Grummer R R, Carroll D J
Dairy Sci. Dept., Coll. of Agric. and Life Sci., University of Wisconsin, Madison 53706.
J Anim Sci. 1988 Dec;66(12):3160-73. doi: 10.2527/jas1988.66123160x.
Cholesterol utilized for steroid synthesis by ovarian tissue may be derived from de novo synthesis or cellular uptake of lipoprotein cholesterol. The majority of blood cholesterol is transported by either low (LDL) or high (HDL) density lipoproteins, depending on the animal species. Prior to vascularization, only HDL are in follicular fluid and contribute sterol to granulosa cells because other lipoproteins are unable to transverse the basement membrane due to their molecular masses. Following vascularization, both LDL and HDL bathe luteal cells. Most species preferentially use LDL cholesterol as a precursor for ovarian steroid synthesis. The LDL uptake by ovarian tissue occurs by receptor-mediated endocytosis. The receptor recognizes apolipoprotein B of LDL and apolipoprotein E found on some, but not all, HDL. Within a species, a positive relationship may exist between HDL apolipoprotein E content and importance of HDL cholesterol as a precursor for steroidogenesis. A "HDL pathway" exists for uptake of sterol from HDL void of apolipoprotein E. The HDL receptor exhibits broad binding specificity. Unlike LDL, the HDL particle is not internalized, and cholesterol preferentially is taken up relative to other HDL constituents. In most species, lipoproteins, rather than de novo synthesis from acetate, contribute the majority of cholesterol used for steroid production. Trophic hormones increase lipoprotein binding, internalization, degradation and conversion of lipoprotein-derived sterol to steroids, effects that are mediate through cyclic adenosine monophosphate. Knowledge recently acquired regarding lipoprotein sterol utilization by the ovary may be useful in developing nutritional, pharmacological or endocrine manipulations that may positively affect cholesterol clearance by the ovary, steroidogenesis and reproductive performance.
卵巢组织用于类固醇合成的胆固醇可能来源于从头合成或脂蛋白胆固醇的细胞摄取。根据动物种类的不同，血液中的大部分胆固醇由低密度脂蛋白（LDL）或高密度脂蛋白（HDL）运输。在血管形成之前，卵泡液中只有HDL，它为颗粒细胞提供固醇，因为其他脂蛋白由于分子质量大而无法穿过基底膜。血管形成后，LDL和HDL都作用于黄体细胞。大多数物种优先使用LDL胆固醇作为卵巢类固醇合成的前体。卵巢组织对LDL的摄取通过受体介导的内吞作用进行。该受体识别LDL的载脂蛋白B以及部分（而非全部）HDL上存在的载脂蛋白E。在一个物种内，HDL载脂蛋白E含量与HDL胆固醇作为类固醇生成前体的重要性之间可能存在正相关关系。存在一条从不含载脂蛋白E的HDL摄取固醇的“HDL途径”。HDL受体表现出广泛的结合特异性。与LDL不同，HDL颗粒不会被内化，胆固醇相对于其他HDL成分优先被摄取。在大多数物种中，用于类固醇生成的胆固醇大部分来自脂蛋白，而非由乙酸盐从头合成。促营养激素会增加脂蛋白的结合、内化、降解以及脂蛋白衍生固醇向类固醇的转化，这些作用是通过环磷酸腺苷介导的。最近获得的关于卵巢对脂蛋白固醇利用的知识，可能有助于开发营养、药理或内分泌干预措施，从而对卵巢胆固醇清除、类固醇生成和生殖性能产生积极影响。
