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N Potau

Publications and source records attributed to N Potau.

61 records · Page 4Linked to original sources
PubMed1984

Effect of intracellular Ca2+ on insulin-like growth factor II. internalization into pancreatic acini. Roles of insulin and cholecystokinin.

Previously, we reported that pancreatic acini have specific receptors for the insulin-like growth factors (IGF) I and II. We now report that the binding of 125I-labeled IGF II to mouse pancreatic acini is maximally increased by 100 nM insulin (51%) and is maximally reduced by 10 nM cholecystokinin octapeptide (CCK8) (34%), but is not affected by other regulatory peptides such as somatostatin or glucagon. Since many polypeptide hormones are internalized, we determined whether this regulation of IGF II binding occurred via a change in internalization. Acid washing or trypsinization has been shown to remove surface-bound hormone while the acid- or trypsin-resistant radioactivity represents internalized radioligand. Insulin increased and CCK8 decreased the internalization of IGF II as determined by these techniques. Studies of IGF II binding to acini at low temperature (15 degrees C) and binding to particulate fractions from acini were also consistent with the effect of insulin to increase and CCK8 to decrease the internalization of IGF II. When insulin and CCK8 were added together, the inhibitory effect of CCK8 predominated, indicating that CCK8 acted distal to the effect of insulin. Several lines of evidence suggest that this effect of CCK8 was via the CCK receptor and was mediated via a change in intracellular Ca2+: the effect of CCK8 on inhibiting IGF II binding was blocked by the cholecystokinin antagonist N2,O2'-dibutyryl cGMP; the cholinergic agent carbachol (1-100 microM), which acts through the muscarinic receptor to increase intracellular Ca2+, also inhibited IGF II binding; the Ca2+ ionophore A23187 (1-5 microM) mimicked the effects of CCK8 and carbachol. These data indicate, therefore, that CCK8 and possibly insulin may regulate the internalization of IGF II via intracellular Ca2+. Moreover, the data raise the possibility that alterations of hormone internalization may be a general phenomenon of hormone-hormone interaction.

Animals↗
PubMed1984

Cholecystokinin and insulin regulate insulin-like growth factor II binding to pancreatic receptors; evidence of a role for intracellular calcium.

The binding of 125I-labeled insulin-like growth factor II (125I-IGF II) to mouse pancreatic acini was stimulated (45%) by insulin and inhibited (30%) by cholecystokinin octapeptide (CCK8). When CCK8 and insulin were added together, the effect on IGF II binding was similar to that seen when CCK8 was added alone. Two lines of evidence suggest that this effect of cholecystokinin on basal and insulin-stimulated 125I-IGF II binding was mediated via a change in intracellular calcium: (1) the cholinergic agent carbachol inhibited IGF II binding to its receptors; (2) addition of the Ca2+ ionophore A23187 mimicked the effects of CCK8 and carbachol. In contrast to its effects on IGF II binding to acini, CCK8 had only small effects on IGF I binding and no effects on insulin binding.

Animals↗
PubMed1984

The dosage dependency of growth and maturity in growth hormone deficiency treated with human growth hormone.

A group of 11 pre-pubertal growth hormone deficient patients were treated with human growth hormone over a period of 4 years. In 6 of the patients the dosage was 4 IU 3 times a week and in 5, 8 IU 3 times a week. Changes in height demonstrated that the "catch up" was significantly greater and of longer duration in the second group. In spite of a more rapid increase of bone age in the second group, the prognosis of final height had improved significantly at the end of the study period. A comparative study of the plasma concentrations significantly at the end of the study period. A comparative study of the plasma concentrations of T4, TSH, gonadotrophins and steroids, to see if the greater velocity of bone maturity in the second group could be due to contamination of the preparation by other could be due to contamination of the preparation by other hypophysary hormones, did not demonstrate significant differences between the groups.

Body Height↗
PubMed1984

Methylamine and monensin do not block insulin internalization but do influence the intracellular distribution and action of insulin in pancreatic acini from diabetic mice.

Methylamine and monensin are two agents known to interfere with the recycling of membrane receptors. In the present investigation, we studied their effects on the binding, intracellular distribution, and action of insulin in isolated pancreatic acini prepared from diabetic mice. These drugs had several similar effects on these cells. In a dose-dependent fashion, both increased the amount of [125I]insulin associated with acini. Methylamine approximately doubled and monensin tripled the amount of insulin associated with cells. Employing electron microscope autoradiographs, we observed the accumulation of hormone in large vacuoles in the Golgi-lysosomal area after treatment with methylamine and in smaller swollen Golgi vesicles after treatment with monensin. The influences of both agents on the biological effects of insulin in acini were then investigated. Both agents blocked insulin stimulation of [3H]2-deoxy-D-glucose uptake in acini. The effect of methylamine was also studied on [3H]leucine incorporation into protein and was found to only partially block the effect of insulin. Since insulin and its receptor are internalized, it is likely that the accumulation of insulin in acini induced by these two agents was due to their inhibition of the cellular processing of insulin and its receptor. Moreover, the effects of these two agents to inhibit insulin-stimulated glucose transport may have resulted from either the inhibition of the recruitment of glucose carriers from the Golgi to the plasma membrane or an abnormal interaction of internalized insulin with the Golgi.

Animals↗
PubMed1981

Insulin receptors in human placenta in relation to fetal weight and gestational age.

Insulin receptors were studied in human placentas from 26 wk to term, according to fetal and placental weight. Insulin-binding studies were performed in purified membranes with monoiodoinsulin biologically active. We found a marked decrease in receptor number in placentas corresponding to small for gestational age infants (S.G.A.) in relation to preterm and full-term adequate for gestational age (A.G.A.). Maximal insulin binding in human placentas was reached before 26 wk of gestation.

Birth Weight↗
PubMed1980

Masculinization of a female fetus by Krukenberg tumor during pregnancy.

A case of fetal masculinization resulting from a Krukenberg tumor in a pregnant woman is reported in a newborn infant with a sexual ambiguity of the external genitals, of the feminine pseudohermaphrodite type. She also had an incarceration of both ovaries and tubes in a right inguinoscrotal hernia that was surgically corrected.

Disorders of Sex Development↗