Spitzer J A, Deaciuc I V
Department of Physiology, Louisiana State University Medical Center, New Orleans.
Cell Calcium. 1990 Jun-Jul;11(6):405-11. doi: 10.1016/0143-4160(90)90052-v.
Lipolytic rates and intracellular Ca2+ concentration ([Ca2+]i) were determined under basal conditions and upon stimulation with adrenocorticotropic hormone (ACTH), norepinephrine (NE) and insulin (I), in adipocytes isolated from control and acutely endotoxin (ET)-treated rats (1 mg/100 g body weight, LD50 at 6 h). [Ca2+]i measurements were done using the fluorescent Ca2(+)-indicator Fura-2. NE and ACTH, but not I, produced a marked increase of [Ca2+]i in cells of both control and ET-treated rats. ET treatment elicited a significant increase in [Ca2+]i of resting cells, and enhanced the ACTH effect on this parameter. The changes in lipolytic activity correlated well with changes of [Ca2+]i induced by ACTH. The results indicate that ET-induced alterations in intracellular calcium homeostasis of adipocytes may contribute to the mediation of effects on fat mobilization during endotoxemia.
在基础条件下以及用促肾上腺皮质激素（ACTH）、去甲肾上腺素（NE）和胰岛素（I）刺激后，测定从对照大鼠和急性内毒素（ET）处理的大鼠（1mg/100g体重，6小时半数致死量）分离的脂肪细胞中的脂解速率和细胞内钙离子浓度（[Ca2+]i）。使用荧光Ca2+指示剂Fura-2进行[Ca2+]i测量。NE和ACTH，但不是I，在对照大鼠和ET处理大鼠的细胞中均引起[Ca2+]i显著增加。ET处理使静息细胞的[Ca2+]i显著增加，并增强了ACTH对该参数的作用。脂解活性的变化与ACTH诱导的[Ca2+]i变化密切相关。结果表明，ET诱导的脂肪细胞内钙稳态改变可能有助于介导内毒素血症期间对脂肪动员的影响。
