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Biomedical subjects

R Cordera

Publications and source records attributed to R Cordera.

69 records · Page 4Linked to original sources
PubMed1979

[Insulin response and NEFA behavior in volunteers with a flat response to oral glucose tolerance test].

The insulin response and the NEFA behaviour of 7 lean and 8 obese subjects with a flat response to an oral glucose tolerance test have been studied. A flat response has been defined as one in which the maximum glycemic increase and the area of increase does not exceed 32 mg% and 18 mg% respectively. The insulin response and the NEFA behaviour were similar both in lean and in obese subjects to controls with normal O.G.T.T. The glucose/I.R.I. ratios were increased. A possible physiopathological interpretation is proposed.

Adolescent↗
PubMed1979

[Special aspects of the curve of the oral glucose tolerance test].

The insulin response of 10 lean and 23 obese subjects with lag-type and borderline O.G.T.T. has been studied. The O.G.T.T. was interpreted according to the criteria of Fajans and Conn. The maximum increase and the area of increase were examined both for blood glucose and plasma I.R.I., and the corresponding I.R.I./glucose ratios calculated. The shape of the insulin response curve is similar to that of glucose curve. The I.R.I./glucose ratios are decreased in the lag-type curves as compared to borderline in the lean subjects while we observed opposite results in obese ones. A possible physiopathological interpretation of this curves is proposed.

Adolescent↗
PubMed1979

[Examination of the early phase of insulin secretion with 3 successive small overloads of glucose (5 g) in normal and obese subjects].

We studied the E.I.R. in eight normal subjects and fifteen obese ones with three successive small glucose pulses (5 g.) e.v. at 30' interval. In normal subjects the three successive loads gave rise to identical responses for both glucose and I.R.I. Obese could be divided, on the basis of their E.I.R. to the first load, into normal responders (group I), hyper-responders (group II) and hypo-résponders (group III); on the basis of the E.I.R. to the second load, group I could be divided in two subgroups: Ia and Ib. We found an identical E.I.R. to all glucose loads in group Ia; a reduced E.I.R. to successive loads in groups Ib and II. Group III didn't have any insulin response to all glucose loads.

Antigens↗
PubMed1979

[Double test of insulin sensitivity in normal and obese subjects].

13 normal and 16 obese subjects have been chosen for a double insulin tolerance test: 0,02 U/Kg of insulin were administered i.v. with an interval of 60'. The glycemic curve of the normal subjects show an identical lay out after both pulses; on the contrary the obese subjects could be divided into two subgroups. In the first one the lowering glucose action can be compared after both pulses, while in the second one the first stimulus causes a weather lowering glucose action, than in the first group, which is furtherly reduced during the subsequent pulse. An insulin resistance in these subjects is thus stressed. In the obese subjects the NEFA have a higher concentration in both groups than in the normal ones, show a normal decrease, but a certain delay is observed in the rebound phase.

Blood Glucose↗
PubMedDate not supplied

Exploration of the early insulin response by two small successive loads of I.V. glucose in normal and obese subjects.

Two 5 g glucose loads at 1-h interval were given to healthy controls and obese subjects with slightly altered or normal OGTT in order to explore the capacity of restoration of the "rapid insulin response" to i.v. glucose. In the normal subjects, the two successive loads gave rise to identical responses as far as maximum increase (delta max), average increase at 2-5 min (delta 2-5 min), area of increase 0-15 min (delta 0-15 min) for both glucose and IRI, were concerned. Obese subjects could be divided on the basis of their insulin response to the first load into normal responders (group I) and high-responders (group II). In group I obese subjects, the responses to the second load were identical to those to the first. In group II obese subjects delta max, delta 2-5 min and delta 0-15 min of the insulin response to the second load were reduced as compared to the first.

Adult↗
PubMedDate not supplied

I.V. glucose tolerance test: correlation between FFA, glucose and IRI in normal, obese and diabetic subjects.

Insulin response and FFA behavior have been evaluated during an IVGTT in 63 subjects of whom 18 were normal, 31 were obese (with varying degrees of carbohydrate tolerance) and 14 were mild non insulin-dependent diabetics. The extreme reduction of insulin secretion in the early phase (delta 0-15 min) and the less severe impairment of the late phase (delta 15-60 min) have been confirmed; obese subjects showed on the average an active insulin response to venous loading; this was more marked and more consistent in the late phase. Compared to controls, FFA concentration both in basal conditions and during IVGTT was progressively higher in obese and diabetic patients. When analyzing the interplay between IRI, KG and FFA in the course of IVGTT, it was observed that: (1) a close correlation exists between IG and early insulin response (r = 0.72); (2) a correlation between delta IRI 0-15 min and percentage decrease of FFA at 45 min is found only in normal subjects; (3) a negative highly significant correlation is found between KG and mean FFA plasma level 0-60 min. This last correlation is evidence of the important role played by FFA in carbohydrate tolerance. The conflicting results reported by others have been discussed.

Adult↗
PubMedDate not supplied

Increased phosphorylation of ribosomal protein S6 following microinjection of insulin receptor-kinase into Xenopus oocytes.

The protein products of several transforming retroviruses as well as the receptors for several hormones and growth factors, including insulin, have been shown to possess a protein kinase activity in vitro specific for tyrosine residues in protein substrates, including themselves. In the case of pp60src and the insulin receptor, autophosphorylation activates the tyrosine kinase activity towards exogenous substrates. Experiments indicate that, in vivo, many of these viruses or growth factors induce an increase in cellular phosphotyrosine, as well as an increase in the phosphorylation of serine residues on proteins, including ribosomal protein S6. It seems likely that some of the effects of insulin might be mediated by phosphorylation of intracellular substrates by its receptor. As the beta subunit of the receptor is a transmembrane protein, such phosphorylation could occur either while the receptor is still in the membrane or after its internalization. In various cell systems, internalized receptors are degraded, reshuttled back to the plasmalemma or maintained in a separate compartment before reinsertion in the membrane; shuttling of the insulin receptor could provide the opportunity for it to phosphorylate various intracellular components as part of its mechanism of signal transduction. To approach directly the question of whether the receptor can elicit a signal while acting at an intracellular location, we have microinjected Xenopus oocytes with the insulin receptor kinase. The results indicate that an S6 protein-serine kinase is stimulated or an S6 protein-serine phosphatase inhibited by the activity of the insulin receptor, supporting the concept that the insulin receptor acting within the cell can elicit a biological response.

Animals↗