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Progesterone decreases the oxidation of 2-deoxyglucose and glucose through the pentose-phosphate pathway in isolated female rat adipocytes and, therefore, the effect of this steroid on the activity of the phosphorylating enzyme, hexokinase, was studied. After a 30-min incubation in vitro, progesterone decreased total hexokinase activity but did not affect the isoenzyme-I activity. Progesterone had no direct effect on fat cell cytosol hexokinase and its action on glucose oxidation was not affected by variations in the concentration of Mg2+, the cofactor of hexokinase. Our data suggest that the decreased activity of hexokinase in the presence of progesterone is due to a decrease in the activity of the insulin-sensitive isoenzyme-II. This results from the steroid acting at a step beyond enzyme activation and may be mediated by a feedback mechanism.
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Pregnancy and progesterone treatment of ovariectomized rats decrease glucose metabolism through the pentose-phosphate pathway in isolated female rat adipocytes. As demonstrated in previous studies, progesterone directly decreases [1-14C]glucose oxidation through the pentose-phosphate pathway and lipogenesis from [6-14C]glucose; the present study therefore compared glucose-induced lipid synthesis during pregnancy (10, 16 and 20 days of pregnancy) with the effect of progesterone treatment (5 mg/rat per day for 14 days) to shed more light on the role of this steroid in glucose metabolism during pregnancy. The inhibition of [6-14C]glucose incorporation into triacylglycerols in the progesterone-treated rats was comparable to that which occurs during late (20 days) and mid-pregnancy (16 days) but not during early pregnancy (10 days). The inhibition of fatty acid synthesis was more important as pregnancy advanced and was different from the decrease in fatty acid synthesis induced by progesterone treatment. The sensitivity to insulin was comparable in virgin, ovariectomized and progesterone-treated ovariectomized rats but not in pregnant rats. This implies that progesterone and insulin affect glucose-induced lipid synthesis by distinct processes and that the impaired glucose metabolism is characterized by a reduction in basal glucose utilization rather than by an impaired insulin response.
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The effects of progesterone on isolated rat adipocytes were studied in vitro during various steps of glucose metabolism, transport, lipogenesis and lipolysis. Progesterone decreased the phosphorylation of glucose into glucose-6-phosphate as assessed by measuring the uptake of 2-deoxyglucose but it had no effect on transmembrane transport of glucose as determined by measuring the entry of 3-0-methylglucose into the cell. As glucose phosphorylation is a rate-limiting step of the pentose-phosphate pathway, these data could explain the inhibition of lipogenesis and the enhancement of lipolysis observed when progesterone is present in incubation medium. Progesterone might thus modulate a regulatory step of glucose metabolism and antagonize insulin action in the fat cell.
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ABSTRACT
The changes in the effects of oestradiol-17β on body weight, food intake and [1-14C]glucose oxidation in adipocytes were followed in sham-operated, ovariectomized and adrenalectomized–ovariectomized rats to eliminate effects of endogenous progesterone and corticosterone. During the first 5 days oestradiol induced a dramatic fall in food intake and body weight concomitant with a decrease in glucose oxidation by adipocytes, when tested 12 h and 3 days after the beginning of treatment. In-vitro incubations with oestradiol showed that this was a direct effect of this hormone. On the other hand, from days 5 to 14 of treatment, body weight and food intake increased, though they were still lower than in sham-operated controls. On day 14, as values of treated rats tended to reach those of controls, glucose oxidation in adipocytes was stimulated by oestradiol treatment. An insulin effect was still observable and none of these effects was dependent on the adrenal gland.
These biphasic changes in the parameters studied could be closely related; moreover, a relationship with other oestradiol actions on metabolism that are known to be corticosterone-dependent could be eliminated.
J. Endocr. (1984) 101, 13–19
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ABSTRACT
Insulin resistance was investigated in the adipose cell of rats which were at days 16 and 20 of pregnancy. Data are presented to relate insulin binding and biological effect, which was evaluated by the ability of insulin to stimulate [1-14C]glucose oxidation. Adipocytes from pregnant rats bound more insulin than fat cells from control (non-pregnant) animals and the number of insulin receptors per adipocyte increased during pregnancy. Basal glucose oxidation rate was decreased at 16 and 20 days of pregnancy: however, the dose–response curve for insulin-stimulated glucose oxidation was significantly depressed only after 20 days of pregnancy. The concentration at which insulin increased glucose oxidation by 50% increased with the duration of pregnancy. We conclude that during pregnancy in the rat the adipocyte response to insulin was decreased, despite an increase in insulin binding. This result suggests that a major determinant of insulin resistance in rat adipocytes during pregnancy is present after the initial insulin–receptor interaction. Consequently, a post-receptor defect may be largely responsible for the insulin resistance.
J. Endocr. (1984) 102, 209–214
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The effects of progesterone and/or oestradiol treatment on the ultrastructural appearance of the pancreatic B cells has been studied in ovariectomized Wistar rats. A morphometric examination of the numerical density of dark and light granules in the B cells was therefore performed in each group of experimental rats as well as in control (olive oil-injected) rats.
In the oestradiol-treated rats, and especially in the rats with combined oestradiol/progesterone treatment, the proportions of light and dark granules in the pancreatic B cells changed, compared with control values, in favour of the light granules. This increase in light granule content was comparable to changes in B cells during pregnancy and it is suggested that the secretory activity of the B cells increases during pregnancy in a manner similar to that seen during oestradiol treatment.