Forearm insulin uptake in healthy subjects after oral glucose and intravenous glipizide

1981 ◽  
Vol 98 (3) ◽  
pp. 407-412 ◽  
Author(s):  
Arne Nygren ◽  
Lars Erik Lindblad ◽  
Lars Sundblad
Keyword(s):  
Healthy Subjects ◽  
Insulin Receptors ◽  
Random Order ◽  
Insulin Binding ◽  
Insulin Concentration ◽  
Oral Glucose ◽  
Healthy Individuals ◽  
Pre Treatment ◽  
Insulin Uptake ◽  
Arterial Insulin

Abstract. In six healthy subjects fasted overnight two different experiments were carried out on separate days and in random order: A. Oral glucose followed 60 min later by iv glipizide. B. Iv glipizide followed 60 min later by oral glucose. Each experiment was divided into two 60 min periods, and the fractionated insulin uptake by forearm tissue was calculated for each 60 min period. When the fractional insulin uptake values for these four 60 min periods were compared it was found that the uptake of insulin was significantly higher for the 60 min period that was obtained in response to glucose without glipizide pre-treatment, than it was for any of the other 60 min periods. Moreover, in some of the participants the venous insulin concentration occasionally exceeded the corresponding arterial insulin concentration after iv glipizide administration. These findings imply that glipizide may decrease insulin binding to peripheral insulin receptors in healthy individuals.

Failure of chronic experimental hyperinsulinism to alter insulin binding to hypothalamic receptors in the rat

1984 ◽  
Vol 107 (1) ◽  
pp. 86-90 ◽  
Author(s):  
Roman B. Melnyk ◽  
J. M. Martin
Keyword(s):  
Food Restriction ◽  
Insulin Treatment ◽  
Binding Capacity ◽  
Insulin Receptors ◽  
Insulin Binding ◽  
Insulin Concentration ◽  
Regulatory Mechanisms ◽  
Hypothalamic Region ◽  
Insulin Levels ◽  
Lateral Area

Abstract. We have previously shown that [125I]insulin binding to medial hypothalamic receptors is attenuated following 14 days of food restriction. Such rats are characterized by considerably reduced circulating insulin levels with unchanged hypothalamic insulin concentration. The present data demonstrate that, in contrast to the effects of starvation, [125I]insulin binding to hypothalamic receptors from rats made hyperinsulinaemic by daily injections of protamine zinc insulin (4–6 U/rat/day for 14 days) is unaffected by this manipulation, even though hypothalamic insulin concentration in insulininjected animals was significantly higher than in salineinjected controls. Insulin binding to partially purified membranes from the medial hypothalamic region was significantly greater than that from the lateral area, confirming a finding in our earlier study. Insulin treatment was associated with slight reductions in maximal insulin-binding capacity of medial hypothalamic receptors, a tendency which appeared to be compensated by reciprocal changes in receptor affinity for this hormone. The data indicate that hypothalamic insulin receptors are not regulated by peripheral or even central insulin levels per se; it appears, rather, that some other, as yet unidentified, correlate(s) of significantly altered food intake and/or body weight can modify hypothalamic insulin receptor function. Perhaps such modifications could, in turn, participate in the activation of regulatory mechanisms involved in correcting energy imbalance.

The Relation Between Glucose Tolerance and Insulin Binding to Circulating Monocytes in Obese Children

PEDIATRICS ◽  
1982 ◽  
Vol 70 (4) ◽  
pp. 633-637
Author(s):  
Kaichi Kida ◽  
Noriyoshi Watanabe ◽  
Yoshiki Fujisawa ◽  
Yoshinori Goto ◽  
Hiroshi Matsuda
Keyword(s):  
Glucose Tolerance ◽  
Insulin Receptors ◽  
Insulin Binding ◽  
Tolerance Test ◽  
Quantitative Relation ◽  
Immunoreactive Insulin ◽  
Oral Glucose ◽  
Obese Children

The quantitative relation between insulin binding to circulating monocytes in vitro and glucose tolerance in obese children in vivo is reported. Sixty-one obese children and 11 healthy control children participated in this study. The oral glucose tolerance test (OGTT) was performed by giving them glucose (1.75 gm/kg of body weight), orally in the morning, and the binding of 125I-labeled insulin to circulating monocytes in vitro was measured prior to OGTT. The glucose tolerance expressed by ΣBS (milligrams/100 ml), the sum of the plasma glucose (blood sugar [BS]) values at OGTT, was significantly correlated with the degree of overweight (r = .316, P < .01) and more highly with ΣIRI (microunits per milliliter), the sum of immunoreactive insulin (IRI) values at OGTT (r = .512, P < .001). Insulin binding to monocytes in vitro (picograms/106 cells) was inversely correlated with the degree of overweight (r = -. 687, P < .001). Furthermore, ΣBS was inversely correlated significantly with insulin binding to monocytes in vitro (r = -.435, P < .002). These data suggest that the decrease of insulin receptors might be one cause for the impairment of the glucose tolerance associated with obesity in children.

Insulin binding, internalization, and receptor regulation in cultured human fibroblasts

1981 ◽  
Vol 241 (3) ◽  
pp. E251-E260
Author(s):  
D. Baldwin ◽  
M. Prince ◽  
P. Tsai ◽  
C. Johnson ◽  
R. Lotan ◽  
...  
Keyword(s):  
Incubation Temperature ◽  
Degradation Products ◽  
Human Fibroblasts ◽  
Insulin Receptors ◽  
Insulin Binding ◽  
Insulin Concentration ◽  
Target Cells ◽  
Kinetic Properties ◽  
Insulin Degradation ◽  
Normal Human

Insulin binding to receptors was studied using monolayers of cultured normal human fibroblasts. Binding was rapid and inversely related to the incubation temperature; prolonged periods of steady-state binding were achieved at all temperatures studied and the amount of degradation of extracellular insulin was minimal. Competition curves demonstrated half-maximal inhibition of 125I-insulin binding at an unlabeled insulin concentration of 125I-insulin binding at an unlabeled insulin concentration of 7 ng/ml. Scatchard plots of the binding data were curvilinear and revealed that fibroblasts contained about 7,000 receptor sites per cell. Bound 125I-insulin dissociated from fibroblasts with a t 1/2 of 10 min at 30 degrees C and 35 min at 16 degrees C. After 60 min dissociation at 30 degrees C, 45% of the dissociated radioactivity consisted of 125I-insulin degradation products, whereas only 8% of the dissociated material was in the form of degraded products after 60 min of dissociation at 16 degrees C. This indicates that fibroblasts possess a temperature-sensitive receptor-mediated process for insulin degradation. Preincubation of the monolayers with insulin led to a hormone-induced loss of insulin receptors. Thus, incubating cells with 25 ng/ml insulin for 6 h at 37 degrees C caused a 50% reduction in subsequently measured 125I-insulin binding. This hormone-induced receptor loss was sensitive to physiologic insulin levels, with approximately 5 ng/ml causing a half-maximal receptor loss. When monolayers were treated with the lysosomotropic agent chloroquine and subsequently incubated with 5 X 10(-11) M 125I-insulin, a 130% increase in cell-associated radioactivity was observed after 120 min at 30 degrees C. In summary, 1) cultured normal human fibroblasts possess insulin receptors that exhibit kinetic properties and specificity identical to that of other insulin target cells; 2) incubation of fibroblasts with physiologic concentrations of insulin causes a marked loss of cell-surface insulin receptors; and 3) receptor-bound 125I-insulin is internalized through an energy-dependent endocytotic pathway and subsequently degraded by a chloroquine-sensitive reaction.

INSULIN RECEPTORS, INSULIN SECRETION, AND GLUCOSE DISAPPEARANCE RATE IN PATIENTS WITH PERIODIC HYPOKALAEMIC PARALYSIS

1979 ◽  
Vol 90 (2) ◽  
pp. 272-282 ◽  
Author(s):  
Torsten Johnsen ◽  
Henning Beck-Nielsen
Keyword(s):  
Insulin Response ◽  
Insulin Receptors ◽  
Normal Subjects ◽  
Insulin Binding ◽  
Oral Glucose ◽  
Oral Glucose Load ◽  
Glucose Disappearance ◽  
Normal Glucose ◽  
Glucose Tolerance Tests ◽  
Male Patients

ABSTRACT In a study of 6 male patients with periodic hypokalaemic paralysis (PHP), we found reduced insulin binding to monocytes as compared with a group of 25 normal subjects (P < 0.1). The decreased insulin binding was caused by the decreased binding affinity. During induction of paralysis by a prolonged oral glucose load, one patient showed 24-h variations in the insulin binding to monocytes not differing from those observed in normals. After iv administration of glucose, these patients showed an elevated initial insulin response compared with the normals (P < 0.1). However, the iv glucose tolerance tests revealed normal glucose disappearance rates. We conclude that changes in insulin receptor binding do not appear to be of pathophysiological significance for eliciting the parese attacks in PHP. However, the increased insulin response, following carbohydrate intake, might be of significance in the generation of paralytic attacks in patients with PHP.

Insulin receptors in normal pregnant women and women with gestational diabetes

1986 ◽  
Vol 113 (3_Suppl) ◽  
pp. S27-S30 ◽  
Author(s):  
Ole Andersen ◽  
Claus Kühl ◽  
Inge Buch
Keyword(s):  
Gestational Diabetes ◽  
Pregnant Women ◽  
Receptor Binding ◽  
Insulin Receptors ◽  
Late Pregnancy ◽  
Insulin Binding ◽  
Normal Weight ◽  
Insulin Concentration ◽  
Isolated Adipocytes ◽  
Normal Controls

Abstract. In a serial study of insulin receptor binding to monocytes from normal pregnant women, a significant increase in insulin binding in mid pregnancy followed by a significant decrease in late pregnancy at tracer insulin concentration was found. No changes in the insulin concentration necessary to reduce tracer binding by 50% (ID50) were observed. At delivery, binding to isolated adipocytes was significantly lower in normal pregnant women than in non-pregnant normal controls while no difference in ID50 was observed. No differences in insulin binding at tracer insulin concentration to monocytes and adipocytes between normal weight women with gestational diabetes and healthy non-diabetic pregnant controls were found, but the ID50 was significantly lower in women with gestational diabetes diagnosed in late pregnancy than in pregnant controls at the same weeks of gestation.

The Effect of the Oral Administration of Leucine on Endothelial Function, Glucose and Insulin Concentrations in Healthy Subjects

2018 ◽  
Vol 127 (08) ◽  
pp. 505-510 ◽  
Author(s):  
Georgia Argyrakopoulou ◽  
Paraskevi Kontrafouri ◽  
Ioanna Eleftheriadou ◽  
Alexander Kokkinos ◽  
Christina Arapostathi ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Healthy Subjects ◽  
Insulin Response ◽  
Random Order ◽  
Serum Glucose ◽  
Glucose Infusion ◽  
The Other ◽  
Healthy Individuals ◽  
Healthy Male ◽  
Glucose Levels

Abstract Objective The aim of our study was to investigate the potential differential effect of hyperglycaemia and hyperinsulinaemia induced by glucose infusion alone and in combination with leucine consumption on endothelial function in healthy individuals. Methods Ten male volunteers were examined in random order twice. In one visit, they consumed 250 ml water (baseline) and 30 min later glucose was infused iv. In the other visit, they consumed 250 ml water with 25 g of leucine and 30 min later the same amount of glucose was infused. Serum glucose and insulin were measured at baseline and every 10 min after glucose infusion for 1 h. Endothelial function was evaluated by measurement of flow mediated vasodilatation (FMD) at baseline, 10 and 60 min after glucose infusion. Results In both visits, glucose levels increased to the same degree, whereas insulin response was significantly higher after leucine administration. FMD values declined significantly compared to baseline 10 min after glucose infusion in the control visit (6.9±2.7 vs. 3.2±3.5%, respectively, p=0.006), while no significant change was observed when glucose infusion was followed by leucine consumption. Conclusions Acute hyperglycaemia impairs endothelial function in healthy male individuals. Leucine administration prevents hyperglycaemia-mediated endothelial dysfunction probably due to enhanced insulin secretion.

scholarly journals Secretion of parathyroid hormone may be coupled to insulin secretion in humans

2020 ◽  
Vol 9 (7) ◽  
pp. 747-754
Author(s):  
Marie Reeberg Sass ◽  
Nicolai Jacob Wewer Albrechtsen ◽  
Jens Pedersen ◽  
Kristine Juul Hare ◽  
Nis Borbye-Lorenzen ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Gut Hormones ◽  
Insulin Receptors ◽  
Underlying Mechanism ◽  
Parathyroid Glands ◽  
Oral Glucose ◽  
Healthy Individuals ◽  
Oral Glucose Tolerance Tests ◽  
Glucose Tolerance Tests ◽  
Calcium Secretion

Objective: Parathyroid hormone (PTH) is a key hormone in regulation of calcium homeostasis and its secretion is regulated by calcium. Secretion of PTH is attenuated during intake of nutrients, but the underlying mechanism(s) are unknown. We hypothesized that insulin acts as an acute regulator of PTH secretion. Methods: Intact PTH was measured in plasma from patients with T1D and matched healthy individuals during 4-h oral glucose tolerance tests (OGTT) and isoglycemic i.v. glucose infusions on 2 separate days. In addition, expression of insulin receptors on surgical specimens of parathyroid glands was assessed by immunochemistry (IHC) and quantitative PCR (qPCR). Results: The inhibition of PTH secretion was more pronounced in healthy individuals compared to patients with T1D during an OGTT (decrementalAUC0–240min: −5256 ± 3954 min × ng/L and −2408 ± 1435 min × ng/L, P = 0.030). Insulin levels correlated significantly and inversely with PTH levels, also after adjusting for levels of several gut hormones and BMI (P = 0.002). Expression of insulin receptors in human parathyroid glands was detected by both IHC and qPCR. Conclusion: Our study suggests that insulin may act as an acute regulator of PTH secretion in humans.

Receptor and postreceptor insulin resistance induced by in vivo hyperinsuiinemia

1983 ◽  
Vol 61 (8) ◽  
pp. 802-807 ◽  
Author(s):  
C. Martin ◽  
K. S. Desai ◽  
G. Steiner
Keyword(s):  
Insulin Resistance ◽  
Glucose Oxidation ◽  
Binding Capacity ◽  
Insulin Receptors ◽  
Insulin Binding ◽  
Insulin Concentration ◽  
Fat Cell ◽  
And Control

We examined the effects of inducing hyperinsuiinemia in vivo in rats on the insulin receptors of, and the glucose oxidation by their adipocytes. Hyperinsulinemia was induced over a 2-week period by injecting NPH insulin subcutaneously. This was given in doses that were gradually increased to a final dose of 6 units/day. Profound hypoglycemia was avoided by providing supplemental sucrose to both the insulin-treated and control rats. The insulin concentration was eight times greater in the insulin-treated rats. However, they were not grossly obese and their adipocytes were not enlarged. The adipocytes of the hyperinsulinemic rats had a 25% lower maximal insulin binding capacity and were resistant to the effects of insulin on glucose oxidation. We felt that the hyperinsuiinemia was sufficient so that, despite their somewhat lower insulin binding capacity, these adipocytes would not bind less insulin in vivo than would adipocytes from control rats. Hence, we postulated that, this massive hyperinsulinemia not only down regulated the insulin receptor, but also led to a postreceptor resistance. This notion was supported by two lines of in vitro data. First, even at maximally effective medium concentrations of insulin, the maximum rate of glucose oxidation by the adipocytes from hyperinsulinemic rats reached a plateau which was less than that reached by cells from controls. Second, when this in vitro glucose oxidation was related not merely to the medium insulin concentration, but to the amount of insulin bound to adipocytes, the response of the hyperinsulinemic rats' cells was always lower than control. These changes occurred in the absence of any difference in fat cell size. Thus, in vivo hyperinsulinemia led to insulin resistance in adipocytes. This was associated both with down regulation of the insulin receptors and with a postreceptor defect.

The disposal of an oral glucose load in healthy subjects. A quantitative study

Diabetes ◽  
1985 ◽  
Vol 34 (6) ◽  
pp. 580-588 ◽  
Author(s):  
E. Ferrannini ◽  
O. Bjorkman ◽  
G. A. Reichard ◽  
A. Pilo ◽  
M. Olsson ◽  
...  
Keyword(s):  
Quantitative Study ◽  
Healthy Subjects ◽  
Oral Glucose ◽  
Oral Glucose Load ◽  
Glucose Load

A Comparative Evaluation of Serum and Salivary Total Proteins and Immunoglobulins in Patients with Hepatitis A and Healthy Subjects

2018 ◽  
Vol 69 (5) ◽  
pp. 1125-1128
Author(s):  
Daniela G. Balan ◽  
Dan Piperea Sianu ◽  
Iulia I. Stanescu ◽  
Dorin Ionescu ◽  
Andra Elena Stroescu Balcangiu ◽  
...  
Keyword(s):  
Healthy Subjects ◽  
Comparative Evaluation ◽  
Hepatitis A ◽  
Hepatitis A Virus ◽  
Point Of View ◽  
Healthy Individuals ◽  
Total Proteins ◽  
Statistical Point ◽  
Immunological Tests ◽  
Acute Hepatitis A

Assessment of changes in total proteins level, serum and saliva IgG and IgA levels, serum IgM level, serum and saliva IgA/IgG ratio. The study was conducted on a group of 40 subjects, divided into 2 lots: the first lot consisting of 20 healthy individuals and the second consisting of 20 patients with hepatitis with hepatitis A virus (HAV). The levels of total proteins, serum and saliva IgG and IgA, serum IgM and serum and saliva IgA/IgG ratio have higher values in patients with hepatitis A, in comparison to healthy subjects, without necessarily exceeding the maximum admitted value. The results are significant from a statistical point of view. Due to the sensitivity and specificity of salivary anti-HAV IgM and IgG in patients with acute hepatitis A, compared with healthy subjects, there is a possibility of using salivary immunological tests instead of serum tests for the diagnosis and epidemiological study of HAV infection.

Sign in / Sign up

Export Citation Format

Share Document