A chalcone analogue, (E)-3-(phenyl)-1-(3,4,5-trimethoxyphenyl)prop-2-en-1-one (DMU 101), was synthesized using classic base catalysis and Claisen-Schmidt condensation, and then screened for its antidiabetic properties. The compound's effects on glucose and lipid metabolism were assayed in rats that were treated acutely and for a short time to elucidate its mechanism of action, evaluating glucose tolerance and lactate dehydrogenase activity in response to chalcone analogue administration. The chalcone's in vitro and ex vivo effects on glycogen, glucose, lipid and lipolysis were also investigated, as well as the mechanism by which it induces ⁴⁵Ca²⁺ influx-mediated insulin secretion. The analogue (10 mg/kg) diminished glycemia, without inducing acute cell damage, increased glycogen content in the skeletal muscle and reduced serum triacylglycerol and total cholesterol, but did not alter high-density lipoprotein or low-density lipoprotein. Chalcone (10 μM) stimulated glucose uptake in the soleus muscle and did not modulate in vitro or ex vivo lipolysis. This analogue also increased insulin secretion by triggering calcium influx and blocking ATP-sensitive K⁺ channels and voltage-dependent calcium channels. However, it also modulated stored calcium via sarco/endoplasmic reticulum calcium ATPase (SERCA) and ryanodine receptor (RYR) activity. These findings indicate that this chalcone may induce cellular repolarization via a mechanism mediated by calcium-dependent potassium channels.

使用经典碱催化和 Claisen-Schmidt 缩合合成查尔酮类似物 (E)-3-(苯基)-1-(3,4,5-三甲氧基苯基)prop-2-en-1-one (DMU 101) ，然后筛选其抗糖尿病特性。在经过短期急性治疗的大鼠中测定了该化合物对葡萄糖和脂质代谢的影响，以阐明其作用机制，评估查耳酮类似物给药后的葡萄糖耐量和乳酸脱氢酶活性。还研究了查耳酮对糖原、葡萄糖、脂质和脂肪分解的体外和离体影响，以及它诱导⁴⁵ Ca ²⁺流入介导的胰岛素分泌的机制。该类似物（10 mg/kg）可降低血糖，但不会引起急性细胞损伤，增加骨骼肌中的糖原含量，降低血清三酰甘油和总胆固醇，但不会改变高密度脂蛋白或低密度脂蛋白。查尔酮 (10 μM) 刺激比目鱼肌中的葡萄糖摄取，并且不调节体外或离体脂肪分解。该类似物还通过触发钙流入并阻断 ATP 敏感 K ⁺通道和电压依赖性钙通道来增加胰岛素分泌。然而，它还通过肌浆/内质网钙 ATP 酶(SERCA) 和兰尼碱受体 (RYR) 活性调节储存的钙。这些发现表明，这种查尔酮可能通过钙依赖性钾通道介导的机制诱导细胞复极化。