del Mar Grasa Maria, Serrano Marta, Fernández-López José Antonio, Alemany Marià
Department of Nutrition and Food Science, Faculty of Biology, University of Barcelona, Av. Diagonal 645, 08028 Barcelona, Spain.
Endocrinology. 2007 Aug;148(8):4056-63. doi: 10.1210/en.2007-0331. Epub 2007 May 17.
Oleoyl-estrone (OE) is an adipose-derived signal that decreases energy intake and body lipid, maintaining energy expenditure and glycemic homeostasis. Glucocorticoids protect body lipid and the metabolic status quo. We studied the combined effects of OE and corticosterone in adrenalectomized female rats: daily OE gavages (0 or 10 nmol/g) and slow-release corticosterone pellets at four doses (0, 0.5, 1.7, and 4.8 mg/d). Intact and sham-operated controls were also included. After 8 d, body composition and plasma metabolites and hormones were measured. OE induced a massive lipid mobilization (in parallel with decreased food intake and maintained energy expenditure). Corticosterone increased fat deposition and inhibited the OE-elicited mobilization of body energy, even at the lowest dose. OE enhanced the corticosterone-induced rise in plasma triacylglycerols, and corticosterone blocked the OE-induced decrease in leptin. High corticosterone and OE increased insulin resistance beyond the effects of corticosterone alone. The presence of corticosterone dramatically affected OE effects, reversing its decrease of body energy (lipid) content, with little or no change on food intake or energy expenditure. The maintenance of glycemia and increasing insulin in parallel to the dose of corticosterone indicate a decrease in insulin sensitivity, which is enhanced by OE. The reversal of OE effects on lipid handling, insulin resistance, can be the consequence of a corticosterone-induced OE resistance. Nevertheless, OE effects on cholesterol were largely unaffected. In conclusion, corticosterone administration effectively blocked OE effects on body lipid and energy balance as well as insulin sensitivity and glycemia.
油酰雌酮（OE）是一种源自脂肪组织的信号，它可减少能量摄入和体内脂质，维持能量消耗和血糖稳态。糖皮质激素可保护体内脂质和代谢现状。我们研究了OE和皮质酮对肾上腺切除的雌性大鼠的联合作用：每日灌胃OE（0或10 nmol/g）以及四种剂量（0、0.5、1.7和4.8 mg/d）的缓释皮质酮丸剂。还纳入了完整和假手术对照组。8天后，测量身体组成、血浆代谢物和激素。OE诱导大量脂质动员（与食物摄入量减少和能量消耗维持平行）。皮质酮增加脂肪沉积并抑制OE引发的身体能量动员，即使在最低剂量时也是如此。OE增强了皮质酮诱导的血浆三酰甘油升高，而皮质酮则阻断了OE诱导的瘦素降低。高剂量皮质酮和OE增加胰岛素抵抗，其作用超过单独使用皮质酮的效果。皮质酮的存在显著影响OE的作用，逆转其对身体能量（脂质）含量的降低，而对食物摄入量或能量消耗几乎没有影响。血糖维持以及胰岛素与皮质酮剂量平行增加表明胰岛素敏感性降低，而OE会增强这种降低。OE对脂质处理、胰岛素抵抗的作用逆转可能是皮质酮诱导的OE抵抗的结果。然而，OE对胆固醇的作用在很大程度上未受影响。总之，给予皮质酮有效地阻断了OE对身体脂质和能量平衡以及胰岛素敏感性和血糖的影响。
