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3. Regulation of food intake by oleoylethanolamide

Author

Lo Verme, J, Gaetani, S, Fu, J, Oveisi, F, Burton, K, and Piomelli, D

Subjects
Nutrition, Adipose Tissue, Animals, Body Weight, Eating, Endocannabinoids, Feeding Behavior, Molecular Structure, Neurons, Afferent, Oleic Acids, PPAR alpha, Receptors, Drug, Signal Transduction, Vagus Nerve, oleoylethanolamide, palmitoylethanolamide, peroxisome proliferator-activated receptor-alpha, lipid, feeding, satiety, energy balance, metabolism, Biochemistry and Cell Biology, Physiology, Clinical Sciences, Biochemistry & Molecular Biology
Abstract

Oleoylethanolamide (OEA), the naturally occurring amide of ethanolamine and oleic acid, is an endogenous lipid that modulates feeding, body weight and lipid metabolism by binding with high affinity to the ligand-activated transcription factor, peroxisome proliferator-activated receptor-alpha (PPAR-alpha). In the present article, we describe the biochemical pathways responsible for the initiation and termination of OEA signaling, and outline the pharmacological properties of this compound in relation to its ability to activate PPAR-alpha. Finally, we discuss the possible role of OEA as a peripheral satiety hormone.

Published
2005

5. An anorexic lipid mediator regulated by feeding

Author

Rodríguez de Fonseca, F, Navarro, M, Gómez, R, Escuredo, L, Nava, F, Fu, J, Murillo-Rodríguez, E, Giuffrida, A, LoVerme, J, Gaetani, S, Kathuria, S, Gall, C, and Piomelli, D

Subjects
Neurosciences, Nutrition, Underpinning research, 1.1 Normal biological development and functioning, Animals, Appetite Depressants, Arachidonic Acids, Drug Tolerance, Eating, Endocannabinoids, Feeding Behavior, Intestine, Small, Oleic Acid, Oleic Acids, Polyunsaturated Alkamides, Rats, Rats, Wistar, General Science & Technology
Abstract

Oleylethanolamide (OEA) is a natural analogue of the endogenous cannabinoid anandamide. Like anandamide, OEA is produced in cells in a stimulus-dependent manner and is rapidly eliminated by enzymatic hydrolysis, suggesting a function in cellular signalling. However, OEA does not activate cannabinoid receptors and its biological functions are still unknown. Here we show that, in rats, food deprivation markedly reduces OEA biosynthesis in the small intestine. Administration of OEA causes a potent and persistent decrease in food intake and gain in body mass. This anorexic effect is behaviourally selective and is associated with the discrete activation of brain regions (the paraventricular hypothalamic nucleus and the nucleus of the solitary tract) involved in the control of satiety. OEA does not affect food intake when injected into the brain ventricles, and its anorexic actions are prevented when peripheral sensory fibres are removed by treatment with capsaicin. These results indicate that OEA is a lipid mediator involved in the peripheral regulation of feeding.

Published
2001

8. P58 IMMEDIATE CORONARY ANGIOGRAPHY AND SYSTEMATIC TARGETED TEMPERATURE MANAGEMENT ARE ASSOCIATED WITH IMPROVED OUTCOME IN COMATOSE SURVIVORS OF CARDIAC ARREST

Author

Dall’Ara, G, primary, Compagnone, M, additional, Spartà, D, additional, Carletti, R, additional, Grotti, S, additional, Guerrieri, G, additional, Gaetani, S, additional, Cortigiani, M, additional, Maitan, S, additional, Fabbri, A, additional, Ottani, F, additional, Caravita, L, additional, Tarantino, F, additional, and Galvani, M, additional

Published
2022
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19. An anorexic lipid mediator regulated by feeding

Author

de Fonseca, F. Rodríguez, Navarro, M., Gómez, R., Escuredo, L., Nava, F., Fu, J., Murillo-Rodríguez, E., Giuffrida, A., LoVerme, J., Gaetani, S., Kathuria, S., Gall, C., and Piomelli, D.

Published
2001

24. Increased intake of energy-dense diet and negative energy balance in a mouse model of chronic psychosocial defeat

Author

Coccurello, R., Romano, A., Giacovazzo, G., Tempesta, B., Fiore, M., Giudetti, A. M., Marrocco, Ilaria, Altieri, F., Moles, A., Gaetani, S., Marrocco I. (ORCID:0000-0002-8225-2177), Coccurello, R., Romano, A., Giacovazzo, G., Tempesta, B., Fiore, M., Giudetti, A. M., Marrocco, Ilaria, Altieri, F., Moles, A., Gaetani, S., and Marrocco I. (ORCID:0000-0002-8225-2177)

Abstract

Purpose: Chronic exposure to stress may represent a risk factor for developing metabolic and eating disorders, mostly driven by the overconsumption of easily accessible energy-dense palatable food, although the mechanisms involved remain still unclear. In this study, we used an ethologically oriented murine model of chronic stress caused by chronic psychosocial defeat (CPD) to investigate the effects of unrestricted access to a palatable high fat diet (HFD) on food intake, body weight, energy homeostasis, and expression of different brain neuropeptides. Our aim was to shed light on the mechanisms responsible for body weight and body composition changes due to chronic social stress. Methods: In our model of subordinate (defeated), mice (CPD) cohabitated in constant sensory contact with dominants, being forced to interact on daily basis, and were offered ad libitum access either to an HFD or to a control diet (CD). Control mice (of the same strain as CPD mice) were housed in pairs and left unstressed in their home cage (UN). In all these mice, we evaluated body weight, different adipose depots, energy metabolism, caloric intake, and neuropeptide expression. Results: CPD mice increased the intake of HFD and reduced body weight in the presence of enhanced lipid oxidation. Resting energy expenditure and interscapular brown adipose tissue (iBAT) were increased in CPD mice, whereas epididymal adipose tissue increased only in HFD-fed unstressed mice. Propiomelanocortin mRNA levels in hypothalamic arcuate nucleus increased only in HFD-fed unstressed mice. Oxytocin mRNA levels in the paraventricular nucleus and neuropeptide Y mRNA levels within the arcuate were increased only in CD-fed CPD mice. In the arcuate, CART was increased in HFD-fed UN mice and in CD-fed CPD mice, while HFD intake suppressed CART increase in defeated animals. In the basolateral amygdala, CART expression was increased only in CPD animals on HFD. Conclusions: CPD appears to uncouple the intake of HFD fr

Published
2018

25. Proteomic identification of altered protein O-GlcNAcylation in a triple transgenic mouse model of Alzheimer's disease

Author

Tramutola, A., Sharma, N., Barone, E., Lanzillotta, C., Castellani, A., Iavarone, F., Vincenzoni, F., Castagnola, M., Butterfield, D. A., Gaetani, S., Cassano, T., Perluigi, M., Di Domenico, F., Iavarone F. (ORCID:0000-0002-2074-5531), Castagnola M. (ORCID:0000-0002-0959-7259), Tramutola, A., Sharma, N., Barone, E., Lanzillotta, C., Castellani, A., Iavarone, F., Vincenzoni, F., Castagnola, M., Butterfield, D. A., Gaetani, S., Cassano, T., Perluigi, M., Di Domenico, F., Iavarone F. (ORCID:0000-0002-2074-5531), and Castagnola M. (ORCID:0000-0002-0959-7259)

Abstract

PET scan analysis demonstrated the early reduction of cerebral glucose metabolism in Alzheimer disease (AD) patients that can make neurons vulnerable to damage via the alteration of the hexosamine biosynthetic pathway (HBP). Defective HBP leads to flawed protein O-GlcNAcylation coupled, by a mutual inverse relationship, with increased protein phosphorylation on Ser/Thr residues. Altered O-GlcNAcylation of Tau and APP have been reported in AD and is closely related with pathology onset and progression. In addition, type 2 diabetes patients show an altered O-GlcNAcylation/phosphorylation that might represent a link between metabolic defects and AD progression. Our study aimed to decipher the specific protein targets of altered O-GlcNAcylation in brain of 12-month-old 3×Tg-AD mice compared with age-matched non-Tg mice. Hence, we analysed the global O-GlcNAc levels, the levels and activity of OGT and OGA, the enzymes controlling its cycling and protein specific O-GlcNAc levels using a bi-dimensional electrophoresis (2DE) approach. Our data demonstrate the alteration of OGT and OGA activation coupled with the decrease of total O-GlcNAcylation levels. Data from proteomics analysis led to the identification of several proteins with reduced O-GlcNAcylation levels, which belong to key pathways involved in the progression of AD such as neuronal structure, protein degradation and glucose metabolism. In parallel, we analysed the O-GlcNAcylation/phosphorylation ratio of IRS1 and AKT, whose alterations may contribute to insulin resistance and reduced glucose uptake. Our findings may contribute to better understand the role of altered protein O-GlcNAcylation profile in AD, by possibly identifying novel mechanisms of disease progression related to glucose hypometabolism.

Published
2018

32. Inhibition of anandamide hydrolysis enhances noradrenergic and GABAergic transmission in the prefrontal cortex and basolateral amygdala of rats subjected to acute swim stress

Author

Besde, G, Romano, A, Tempesta, B, Lavecchia, Ma, Pace, L, Bellomo, A, Duranti, Andrea, MICIONI DI BONAVENTURA MV, Cifani, C, Cassano, T, and Gaetani, S.

Subjects
Male, Polyunsaturated Alkamides, Microdialysis, Arachidonic Acids, Norepinephrine, GABA, Animals, anandamide, Rats, Wistar, Chromatography, High Pressure Liquid, Swimming, gamma-Aminobutyric Acid, Analysis of Variance, prefrontal cortex, Basolateral Nuclear Complex, Extracellular Fluid, URB597, basolateral amygdala, noradrenaline, Rats, Disease Models, Animal, Benzamides, Carbamates, Stress, Psychological, Endocannabinoids
Abstract

Limbic forebrain endocannabinoid (eCB) signaling is critically involved in stress integration by modulating neurotransmitters release. The purpose of this study was to examine, by brain microdialysis, the effects of fatty acid amide hydrolase (FAAH) inhibition on noradrenergic and γ-aminobutyric acid (GABA)-ergic neurotransmission in the prefrontal cortex (PFC) and basolateral amygdala (BLA) of rats subjected to a 20-min swim stress. Microdialysis started on stress- and drug-naïve rats that were treated with the FAAH inhibitor URB597 (0.1 or 0.3 mg/kg) 30 min before undergoing the stress procedure. Dialysate samples were collected every 20 min from the beginning of the experiment. Concentrations of noradrenaline (NA) and GABA were determined by HPLC coupled to electrochemical and fluorescence detection, respectively. We found that neither URB597 treatment nor 20 min of swim stress exposure per se altered NA and GABA extracellular levels in PFC or BLA. Interestingly, rats treated with 0.1 mg/kg of URB597 followed by 20 min of stress showed significantly higher NA and GABA levels in PFC and BLA. These effects were absent in rats treated with 0.3 mg/kg URB597, indicating a dose-specific effect. Moreover, we found that the pretreatment with the CB1 receptor antagonist rimonabant blocked the URB597 effects on NA and GABA release in PFC and BLA of animals subjected to forced swimming. The present study might provide an important first step toward understanding the mechanisms through which URB597 modulates stress-induced neuroendocrine secretion and behavioral coping strategies.

Published
2015

40. WAG/Rij rats show a reduced expression of CB1 receptors in thalamic nuclei and respond to the CB1 receptor agonist, R(+)WIN55,212-2, with a reduced incidence of spike-wave discharges

Author

Rijn, C.M. van, Gaetani, S., Santolini, I., Badura, A., Fu, J., Watanabe, M., Cuomo, V., Luijtelaar, E.L.J.M. van, Nicoletti, F., and Ngomba, R.T.

Subjects
Biological psychology, Plasticity and Memory [DI-BCB_DCC_Theme 3], Biologische psychologie
Abstract

Contains fulltext : 90547.pdf (Publisher’s version ) (Closed access) Purpose: Genetically epileptic WAG/Rij rats develop spontaneous absence-like seizures after 3 months of age. We used WAG/Rij rats to examine whether absence seizures are associated with changes in the expression of type-1 cannabinoid (CB1) receptors. Methods: Receptor expression was examined by in situ hybridization and western blot analysis in various brain regions of “presymptomatic” 2-month old and “symptomatic” 8-month-old WAG/Rij rats relative to age-matched nonepileptic control rats. Furthermore, we examined whether pharmacologic activation of CB1 receptor affects absence seizures. We recorded spontaneous spike-wave discharges (SWDs) in 8-month old WAG/Rij rats systemically injected with the potent CB1 receptor agonist, R(+)WIN55,212-2 (3–12 mg/kg, s.c.), given alone or combined with the CB1 receptor antagonist/inverse agonist, AM251 (12 mg/kg, s.c.). Results: Data showed a reduction of CB1 receptor mRNA and protein levels in the reticular thalamic nucleus, and a reduction in CB1 receptor protein levels in ventral basal thalamic nuclei of 8-month-old WAG/Rij rats, as compared with age-matched ACI control rats. In vivo, R(+)WIN55,212-2 caused a dose-dependent reduction in the frequency of SWDs in the first 3 h after the injection. This was followed by a late increase in the mean SWD duration, which suggests a biphasic modulation of SWDs by CB1 receptor agonists. Both effects were reversed or attenuated when R(+)WIN55,212-2 was combined with AM251. Discussion: These data indicate that the development of absence seizures is associated with plastic modifications of CB1 receptors within the thalamic-cortical-thalamic network, and raise the interesting possibility that CB1 receptors are targeted by novel antiabsence drugs.

Published
2010

49. Role of Bed Nucleus of the Stria Terminalis Corticotrophin-Releasing Factor Receptors in Frustration Stress-Induced Binge-Like Palatable Food Consumption in Female Rats with a History of Food Restriction

Author

Micioni Di Bonaventura, M. V., primary, Ciccocioppo, R., additional, Romano, A., additional, Bossert, J. M., additional, Rice, K. C., additional, Ubaldi, M., additional, St. Laurent, R., additional, Gaetani, S., additional, Massi, M., additional, Shaham, Y., additional, and Cifani, C., additional

Published
2014
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