Tisdale M J, Threadgill M D
Cancer Biochem Biophys. 1984 Sep;7(3):253-9.
Of a range of glycerol analogues, (+/-)-2,3-dihydroxypropyl dichloroacetate (III) has been shown to be the most potent inhibitor of glycerol kinase in vitro. Inhibition is noncompetitive with a Ki value of 1.8 X 10(-3) M. The presence of ATP seems essential for effective inhibition of the enzyme, suggesting that the inhibitor is phosphorylated to a glycerol-3-phosphate analogue. In vivo III causes a decrease in the specific activity of liver glycerol kinase and produces a dose-dependent reduction in blood glucose levels. There is a reduction in the conversion of [U-14C] glycerol into glucose after administration of III to CBA/CA mice while gluconeogenesis from fructose is increased. This suggests that of the enzymes of gluconeogenesis only glycerol kinase is inhibited by III. This compound may be useful in reducing the lipid contribution to gluconeogenesis in advancing cancer.
在一系列甘油类似物中,(±)-2,3 - 二羟基丙基二氯乙酸酯(III)已被证明是体外甘油激酶最有效的抑制剂。抑制作用是非竞争性的,Ki值为1.8×10⁻³ M。ATP的存在似乎是有效抑制该酶所必需的,这表明抑制剂被磷酸化为甘油 - 3 - 磷酸类似物。在体内,III会导致肝脏甘油激酶的比活性降低,并使血糖水平产生剂量依赖性降低。给CBA/CA小鼠施用III后,[U - ¹⁴C]甘油向葡萄糖的转化减少,而果糖的糖异生增加。这表明在糖异生的酶中,只有甘油激酶被III抑制。这种化合物可能有助于减少晚期癌症中脂质对糖异生的贡献。