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Biomedical subjects

C J Hubinont

Publications and source records attributed to C J Hubinont.

8 recordsLinked to original sources
PubMed1988

Effects of chronic renal failure and hemodialysis on hormonal evaluation of pregnancy.

Different hormonal parameters are studied in a pregnant woman with chronic renal failure undergoing hemodialysis. Serum concentrations of human chorionic gonadotropin, progesterone, 17-hydroxyprogesterone, alpha-fetoprotein, human placental lactogen were all higher than the normal range. This is probably related to a decreased metabolic clearance rate of these hormones. Dehydroepiandrosterone sulfate (DHEAS), which is low before pregnancy and during the first week of gestation, tends to increase later. Serum estradiol is lower than the normal range. This decrease probably results from the low concentration of DHEAS available to placental aromatization. Finally, pregnancy-specific beta 1-glycoprotein concentration follows the normal range and may be considered as the most reliable parameters to evaluate the fetoplacental well-being in these high-risk pregnancies.

Adult↗
PubMed1988

Changes in pancreatic B cell function during late pregnancy, early lactation and postlactation.

Oral glucose tolerance tests were performed in 10 normal women during late pregnancy (36 +/- 1 weeks of gestation), early lactation (5 days after delivery) and postlactation (1 week after weaning). A marked decrease in basal plasma insulin and C peptide concentrations, as well as in the B cell secretory response to hyperglycemia, was observed at the 5th day of postpartum, compared to the high values recorded in late pregnancy. Except for a higher basal C peptide level and a lower plasma prolactin concentration, there was no major difference between early lactation and postlactation. At the 5th day after delivery, the insulin response to hyperglycemia was lower in lactating than in nonlactating women (14 subjects in each group). It is concluded that, in normal women, pancreatic B cell function undergoes a rapid normalization during the postpartum, at least when the latter coincides with the onset of lactation.

Adult↗
PubMed1987

Luteal function in ectopic pregnancy.

Human chorionic gonadotropin, estradiol, progesterone, and 17-hydroxyprogesterone have been measured in the serum of 46 patients with ectopic pregnancy. All these hormones were significantly lower than in normal pregnancy. Unruptured ectopic pregnancy differed from the ruptured state by a lower serum human chorionic gonadotropin concentration, a slower human chorionic gonadotropin increment, a higher incidence of metrorrhagia, and an earlier diagnosis. The concentration of estradiol, progesterone, and 17-hydroxyprogesterone in the serum of patients with ectopic pregnancy was lower than could be expected from the decrease of human chorionic gonadotropin, often lower than in a normal luteal phase. It is suggested that, as long as ultrasonography fails to show an intrauterine pregnancy, the simultaneous determination of serum human chorionic gonadotropin and progesterone could aid in the early diagnosis of ectopic pregnancy and in the improvement of subsequent fertility; to that regard any progesterone level below 15 ng/ml in the presence of detectable amounts of human chorionic gonadotropin is highly suggestive of either a threatened abortion or an ectopic pregnancy, whatever the gestational age.

17-alpha-Hydroxyprogesterone↗
PubMed1987

Lactation-induced changes in calcium handling by rat pancreatic islets.

Glucose-stimulated insulin release occurred at a lower rate in pancreatic islets removed from lactating than non-lactating rats. This defect was corrected in the presence of either gliclazide or a calcium-agonist. With both agents present, insulin release from islets of lactating rats was greater. When islets were prelabelled with 45calcium, gliclazide stimulated to the same extent 45Ca outflow in islets from lactating and non-lactating rats, respectively. However, when the islets were prelabelled with 45Ca in the presence of gliclazide, the administration of Ba2+ increased effluent radioactivity more markedly in islets from non-lactating than lactating rats. This suggests that lactation favours, in gliclazide-stimulated islets, the sequestration of 45Ca in non-labile subcellular pools. When D-glucose was used instead of Ba2+, the greater lability of 45Ca in islets from non-lactating animals was apparently masked by a lesser efficiency in the metabolism and cationic effects of D-glucose in the non-lactating rats. The calcium-ionophoretic effect of islet extracts was higher in lactating than non-lactating rats. These results support the view that a depletion of endogenous calcium stores accounts, in part at least, for the decreased insulin secretory responsiveness to D-glucose in lactation, since the latter apparently favours the function of those systems involved in either the entry of calcium into or its sequestration within the islet cells.

Animals↗
PubMed1986

Influence of lactation upon pancreatic islet function.

The activity of adenylate cyclase, its responsiveness to NaF and forskolin, the activity of the protein kinases A and C, and the oxidation of exogenous D-glucose, L-leucine, and L-glutamine were all higher in pancreatic islets removed from lactating, as distinct from nonlactating, rats. Yet, the release of insulin evoked by D-glucose or the association of L-leucine and L-glutamine was lower in the islets obtained from lactating animals. The lactation-induced decrease in secretory activity was not attributable to a change in the insulin content of the islets, was not corrected by exposure of the islets to theophylline or forskolin, and was also observed in response to stimulation by Ba2+. The rapidly exchangeable islet Ca pool, as estimated from the basal value for 45Ca net uptake, was severely decreased in lactation. Moreover, a hypoglycemic sulfonylurea, which stimulated islet 45Ca net uptake much more markedly in lactating than nonlactating animals, provoked, in association with 12-O-tetradecanoylphorbol-13-acetate, a greater insulin output in lactating than nonlactating rats. It is speculated that the decreased secretory activity in islets removed from lactating rats may be accounted for, in part at least, by a decreased Ca content of the islet cells.

Adenylyl Cyclases↗
PubMed1985

Protein kinase C activity in pancreatic islets: effects of Ca2+, calmodulin and retinoic acid.

Pancreatic islet homogenates display protein kinase C activity. Although the rate of histone phosphorylation by islet homogenates is not enhanced by Ca2+ alone, the Ca2+ ion markedly augments reaction velocity in the presence of phosphatidylserine and at low concentrations (20 nM--0.2 microM) of the tumor-promoting agent 12-0-tetradecanoylphorbol-13-acetate (TPA). At a higher concentration (2.0 microM), TPA stimulates histone phosphorylation even in the absence of Ca2+. Ca-calmodulin also stimulates protein phosphorylation but the latter effect is apparently mediated by a Ca-calmodulin-responsive protein kinase distinct from the protein kinase C. In the presence of phosphatidylserine, retinoic acid (0.1 microM) fails to cause any obvious change in protein kinase C activity. However, in the 0.1-100.0 microM range, retinoic acid confers a limited responsiveness to TPA in the absence of phosphatidylserine. These findings support the view that Ca2+ may regulate protein phosphorylation in the pancreatic B-cell through several distinct pathways.

Animals↗
PubMed1984

Activation of protein kinase C by a tumor-promoting phorbol ester in pancreatic islets.

Rat pancreatic islet homogenates display protein kinase C activity. This phospholipid-dependent and calcium-sensitive enzyme is activated by diacylglycerol or the tumor-promoting phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA). In the presence of TPA, the Ka for Ca2+ is close to 5 microM. TPA does not affect phosphoinositide turnover but stimulates [32P]- and [3H]choline-labelling of phosphatidylcholine in intact islets. Exogenous phospholipase C stimulates insulin release, in a sustained and glucose-independent fashion. The secretory response to phospholipase C persists in media deprived of CaCl2. It is proposed that protein kinase C participates in the coupling of stimulus recognition to insulin release evoked by TPA, phospholipase C and, possibly, those secretatogues causing phosphoinositide breakdown in pancreatic islets.

Animals↗