Cho B H, Park J R
Harlan E. Moore Heart Research Foundation, Champaign, Illinois 61820.
Proc Soc Exp Biol Med. 1990 Feb;193(2):104-9. doi: 10.3181/00379727-193-43009.
To determine whether the estrogen-induced hyperlipidemia is affected by fasting, male growing chicks were administered subcutaneously a single dose of 17 beta-estradiol (25 mg/kg body wt), and the hormone treatment lasted for 2 days with or without feed (Experiment 1). In the second experiment, chicks were initially fasted for 1 or 3 days, and then treated with the same dosage of 17 beta-estradiol as in Experiment 1 for 2 days without feed. Plasma and liver lipids, and the activities of hepatic malic enzyme, glucose-6-phosphate dehydrogenase, and hormone-sensitive lipase in the adipose tissue were determined. Compared with fed control chicks, estrogen treatment in fed birds resulted in a marked elevation of plasma lipids, especially triglyceride during the 2-day period (137 vs 2263 mg/dl). In fasted chicks, the present finding that estrogen also induced a marked hyperlipidemia is noteworthy. Upon estrogen treatment (Experiment 1), the level of plasma triglyceride in fasted birds increased about 16 times over that of the fasted control group (133 vs 2093 mg/dl). Even in chicks fasted for 5 days (Experiment 2), estrogen treatment resulted in a persistent hypertriglyceridemia (75 vs 1369 mg/dl). In fed chicks, estrogen treatment also induced a fatty liver with massive accumulation of triglyceride, but the liver of estrogen-treated/fasted chicks appeared to be normal. In both fed and fasted chicks, malic enzyme was found to be the major NADPH producing enzyme in the liver. Upon fasting, both malic enzyme and glucose-6-phosphate dehydrogenase activities decreased significantly (P less than 0.05). In fed chicks, the total activities of both enzymes increased with estrogen treatment, whereas the effect of hormone on these enzymes was less obvious in fasted chicks. The hormone-sensitive lipase activity in the adipose tissue was much lower in fed chicks compared with that of fasted birds (0.15 vs 0.33 nmol of oleic acid released/min/mg protein). Estrogen treatment in fed chicks had no effect on the hormone-sensitive lipase activity, but its activity was enhanced by the hormone treatment in fasted chicks. The present finding that hyperlipidemia persisted in estrogenized chicks during the fasting seems to indicate the complex nature of this hormonal influence on lipid metabolism.
为了确定雌激素诱导的高脂血症是否受禁食影响，对雄性生长中的雏鸡皮下注射单剂量的17β-雌二醇（25毫克/千克体重），激素处理持续2天，期间有或没有喂食（实验1）。在第二个实验中，雏鸡先禁食1天或3天，然后用与实验1相同剂量的17β-雌二醇处理2天，期间不喂食。测定血浆和肝脏脂质，以及肝脏苹果酸酶、葡萄糖-6-磷酸脱氢酶的活性和脂肪组织中激素敏感性脂肪酶的活性。与喂食的对照雏鸡相比，喂食的雏鸡经雌激素处理后，在2天内血浆脂质显著升高，尤其是甘油三酯（137对2263毫克/分升）。在禁食的雏鸡中，雌激素也诱导明显的高脂血症这一发现值得注意。经雌激素处理后（实验1），禁食雏鸡的血浆甘油三酯水平比禁食对照组增加了约16倍（133对2093毫克/分升）。即使在禁食5天的雏鸡中（实验2），雌激素处理也导致持续的高甘油三酯血症（75对1369毫克/分升）。在喂食的雏鸡中，雌激素处理也诱导了脂肪肝，甘油三酯大量积累，但经雌激素处理/禁食的雏鸡的肝脏似乎正常。在喂食和禁食的雏鸡中，苹果酸酶被发现是肝脏中产生NADPH的主要酶。禁食后，苹果酸酶和葡萄糖-6-磷酸脱氢酶的活性均显著降低（P<0.05）。在喂食的雏鸡中，两种酶的总活性随雌激素处理而增加，而在禁食的雏鸡中，激素对这些酶的影响不太明显。与禁食的雏鸡相比，喂食的雏鸡脂肪组织中激素敏感性脂肪酶的活性要低得多（0.15对0.33纳摩尔油酸释放/分钟/毫克蛋白质）。喂食的雏鸡经雌激素处理对激素敏感性脂肪酶活性没有影响，但在禁食的雏鸡中，激素处理增强了其活性。雌激素化的雏鸡在禁食期间持续存在高脂血症这一发现似乎表明这种激素对脂质代谢的影响具有复杂性。
