Abstract
ObjectiveAcute administration of cannabinoid CB1 receptor agonists, or the ingestion of cannabis, induces short-term hyperphagia. However, the incidence of obesity is lower in frequent cannabis users compared to non-users. Gut microbiota affects host metabolism and altered microbial profiles are observed in obese states. Gut microbiota modifies adipogenesis through actions on the endocannabinoid system. This study investigated the effect of chronic THC administration on body weight and gut microbiota in diet-induced obese (DIO) and lean mice.MethodsAdult male DIO and lean mice were treated daily with vehicle or THC (2mg/kg for 3 weeks and 4 mg/kg for 1 additional week). Body weight, fat mass, energy intake, locomotor activity, whole gut transit and gut microbiota were measured longitudinally.ResultsTHC reduced weight gain, fat mass gain and energy intake in DIO but not lean mice. DIO-induced changes in select gut microbiota were prevented in mice chronically administered THC. THC had no effect on locomotor activity or whole gut transit in either lean or DIO mice.ConclusionsChronic THC treatment reduced energy intake and prevented high fat diet-induced increases in body weight and adiposity; effects that were unlikely to be a result of sedation or altered gastrointestinal transit. Changes in gut microbiota potentially contribute to chronic THC-induced actions on body weight in obesity.
Highlights
Obesity has reached epidemic proportions worldwide placing a huge health and economic burden on society
DIOinduced changes in select gut microbiota were prevented in mice chronically administered THC
THC had no effect on locomotor activity or whole gut transit in either lean or diet-induced obese (DIO) mice
Summary
Obesity has reached epidemic proportions worldwide placing a huge health and economic burden on society. Lifestyle modifications such as improved diet and increased physical activity can initially be successful in reducing weight, but maintaining weight loss through these measures proves difficult [1]. Cannabinoid receptor antagonists/inverse agonists [5, 6] and neutral antagonists [7,8,9] inhibit food intake. CB1 receptor activation by agonists stimulates short-term feeding when administered acutely [10]. Smoking cannabis is associated with increased short-term energy intake. The major psychoactive constituent of cannabis, Δ9 tetrahydrocannabinol (THC) increases food intake and synthetic THC, Dronabinol, is prescribed as an appetite-stimulant in HIV-related anorexia [15]. Contrary to what might be expected, the body mass index of regular cannabis smokers was lower than that of non-users [16]
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