Habib M P, Dickerson F D, Mooradian A D
Tucson Veterans Affairs Medical Center, AZ 85723.
Metabolism. 1994 Nov;43(11):1442-5. doi: 10.1016/0026-0495(94)90042-6.
Lipid peroxidative activity in rats made diabetic with streptozocin and rats made acutely hyperglycemic by intraperitoneal dextrose administration was determined by measurement of exhaled ethane during exposure in vivo to ethane-free air (EFA). Diabetic rats demonstrated increased ethane in the expired breath while breathing EFA (5.82 +/- 0.56 pmol/min/100 g) compared with control rats (4.02 +/- 0.23 pmol/min/100 g). Insulin treatment of diabetic rats attenuated the ethane produced (4.88 +/- 0.23 pmol/min/100 g). Acute hyperglycemia increased exhaled ethane to levels higher than those seen in diabetic rats (9.87 +/- 0.98 pmol/min/100 g). Saline injected intraperitoneally to control rats produced ethane levels similar to those of untreated nondiabetic controls (4.11 +/- 0.52 pmol/min/100 g). Chronic uncontrolled hyperglycemia and acute hyperglycemia are associated with increased in vivo ethane production.
通过在体内暴露于无乙烷空气（EFA）期间测量呼出的乙烷，来测定用链脲佐菌素诱导糖尿病的大鼠以及通过腹腔注射葡萄糖诱导急性高血糖的大鼠的脂质过氧化活性。与对照大鼠（4.02±0.23皮摩尔/分钟/100克）相比，糖尿病大鼠在呼吸EFA时呼出的乙烷增加（5.82±0.56皮摩尔/分钟/100克）。对糖尿病大鼠进行胰岛素治疗可减少产生的乙烷（4.88±0.23皮摩尔/分钟/100克）。急性高血糖使呼出的乙烷增加到高于糖尿病大鼠的水平（9.87±0.98皮摩尔/分钟/100克）。向对照大鼠腹腔注射生理盐水产生的乙烷水平与未治疗的非糖尿病对照大鼠相似（4.11±0.52皮摩尔/分钟/100克）。慢性未控制的高血糖和急性高血糖与体内乙烷产生增加有关。
