Recognizing that the endocannabinoids anandamide (AEA) and 2-arachidonoylglycerol (2-AG) are bioactive lipid mediators derived from long-chain polyunsaturated fatty acids, and are released on demand through cannabinoid CB1 and CB2 receptors, whose presence has been verified in adipose tissue, and recognizing that there are other congeners, likeN-palmitoyl-,N-oleoyl-ethanolamine (PEA, OEA), 2-oleoyl-, 2-linoleoyl-glycerol (2-OG, 2-LG), and 2-arachidonoyl glyceryl ether (2-AGE, noladin ether), that share molecular targets and are activated by the same enzymes as endocannabinoids, it should be no surprise that the endocannabinoid system, in this extended way, mediates processes that include appetite, energy balance, and metabolism. (We have written elsewhere on the possible role that cannabinoid therapy might eventually have in treatment for anorexia and bulimia.) The literature is quite clear that the body’s endocannabinoid system is upregulated in obesity. Serum 2-AG’s upregulation in hyperglycemia correlates with body fat content, visceral fat mass, and fasting plasma triacylglyceride, for example. There is substantial correlation between AEA level and body mass index value, too, though interestingly, patients with non-alcoholic fatty liver disease have significantly increased levels of 2-AG but no change in AEA levels. All of this is the rationale behind the anti-obesity drug rimonabant (SR141716A), a selective antagonist of CB1 receptors controlling energetic homeostasis of the liver, muscle, and adipose tissue. (We have written on this drug, since withdrawn for psychotropic effects, as well.) Other studies have shown positive preclinical anti-obesity effects of the inverse agonists AM6545 and JD5037.  

Cannabidiol (CBD) is a negative allosteric modulator of the CB1 receptor, with some affinity for CB2, either as an agonist or an inverse agonist, and also for GPR55, α1-adrenoreceptors, 5-HT1A, TRPV channels and PPARγ, the last known for its crucial role in regulating glucose homeostasis and lipoprotein metabolism. There are a handful of studies that have investigated anti-obesity effects of CBD. In rats and mice, results have been mixed. Dosages need to be standardized for more intelligible data. 

In adipose tissue studies, CBD has been observed to reduce triacylglycerol accumulation in 3T3-L1 adipocytes treated with oleic acid, and to induce mitochondrial activation and increase oxygen consumption, which may explain the reduced fat accumulation in adipocytes in some rats exposed to  increased glucose uptake. In those studies, animals that should have gained weight, but were treated with CBD, did not gain weight. 

Focussed studies on obesity models have shown positive influence of CBD on the liver, specifically in reduction of intracellular lipid content, possibly by having enhanced lipolysis and mitochondrial activity through increased fatty acid oxidation. CBD increases the expression of proteins involved in upregulating lipid metabolism, by modulating one catalytic subunit of 5′AMP-activated protein kinase (AMPKa2), extracellular signal-regulated kinase (ERK1/2), and signal transducers and transcription activators in hepatocytes. CBD has also enhanced levels of glutathione, adenosine triphosphate, and nicotinamide adenine dinucleotide. 

DiolPure products contain PureForm CBD™ transformed from aromatic terpenes for pharmaceutical-grade purity. PureForm CBD™ is bioidentical to CBD extracted from hemp and cannabis, but free of any residual cannabinoids like THC or impurities or chemicals that can associate with traditional plant-derived production processes. 

The foregoing is a report on trends and developments in cannabinoid industry research. No product description herein is intended as a recommendation for diagnosis, treatment, cure or prevention of any disease or syndrome.