hyperphagia/cannabis

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A low-Δ9 tetrahydrocannabinol cannabis extract induces hyperphagia in rats.

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Appetite stimulation via partial agonism of cannabinoid type 1 receptors by Δtetrahydrocannabinol (ΔTHC) is well documented and can be modulated by non-ΔTHC phytocannabinoids. ΔTHC concentrations sufficient to elicit hyperphagia induce changes to both appetitive (reduced latency to feed) and

N-Oleoylglycine-Induced Hyperphagia Is Associated with the Activation of Agouti-Related Protein (AgRP) Neuron by Cannabinoid Receptor Type 1 (CB1R).

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N-Acyl amino acids (NAAAs) are conjugate products of fatty acids and amino acids, which are available in animal-derived food. We compared the effects of N-arachidonoylglycine (NAGly), N-arachidonoylserine (NASer), and N-oleoylglycine (OLGly) on in vivo food intake and in vitro [Ca2+]i of

Cannabis constituents modulate δ9-tetrahydrocannabinol-induced hyperphagia in rats.

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BACKGROUND The hyperphagic effect of Delta9-tetrahydrocannabinol (Delta9THC) in humans and rodents is well known. However, no studies have investigated the importance of Delta9THC composition and any influence other non-Delta9THC cannabinoids present in Cannabis sativa may have. We therefore

Anandamide induces overeating: mediation by central cannabinoid (CB1) receptors.

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BACKGROUND Central cannabinoid systems have been implicated in appetite regulation by the respective hyperphagic actions of exogenous cannabinoids, such as delta9-THC, and hypophagic effects of selective cannabinoid receptor antagonists. OBJECTIVE This study examined whether an endogenous

Cannabidiol inhibits the hyperphagia induced by cannabinoid-1 or serotonin-1A receptor agonists.

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Δ9-THC is a component of Cannabis sativa that increases food intake in animals and humans, an effect prevented by selective CB1 receptor antagonists. Cannabidiol (CBD) is another constituent of this plant that promotes several opposite neuropharmacological effects compared to Δ9-THC. CBD mechanisms

Cannabinoid-induced hyperphagia: correlation with inhibition of proopiomelanocortin neurons?

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We tested the hypothesis that cannabinoids modulate feeding in male guinea pigs, and correlated cannabinoid-induced changes in feeding behavior with alterations in glutamatergic synaptic currents impinging upon proopiomelanocortin (POMC) neurons of the hypothalamic arcuate nucleus. Feeding

Effect of opioid and cannabinoid receptor antagonism on orphanin FQ-induced hyperphagia in rats.

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Feeding induced in rats by cerebroventricular (i.c.v.) injection of orphanin FQ was potently and dose-dependently reversed by peripheral injection of either the opioid antagonist naloxone or the cannabinoid CB(1) receptor antagonist SR

A cannabigerol-rich Cannabis sativa extract, devoid of [INCREMENT]9-tetrahydrocannabinol, elicits hyperphagia in rats.

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Nonpsychoactive phytocannabinoids (pCBs) from Cannabis sativa may represent novel therapeutic options for cachexia because of their pleiotropic pharmacological activities, including appetite stimulation. We have recently shown that purified cannabigerol (CBG) is a novel appetite stimulant in rats.

Body mass index and marijuana use.

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Though marijuana has been reported to stimulate appetite, we searched for a correlation between obesity and decreased marijuana use. We examined charts of all females referred for morbid obesity/weight management in a 12-month period. BMI and substance use data were collected from 297 charts. While

Cannabis Smoking and Diabetes Mellitus: Results from Meta-analysis with Eight Independent Replication Samples.

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BACKGROUND In preclinical animal studies, evidence links cannabis with hyperphagia, obesity, and insulin resistance. Epidemiologic data, however, suggest an inverse cannabis smoking-diabetes mellitus association. Here, we offer epidemiologic estimates from eight independent replications from (1) the

Cannabinoid-glutamate interactions in the regulation of food intake in neonatal layer- type chicks: role of glutamate NMDA and AMPA receptors.

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The involvement of the endocannabinoid system in the brain functions is likely the conclusion of its capability to interact with specific neurotransmitters in several brain regions. The present study was designed to examine the role of the glutamatergic system on cannabinoid-induced hyperphagia in

Cannabinoid 1 G protein-coupled receptor (periphero-)neutral antagonists: emerging therapeutics for treating obesity-driven metabolic disease and reducing cardiovascular risk.

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BACKGROUND Obesity and related cardiometabolic derangements are spiraling global health problems urgently in need of safe, effective and durable pharmacotherapy. METHODS As an orexigenic and anabolic biosignaling network, the endocannabinoid system interacts with other information-transducing

Endogenous opioids and cannabinoids: system interactions in the regulation of appetite, grooming and scratching.

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Growing evidence suggests substantial crosstalk between endogenous opioid and cannabinoid systems in the regulation of appetite. Not only is cannabinoid-induced hyperphagia abolished by opioid receptor antagonists (and vice versa), but several laboratories have reported supra-additive anorectic

Heavy Cannabis Use Associated with Wernicke's Encephalopathy.

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Cannabis use accounts for more than 149,000 hospital visits annually. As more states legalize recreational Cannabis, side effects that are currently rare or unknown will become increasingly more common. Here, we present one such rare case of Cannabis-induced hyperemesis causing Wernicke's

Antiobesity effects of chronic cannabinoid CB1 receptor antagonist treatment in diet-induced obese mice.

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We determined the effect of a cannabinoid CB1 receptor antagonist (AM-251; N-(Piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide) on food intake, body weight and adipose tissue mass in Western diet-induced obese (DIO) mice using a chronic, interrupted, oral

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