Oxygen and Glucose Uptake and Lactate Production in Polycystic Rat Ovary1
B. O. SURWILO, KENNETH A. DOEG
Abstract
B. O. SURWILO, KENNETH A. DOEG
Abstract
The polycystic ovary, induced in vivo by hypothyroidism and hCG, was used as a model to study changes in oxygen and glucose uptake and lactate production all measured in vitro during the development of an ovarian dysfunction. Besides the polycystic ovary, three control groups were monitored: a) normal ovarian tissue; b) hypothyroid ovarian tissue; and c) luteinized (hCG) ovarian tissue. There were early differences between normal and hypothyroid ovarian tissue with respect to oxygen consumption, glucose uptake or lactate production that disappeared with prolonged treatment. hCG markedly stimulated all of the measured parameters in both the euthyroid and hypothyroid rats. HCG stimulated oxygen uptake 1.4-fold in both the euthyroid and hypothyroid rats after 20 injections. Aerobic glucose uptake was stimulated by hCG 2.7-fold in normal ovarian tissue and 3.5-fold in hypothyroid ovarian tissue. Anaerobiosis stimulated glucose uptake 1.6 to 2.6-fold in both the hypothyroid and euthyroid ovaries indicating the presence of a Pasteur effect in these tissues. Anaerobiosis did not further stimulate glucose uptake in ovarian tissue which had been previously stimulated by hCG; thus the rates of glucose uptake in luteinized and polycystic ovarian tissue were essentially identical under both aerobic and anaerobic conditions. A substantial difference existed between the luteinized and polycystic ovary with respect to aerobic lactate production. Aerobic lactate production was stimulated by hCG 2.1-fold in the euthyroid ovarian tissue which was in striking contrast to an 11-fold stimulation in hypothyroid ovarian tissue. Anaerobiosis stimulated lactate production 5- to 10-fold in the euthyroid and hypothyroid ovarian tissues. Anaerobiosis produced a 3.4–3.9-fold increase in lactate production in luteinized ovaries indicating that prior hCG stimulation had not induced maximal production of lactate. The anaerobic effect on lactate production was virtually nonexistent, however, in the polycystic ovary since anaerobiosis did not stimulate lactate production much beyond that observed in the polycystic ovary under aerobic conditions. Herein lies a striking difference between the polycystic and luteinized ovarian tissues. The polycystic ovary has apparently developed an inability to process pyruvate through normal, aerobic pathways since virtually all of the in vitro glucose uptake appears as in vitro lactate production under aerobic conditions. (Endocrinology93: 652, 1973)
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The polycystic ovary, induced in vivo by hypothyroidism and hCG, was used as a model to study changes in oxygen and glucose uptake and lactate production all measured in vitro during the development of an ovarian dysfunction. Besides the polycystic ovary, three control groups were monitored: a) normal ovarian tissue; b) hypothyroid ovarian tissue; and c) luteinized (hCG) ovarian tissue. There were early differences between normal and hypothyroid ovarian tissue with respect to oxygen consumption, glucose uptake or lactate production that disappeared with prolonged treatment. hCG markedly stimulated all of the measured parameters in both the euthyroid and hypothyroid rats. HCG stimulated oxygen uptake 1.4-fold in both the euthyroid and hypothyroid rats after 20 injections. Aerobic glucose uptake was stimulated by hCG 2.7-fold in normal ovarian tissue and 3.5-fold in hypothyroid ovarian tissue. Anaerobiosis stimulated glucose uptake 1.6 to 2.6-fold in both the hypothyroid and euthyroid ovaries indicating the presence of a Pasteur effect in these tissues. Anaerobiosis did not further stimulate glucose uptake in ovarian tissue which had been previously stimulated by hCG; thus the rates of glucose uptake in luteinized and polycystic ovarian tissue were essentially identical under both aerobic and anaerobic conditions. A substantial difference existed between the luteinized and polycystic ovary with respect to aerobic lactate production. Aerobic lactate production was stimulated by hCG 2.1-fold in the euthyroid ovarian tissue which was in striking contrast to an 11-fold stimulation in hypothyroid ovarian tissue. Anaerobiosis stimulated lactate production 5- to 10-fold in the euthyroid and hypothyroid ovarian tissues. Anaerobiosis produced a 3.4–3.9-fold increase in lactate production in luteinized ovaries indicating that prior hCG stimulation had not induced maximal production of lactate. The anaerobic effect on lactate production was virtually nonexistent, however, in the polycystic ovary since anaerobiosis did not stimulate lactate production much beyond that observed in the polycystic ovary under aerobic conditions. Herein lies a striking difference between the polycystic and luteinized ovarian tissues. The polycystic ovary has apparently developed an inability to process pyruvate through normal, aerobic pathways since virtually all of the in vitro glucose uptake appears as in vitro lactate production under aerobic conditions. (Endocrinology93: 652, 1973)
Key concepts: Internal medicine, Endocrinology, Euthyroid, Polycystic ovary, Ovary, Carbohydrate metabolism, Biology, Anaerobic exercise