The ability of umbelliferone to stimulate muscle glucose uptake and its effect on glucose and fatty acid metabolism as well as nucleotide hydrolysis and cholinergic activity were investigated in isolated psoas muscles. Incubation of umbelliferone with muscles led to increase glucose uptake, elevated GSH, SOD and catalase activities, as well as depleted malondialdehyde and nitric oxide levels. It also led to decrease ATPase activity with concomitant increase in ENTPDase and 5′nucleotidiase activities. The activities of chymotrypsin and acetylcholinesterase, glycogen phosphorylase, glucose-6-phosphatase, fructose-1,6-phosphatase and lipase were also suppressed. Umbelliferone reversed the altered lipid metabolites, and deactivated pathways induced by incubation with glucose. These were however reversed in umbelliferone-incubated muscles with concomitant deactivation of steroid biosynthesis. Taken together, these results further support the antidiabetic properties of umbelliferone. Its antidiabetic mechanism involves stimulation of muscle glucose uptake, with concomitant modulation of lipid metabolism and nucleotide hydrolysis, while stalling gluconeogenesis and oxidative stress.

在分离的腰肌中研究了伞形酮刺激肌肉摄取葡萄糖的能力及其对葡萄糖和脂肪酸代谢的影响以及核苷酸水解和胆碱能活性。伞形酮与肌肉的孵育导致葡萄糖摄取增加，GSH，SOD和过氧化氢酶活性升高，以及丙二醛和一氧化氮水平降低。它也导致ATPase活性降低，同时ENTPDase和5'核苷酸酶活性增加。还抑制了胰凝乳蛋白酶和乙酰胆碱酯酶，糖原磷酸化酶，葡萄糖-6-磷酸酶，果糖-1,6-磷酸酶和脂肪酶的活性。伞形酮逆转了改变的脂质代谢产物，并使葡萄糖孵育诱导的通路失活。然而，在伞形酮培养的肌肉中这些被逆转，伴随类固醇生物合成的失活。综上所述，这些结果进一步支持伞形酮的抗糖尿病特性。它的抗糖尿病机制包括刺激肌肉吸收葡萄糖，同时调节脂质代谢和核苷酸水解，同时阻止糖异生和氧化应激。