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Biomedical subjects

L Adezati

Publications and source records attributed to L Adezati.

At least 37 records · Page 2Linked to original sources
PubMed1987

Species specificity of insulin binding and insulin receptor protein tyrosine kinase activity.

The effect of monoclonal anti-insulin receptor antibody MA 10 on [125I]insulin binding and on insulin receptor protein tyrosine kinase activity was investigated in human and rat tissues. It was observed that MA 10 inhibits insulin binding to human, but not rat, tissues while inhibiting insulin-stimulated receptor autophosphorylation and protein tyrosine kinase activity in both human and rat tissues. These data suggest that MA 10 is directed against a region of the insulin receptor that is in between the insulin-binding domain and the beta-subunit and that in human, but not rat, tissues, this region is involved in insulin binding.

Adipose Tissue↗
PubMed1986

Insulin-like growth factor I (IGF I) receptor autophosphorylation and kinase activity. Effect of a human polyclonal antibody (pIgG)

IGF I receptor is a tyrosine kinase capable of phosphorylating the receptor itself and other substrates. A high degree of homology does exist in tyrosine kinase domain among receptors for several polypeptide growth factor receptors and this enzymic activity has been indicated as a possible mediator of biological action. Nevertheless growth factor receptors possess peculiar specificities both in their functions and tissue distribution. A human polyclonal IgG (pIgG), previously characterized as anti insulin receptor antibody, able to inhibit insulin receptor kinase activity, was used to further investigate subunit homologies and differences in antigenicity and functional regulation between IGF I and insulin receptors, IGF I receptor tyrosine kinase was stimulated by a IGF I analog (aIGF I), produced by DNA recombinant technology, pIgG was able to inhibit IGF I receptor kinase activity, thus revealing antigenic homologies between the kinase domains of insulin and IGF I receptors. However the more pronounced inhibition of IGF I receptor-compared with insulin receptor kinase activity by pIgG suggests the existence of different regulatory mechanisms.

Antigen-Antibody Reactions↗
PubMed1986

[Left ventricular diastolic function in type I diabetes. A longitudinal echocardiographic study].

The present study was performed to assess the extent of left ventricular diastolic abnormalities and their possible progression with time in patients with type I (insulin dependent) diabetes. Two echocardiographic examinations were performed at an interval of 5 years in 18 study patients. Left ventricular diastolic function was assessed by computer digitized analysis of the M-mode echocardiographic tracings. During the study period all patients remained in satisfactory metabolic control and without retinopathy. Twelve normal subjects, matched for age and sex, were used as control group. Peak rate of left ventricular posterior wall excursion and the peak rate of increase in left ventricular internal dimensions were significantly reduced in patients with diabetes (14.12 +/- 2.5; 16.48 +/- 3.9 cm/sec) compared with controls (17.25 +/- 2.8; 20.41 +/- 3.6 cm/sec) (p less than .005; p less than .01). In addition time to peak rate of increase in left ventricular internal dimensions, isovolumic relaxation index and isovolumic relaxation time were significantly prolonged in patients with diabetes (63.66 +/- 16.5; 23.9 +/- 9; 72.7 +/- 14 msec) compared to controls (46.83 +/- 9.8; 13.4 +/- 4; 61.1 +/- 12 msec) (p less than .005; p less than .001; p less than .05). In the study patients, no relation was found between the extent of diastolic abnormalities and age, duration of the disease and insulin dosage. The extent of left ventricular diastolic dysfunction did not show significant changes during follow-up. Our results indicate that diastolic abnormalities are common in patients with type I diabetes and are not related to the duration of the disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Diabetes Mellitus, Type 1↗
PubMed1985

Inhibition of insulin and epidermal growth factor (EGF) receptor autophosphorylation by a human polyclonal IgG.

The immunoglobulin G of a polyclonal antiserum (pIgG) from a patient with insulin resistance and hypoglycemia was tested for its ability to inhibit insulin binding and to affect the autophosphorylation of partially-purified insulin receptors extracted from rat liver membranes. pIgG, when added 4 hr prior to insulin, inhibited subsequent insulin binding by 50% at 30 micrograms added protein; however, insulin previously bound to the receptor could not be displaced by a 4 hr subsequent exposure of up to 70 micrograms pIgG. pIgG, independent of its effect on insulin binding, inhibited both basal and insulin-stimulated autophosphorylation of the insulin receptor in a dose-dependent manner with a half maximal effect at 3.3 to 7 micrograms protein. Furthermore, pIgG also reduced basal autophosphorylation of the EGF receptor. The effect of pIgG to inhibit basal autophosphorylation of insulin and EGF receptors, together with its ability to reduce autophosphorylation of insulin receptors fully occupied by insulin, imply that the effect of pIgG on receptor autophosphorylation is largely independent of its effect on ligand binding. Moreover, these findings suggest that pIgG may inhibit autophosphorylation by acting on domains which are similar in the insulin and EGF receptors.

Animals↗
PubMed1985

Influence of cell age and ketoaminic linkage on rapid glycosylation of hemoglobin in human red cells in vitro.

In vitro the rate of synthesis of the aldiminic linkage between Hb and glucose depends on glucose concentration, length of incubation and some other physiological factors. To understand better the regulation of this synthesis and to verify the role of cell age and of basal HbA1 levels on the rate of synthesis of pre-A1, we studied red cells from 7 normal controls and 7 diabetics, with high HbA1 levels. We found that the content of HbA1 (stable glycosylated hemoglobin) is able to negatively affect the rate of synthesis of new pre-A1, according to a curvilinear model. These results suggest that in vitro the glycosylation process is saturable, and that elevated values of HbA1 are able to slow the synthesis of pre-A1 in vitro.

Adult↗
PubMed1985

Insulin receptor regulation in human mature red cells in vitro.

We have studied the ability of mature red cells to regulate the number and affinity of their insulin receptors, in vitro. Our data show that mature red cells are not able to change either the number and the affinity of their insulin receptors, after preincubation with high concentrations of insulin alone or insulin and glucose. We conclude that mature red cells possess an insulin receptor system not completely similar to that of major target cells such as hepatocytes and adipocytes, and therefore we suggest some criticism in evaluating these cells in clinical studies, regarding the insulin receptor status.

Animals↗
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↗