Erukainure Ochuko L, Matsabisa Motlalepula G, Salau Veronica F, Olofinsan Kolawole A, Oyedemi Sunday O, Chukwuma Chika I, Nde Adeline Lum, Islam Md Shahidul
Department of Pharmacology, School of Clinical Medicine, Faculty of Health Sciences, University of the Free State, Bloemfontein 9300, South Africa.
Department of Pharmacology, School of Clinical Medicine, Faculty of Health Sciences, University of the Free State, Bloemfontein 9300, South Africa.
Biomed Pharmacother. 2022 May;149:112863. doi: 10.1016/j.biopha.2022.112863. Epub 2022 Mar 30.
Reduced glucose uptake and utilization, with concomitant lipolysis in adipose tissues has been linked to the pathogenesis of obesity and its complications. The present study investigated the effect of cannabinoid-stimulated glucose uptake on redox imbalance, glucose and lipid metabolisms, as well as cholinergic and purinergic dysfunctions in isolated rats' adipose tissues. Freshly Isolated rats' adipose tissues were incubated with glucose and different concentrations of cannabidiol for 2 h at 37 °C. The negative control consisted of incubation without cannabidiol, while normal control consisted of incubations without glucose and/or cannabidiol and Metformin served as the standard drug. Cannabidiol caused an increase in adipose-glucose uptake, with concomitant elevation of glutathione, triglyceride level, superoxide dismutase, catalase and 5'nucleoidase activities. It also caused suppression in malondialdehyde and cholesterol levels, acetylcholinesterase, ENTPDase, fructose-1,6-biphosphatase, glucose 6-phosphatase, glycogen phosphorylase, and lipase activities. In silico studies revealed a strong molecular interaction of cannabidiol with adipose triglyceride lipase, hormone-sensitive lipase, and monoglyceride lipase. These results indicate that cannabidiol-enhanced glucose uptake in adipose tissues is associated with enhanced antioxidative activities, concomitant modulation of cholinergic and purinergic dysfunctions, and improved glucose - lipid homeostasis.
葡萄糖摄取和利用的减少，以及脂肪组织中伴随的脂解作用，与肥胖及其并发症的发病机制有关。本研究调查了大麻素刺激的葡萄糖摄取对分离的大鼠脂肪组织中氧化还原失衡、葡萄糖和脂质代谢以及胆碱能和嘌呤能功能障碍的影响。将新鲜分离的大鼠脂肪组织与葡萄糖和不同浓度的大麻二酚在37℃下孵育2小时。阴性对照为不添加大麻二酚的孵育，正常对照为不添加葡萄糖和/或大麻二酚的孵育，二甲双胍作为标准药物。大麻二酚导致脂肪组织对葡萄糖的摄取增加，同时谷胱甘肽、甘油三酯水平、超氧化物歧化酶、过氧化氢酶和5'核苷酸酶活性升高。它还导致丙二醛和胆固醇水平、乙酰胆碱酯酶、ENTPD酶、果糖-1,6-双磷酸酶、葡萄糖6-磷酸酶、糖原磷酸化酶和脂肪酶活性受到抑制。计算机模拟研究揭示了大麻二酚与脂肪甘油三酯脂肪酶、激素敏感性脂肪酶和单甘油酯脂肪酶之间有很强的分子相互作用。这些结果表明，大麻二酚增强脂肪组织对葡萄糖的摄取与增强抗氧化活性、同时调节胆碱能和嘌呤能功能障碍以及改善葡萄糖-脂质稳态有关。
