|WIN55,AM6545||weight loss,obesity in mice via experiment||Cannabinoid CB1 Receptors Inhibit Gut-Brain Satiation Signaling in Diet-Induced Obesity||Mar 2019|
Action Pathway: CB1|
Collectively, these results provide evidence that hyperphagia associated with DIO is driven by a mechanism that includes CB1R-mediated inhibition of gut-brain satiation signaling.
|AM6545||obesity in mice||Peripheral CB1 cannabinoid receptor blockade improves cardiometabolic risk in mouse models of obesity||Aug 2010|
Action Pathway: CB1|
Here we have demonstrated that a CB1R neutral antagonist largely restricted to the periphery does not affect behavioral responses mediated by CB1R in the brains of mice with genetic or diet-induced obesity, but it does cause weight-independent improvements in glucose homeostasis, fatty liver, and plasma lipid profile
|AM6545||obesity,appetite supress in vitro||A novel peripherally restricted cannabinoid receptor antagonist, AM6545, reduces food intake and body weight, but does not cause malaise, in rodents||Oct 2010|
|Peripherally active, cannabinoid receptor antagonists with limited brain penetration may be useful agents for the treatment of obesity and its complications.|
|AM6545||obesity,appetite supress in rats via experiment||THE NOVEL CANNABINOID CB1 ANTAGONIST AM6545 SUPPRESSES FOOD INTAKE AND FOOD-REINFORCED BEHAVIOR||Aug 2010|
Ingestion Method: 16mg/kg|
AM6545 also produced a strong suppression of the intake of high carbohydrate and high fat diets in the same dose range, but only produced a mild suppression of lab chow intake at the highest dose (16.0 mg/kg). Although AM6545 did not affect food handling, it did reduce time spent feeding and feeding rate. Taken together, these results suggest that AM6545 is a compound that warrants further study as a potential appetite suppressant drug.
|cannabinoids||pain,addiction,obesity via article||Cannabinoids: Friend or Foe?||Jun 2016|
|These are interesting time for cannabinoid research and clinical application; much more needs to be done to translate the potential of cannabinoid drugs to medicinal use and to identify the conditions that could benefit from this class of drugs. There is as yet untapped potential in the areas of pain and addiction, obesity, metabolic syndrome and epilepsy|
|cannabis||obesity,diabetes in humans via survey (n=786)||Cannabis use in relation to obesity and insulin resistance in the Inuit population.||Feb 2015|
|Positive Cannabis use was highly prevalent in the study population (57.4%) and was statistically associated with lower body mass index (BMI) (P < 0.001), lower % fat mass (P < 0.001), lower fasting insulin (P = 0.04), and lower HOMA-IR (P = 0.01), after adjusting for numerous confounding variables. Further adjustment for BMI rendered fasting insulin and HOMA-IR differences statistically nonsignificant between past-year cannabis users and nonusers. Mediation analysis showed that the effect of cannabis use on insulin resistance was indirect, through BMI.|
|Cymene||obesity,diabetes in mice (n=48)||Cymene and Metformin treatment effect on biochemical parameters of male NMRI mice fed with high fat diet.||June 2015|
|Non-fasting glucose serum levels, ALT, and ALP of E2 and E3 decreased significantly compared to HFD control group.|
|CBD||obesity,weight loss in rats via experiment||Cannabidiol inhibits sucrose self-administration by CB1 and CB2 receptor mechanisms in rodents||Jun 2019|
Ingestion Method: 10, 20, and 40 mg/kg, ip|
Action Pathway: CB1,CB2
Taken together, the present findings suggest that CBD may have therapeutic potential in reducing binge eating and the development of obesity.