Mayer D, Weber E, Moore M A, Letsch I, Filsinger E, Bannasch P
Institut für Experimentelle Pathologie, Deutsches Krebsforschungszentrum, Heidelberg, FRG.
Carcinogenesis. 1988 Nov;9(11):2039-43. doi: 10.1093/carcin/9.11.2039.
Long-term dietary administration of the adrenal hormone dehydroepiandrosterone (DHEA) to male Sprague-Dawley rats induced significant alterations in the activities of enzymes involved in liver carbohydrate metabolism. Although glycogen synthase activity was increased and phosphorylase decreased, glycogen stores were reduced. This was presumably related to lysosomal glycogen degradation, since alpha-glucosidase was increased. All rate-limiting enzymes of glucose metabolism which were studied (glucose-6-phosphate dehydrogenase, total hexokinases, pyruvate kinase, fructose-1,6-bisphosphatase) revealed markedly reduced activity, only glucose-6-phosphatase activity was increased. These enzymatic changes point to a far-reaching metabolic shift towards energy loss via decreased glucose consumption and increased glucose output. The enzyme pattern induced by DHEA is in many respects opposite to that induced in preneoplastic and neoplastic liver lesions by chemical hepatocarcinogens.
对雄性斯普拉格-道利大鼠长期进行肾上腺激素脱氢表雄酮（DHEA）的饮食给药，会导致参与肝脏碳水化合物代谢的酶活性发生显著改变。尽管糖原合酶活性增加而磷酸化酶活性降低，但糖原储备却减少了。这可能与溶酶体糖原降解有关，因为α-葡萄糖苷酶增加了。所研究的所有葡萄糖代谢限速酶（葡萄糖-6-磷酸脱氢酶、总己糖激酶、丙酮酸激酶、果糖-1,6-二磷酸酶）活性均显著降低，只有葡萄糖-6-磷酸酶活性增加。这些酶促变化表明，通过减少葡萄糖消耗和增加葡萄糖输出，代谢发生了深远的转变，朝着能量损失的方向发展。DHEA诱导的酶模式在许多方面与化学致癌物在癌前和肿瘤性肝脏病变中诱导的模式相反。
