Rapid non-genomic and genomic responses to progestogens, estrogens, and glucocorticoids in the endocrine pancreatic B cell, the adipocyte and other cell types.

Rapid biologic responses to injected steroids were described as early as 60 years ago. More recently, evidence has been presented that 17beta-estradiol given i.v.

Acute effects of progesterone on glucose metabolism in rat adipocytes: are they modulated by endogenous adenosine?

Progesterone rapidly inhibits glucose oxidation of isolated rat adipocytes. Because this inhibition is triggered by endogenous adenosine, the present study was designed to examine the effect of the steroid on cyclic adenosine monophosphate (cAMP) accumulation, its relation to lipolysis, and the possible participation of adenosine. The results strongly indicate that physiological concentrations of progesterone increase the release of adenosine by isolated adipocytes, with maximal release at the end of a 20-minute incubation.

The isolation of glucose tolerance factors from brewer's yeast and their relation to chromium.

A new dietary factor, the glucose tolerance factor (GTF), was reported in 1957 that improved impaired glucose tolerance in rats. Most studies on GTF have used brewer's yeast as the starting material, and it has been postulated that the active material is a low-mol wt organic complex containing Cr3+. It seemed thus important to isolate an active GTF from chromium-rich yeast (228 ppm Cr) obtained by incubation with chromium and to compare each fraction with corresponding ones from untreated yeast (0.

Inhibition of glucose metabolism by progesterone in adipocytes: role of protein synthesis.

Progesterone decreases [I-14C]glucose oxidation in isolated female rat adipocytes within 20 min of incubation. Because steroids regulate transcription mechanisms, the relationship between protein synthesis and glucose metabolism was studied in the presence of progesterone. Actinomycin D does not affect basal glucose oxidation or the progesterone effects on it; cycloheximide and puromycin decrease basal glucose oxidation, but only puromycin decreases the inhibitory progesterone effect.

Effects of placental lactogen and progesterone on insulin stimulated glucose metabolism in rat muscles in vitro.

The short term effects of ovine placental lactogen and progesterone have been studied on skeletal muscle glucose metabolism in order to determine their respective roles in pregnancy-induced insulin resistance. The rates of hexose transport, glycogen synthesis, and glycolysis were measured in vitro by incubating stretched soleus, extensor digitorum longus (EDL) and epitrochlearis from virgin rats. When incubated in plasma from late pregnant rats, EDL glucose metabolism was reduced by 30% when compared to EDL incubated in plasma from virgin rats despite similar glucose (8 mM) and insulin (200 microU/ml) concentrations.

Progesterone and synthetic steroids produce insulin resistance at the post-receptor level in adipocytes of female rats.

The effects of progesterone, its agonists (progestin RU-5020, glucocorticoid RU-26988) and antagonist (antiprogesterone, anti-glucocorticoid RU-486) were tested on isolated fat cells in vitro. When added to the incubation medium, all four steroids decreased basal glucose oxidation. The inhibitory effect of the steroids appeared early (20 min incubation) and was sustained during a 2-h incubation.

Effects of constant magnetic fields on the B-cells and insulin target cells in the rat.

Young male rats were exposed to constant uniform magnetic fields of 400 and 800 millitesia (mT). No changes were observed in the body and in the pancreas weight, in the pancreatic insulin content and in the in vitro insulin release of Langerhans islets, in glucose and insulin plasma levels. The magnetic fields abolished the insulin effect on glucose uptake of diaphragms, but not on 1-14C-glucose oxidation.

Carbohydrate metabolism of female rat adipocytes: effects and mechanisms of action of progesterone.

This short review describes the role of progesterone in the insulin-resistance of pregnancy and the present knowledge of the intracellular mechanisms of action of the steroid in carbohydrate metabolism of female rat adipocytes. Observations concerning steroid effects on the binding of insulin to its specific receptors are often contradictory, and depend on cells used to study it. It is now generally accepted that, in isolated adipocytes, the decreased responsiveness to insulin produced by progesterone is due to a post-receptor effect.

Effects of constant magnetic fields on rats and mice: a study of weight.

Variations in the growth of animals from exposure to a magnetic field have been reported by several authors. In this study, young rats and mice were exposed daily to constant uniform magnetic fields. The strength of the field was 400, 600 or 800 mT.

Insulin binding and action in adipocytes of pregnant rats: evidence that insulin resistance is caused by post-receptor binding defects.

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.

Immediate, short- and long-term opposite effects of oestradiol-17 beta on glucose metabolism in rat adipocytes: relationship with the biphasic changes in body weight and food intake.

The changes in the effects of oestradiol-17 beta 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.

Glucose metabolism in the female rat adipocyte: lipid synthesis from glucose during pregnancy and progesterone treatment.

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).

Ovarian-adrenal interactions in regulation of endocrine pancreatic function in the rat.

The interference of adrenal hormones with the oestradiol-induced modifications of endocrine pancreatic function remains controversial. For this reason, we compared sham-operated, ovariectomized and adrenalectomized-ovariectomized female rats. In each group, control and 17-beta-oestradiol-treated rats (0.

Progesterone and glucose metabolism in the female rat adipocyte: effect on hexokinase activity.

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 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.

Progesterone and insulin resistance. III. Time-course study of progesterone action on differentially labelled 14C-glucose utilization by adipose tissue and isolated adipocytes of the female rat.

Progesterone action on glucose metabolism was evaluated on parametrial fat pads and on isolated adipocytes using glucose labelled on C1, C2 and C6, (1) The steroid decreased the pentose cycle, but had no effect on the krebs cycle as judged by the C5/C1 ratio. (2) The radiorespirometric method, in combination with appropriately labelled glucose, demonstrated a rapid in vitro effect of progesterone on oxidation of (1-14C)-glucose. This finding suggest that progesterone acts on the glucose metabolism of the adipose tissue by a non-classical mechanism of steroid hormone action.

Progesterone and insulin-resistance in the pregnant rat. I. In vivo and in vitro studies.

The effects of pregnancy, progesterone treatment and of progesterone added in vitro on insulin-resistance have been assessed in rat adipocytes and hemidiaphragms. In progesterone treated female rats, the steroid antagonized in vivo the hypoglycemic effect of intravenously injected porcine insulin; the same results were obtained when the steroid was injected at the same time as insulin and there was no lag period between its appearance in the blood and its effect on blood glucose levels. Such a rapid effect differs from the generally accepted scheme for steroidal mode of action.

Progesterone and insulin-resistance: studies of progesterone action on glucose transport, lipogenesis and lipolysis in isolated fat cells of the female rat.

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.

Effects of treatment with progesterone and oestradiol-17 beta on the endocrine pancreas in ovariectomized rats: ultrastructural variations in the B cells.

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 numberical density of dark and high 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.

Effects of pregnancy and progesterone and/or oestradiol on the insulin secretion and pancreatic insulin content in the perfused rat pancreas.

Progesterone and oestradiol treatment of ovariectomized rats was administered leading to plasma steroid concentrations comparable to those of the pregnant rat. In these experimental conditions oestradiol enhanced insulin secretion but progesterone had little effect on B cell response to glucose (0.8 g/l and 1.

[Role of progesterone in the insulin-resistance during pregnancy in the rat (author's transl)].

Progesterone inhibits insulin action in vivo and in vitro. In vivo the hypoglycemic action of an intravenous injection of insulin is counteracted by a simultaneous injection of progesterone. In vitro, insulin effect on glucose uptake and on 14CO2 production from 14C-glucose is inhibited by progesterone in female rat diaphragme muscle, adipose tissue and isolated adipocytes.

Insulin secretion from isolated pancreatic islets in the female rat. Short and long term oestradiol influence.

An increase in the two phases of glucose-induced insulin response is observed after an oestradiol (E2) treatment or after a direct E2 action on the female rat perfused pancreas. To study such effects, experiments were carried out with isolated islets of Langerhans, and especially with a dynamic method : perifusion of the islets. The same long term E2 permissive effect was obtained with isolated islets submitted to a glucose stimulation.