus a majority of neurons induced for c-fos expression also expressed the serotonin 5-HT7 receptor, an allosteric target for oleamide in in vitro studies [6].
• Intraperitoneal injections of oleamide elicited dramatic increases in content of c-fos mRNA and Fos protein in distinct brain regions, including cingulate and somatosensory cortical areas and numerous nuclei of the thalamus and hypothalamus, indicating that there are explicit targets for its action [6].
• Because cannabinoid receptor agonists are known to inhibit the excitatory effects of serotonin on nodose ganglion cells, we examined the effects of endogenous (oleamide) and exogenous (delta9-tetrahydrocannabinol; delta9THC) cannabimimetic agents on sleep-related apnea [4].

Associations of Armoslip CP with other chemical compounds

• Of the naturally occurring fatty acids, the primary amide of oleic acid (oleamide) is the most effective at potentiating the 5-HT2A receptor response [19].
• The effects of oleamide, an amidated lipid isolated from the cerebrospinal fluid of sleep-deprived cats, on serotonin receptor-mediated responses were investigated in cultured mammalian cells [15].
• Fatty acid amide hydrolase (FAAH) is a mammalian integral membrane enzyme responsible for the hydrolysis of a number of neuromodulatory fatty acid amides, including the endogenous cannabinoid anandamide and the sleep-inducing lipid oleamide [20].
• Pretreatment with the GJIC blockers 18beta-glycyrrhetinic acid and oleamide did not affect the changes induced by Cx26 transfection [21].
• Oleoyl-CoA formation from oleic acid has been demonstrated in vitro and in vivo while, to date, N-oleoylglycine cleavage to oleamide has been established only in vitro [3].

Gene context of Armoslip CP

• One of these, denoted metastasis inhibitor-18 (MI-18), inhibited the GJIC formed by Cx26 as well as oleamide but unlike oleamide, which is a non-selective inhibitor of connexin, it did not inhibit the GJIC formed by Cx43 [2].
• Enhanced radiosensitization of p53 mutant cells by oleamide [22].
• In p53 wild-type cells, both oleamide and radiation induced Bax translocation to mitochondria [22].
• Fatty acid amide hydrolase (FAAH) is an integral membrane protein that degrades oleamide and potent inhibitors with physiological sleep-inducing properties have been disclosed [23].
• Fatty acid amide hydrolase (FAAH) is a membrane-bound enzyme activity that degrades neuromodulatory fatty acid amides, including oleamide and anandamide [24].

Analytical, diagnostic and therapeutic context of Armoslip CP

• INTERVENTIONS: Animals were recorded following intraperitoneal injection of various doses of delta9THC, oleamide, and serotonin, alone and in combination [4].
• Therefore, the effects of oleamide on the performance of rats in tests of motor function, analgesia, and anxiety were investigated [25].
• The combined effect of IR and oleamide to suppress tumor growth was studied by use of xenografts in the thighs of nude mice [22].
• The effect of oleamide, a sleep-inducing endogenous lipid in animal models, on intracellular free levels of Ca(2+) ([Ca(2+)](i)) in non-excitable and excitable cells was examined by using fura-2 as a fluorescent dye [26].
• Determination of oleamide and erucamide in polyethylene films by pressurised fluid extraction and gas chromatography [27].

References