glycogen and Endometrial-Hyperplasia

The effect of 17-oxyprogesterone capronate on the proliferative activity and metabolic processes in the endometrium of patients with glandular hyperplasia of the endometrium was studied. It was shown that the proliferative activity was inhibited while the secretory processes in the glandular epithelium were activated. This effect was achieved only after a long-term (6-9 months) administration of the hormone.

Topics: Adult; Cell Division; Drug Evaluation; Endometrial Hyperplasia; Endometrium; Enzyme Activation; Female; Glycogen; Humans; Hydroxyprogesterones; Karyometry; Middle Aged; Time Factors; Uterine Hemorrhage

This paper presents preliminary data concerning the relationship of various components of glandular epithelium and effect of enzymes on metabolism, storage, and release of certain substances in normal and abnormal endometria. Activity of these endometrial enzymes has been compared between two groups: 252 patients with normal menstrual histories and 156 patients, all over the age of 40, with abnormal uterine bleeding. Material was obtained by endometrial biopsy or curettage. In the pathologic classification of the group of 156, 30 patients had secretory endometria, 88 patients had endometria classified as proliferative, 24 were classified as endometrial hyperplasia, and 14 were classified as adenocarcinoma. All tissue was studied by histologic, histochemical, and biochemical methods. Glycogen synthetase activity caused synthesis of glucose to glycogen, increasing in amount until midcycle, when glycogen phosphorylase activity caused the breakdown to glucose during the regressive stage of endometrial activity. This normal cyclic activity did not occur in the abnormal endometria, where activity of both enzymes continued at low constant tempo. Only the I form of glycogen synthetase increased as the tissue became more hyperplastic. With the constant glycogen content and the increased activity of both the TPN isocitric dehydrogenase and glucose-6-phosphate dehydrogenase in the hyperplastic and cancerous endometria, tissue energy was created, resulting in abnormal cell proliferation. These altered biochemical and cellular activities may be the basis for malignant cell growth.

Topics: Adenocarcinoma; Alkaline Phosphatase; Carbohydrate Metabolism; Cell Membrane Permeability; Citric Acid Cycle; Endometrial Hyperplasia; Endometrium; Estradiol; Female; Glucosephosphate Dehydrogenase; Glycogen; Glycogen Synthase; Hexosephosphates; Humans; Menstruation; Middle Aged; Phosphorylases; Progestins; Uterine Diseases; Uterine Neoplasms

Topics: Disease; Endometrial Hyperplasia; Endometrium; Female; Glycogen; Glycogenolysis; Humans; Uterine Diseases