Cannabidiol (CBD) does not influence blood glucose in diabetic animals or humans. Nor, in patients with type 2 diabetes does it affect glycemic control, insulin sensitivity, lipid profile, body mass, or hemodynamic parameters. But, because it has antioxidative, anti-inflammatory, and vasculo-, cardio- and neuroprotective properties, CBD does show some ability to mitigate cardiovascular complications of diabetes, like atherosclerosis, retinopathy, and cardiomyopathy. These are associated with vascular endothelial dysfunction, increased inflammation, and oxidative stress, all known to be within CBD’s modulatory reach.
In the human coronary artery endothelium degrades when it is exposed to high glucose, with increased mitochondrial superoxide generation, 3-nitrotyrosine formation, NF-κB activation, nitrous oxide synthase and adhesion molecules expression, and migration and adhesion of monocytes. Pretreatment with CBD has been reported to attenuate all of these effects, and to reverse glucose-induced disruption of endothelial barrier function. The mechanism of action is not known, but it appears to be independent of either of the known cannabinoid receptor sites.
CBD has enhanced acetylcholine-induced vasodilation in the aortas and femoral arteries of type 2 diabetic rats, and in a more pronounced way than in non-diabetic controls. CBD appears to activate cyclooxygenase, as well, which produces compounds that activate EP4 prostanoid receptors. Superoxide dismutase and CB2 receptors are apparently involved, the latter acted on by the CB2 agonist HU308, which in the absence of CBD does not show any vasodilatory effect. CBD has also been observed to lower some serum metabolic and cardiovascular biomarkers, though for reasons not known, it has also increased circulating levels of endothelin 1. In humans with type 2 diabetes, these effects have been less pronounced. CBD has not enhanced vasodilatory properties and has elicited only moderate vasorelaxant responses.
There is possibly better news in diabetic retinopathy, which is a function of increased vascular permeability and neurotoxicity. In one rat model of type 1 diabetes, long-term CBD therapy did improve the blood-retina barrier function, by lowering retinal levels of vascular endothelial growth factor, and it reduced oxidative and nitrative stress, decreased levels of TNF-α and ICAM-1 as well, and prevented neuronal apoptosis. The opposite effect on VEGF has been observed elsewhere, however, so more investigation of this particular mechanism is needed.
The etiology of diabetic cardiomyopathy involves oxidative and nitrative stress, inflammation, cardiac fibrosis and cardiomyocyte death. In mouse models, long-term CBD mitigates all of these, by inhibiting pro-inflammatory and cell death pathways (NF-κB, p38 and p38α MAPK, JNK) and enhancing the prosurvival Akt pathway. It has done the same in human cardiomyocytes.
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The foregoing is a report on trends and developments in the cannabinoid industry. No product described herein is intended to diagnose, treat, cure or prevent any disease or syndrome.
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