Insulin secretion, insulin sensitivity and hepatic insulin extraction in primary hyperparathyroidism before and after surgery

1992 ◽  
Vol 37 (2) ◽  
pp. 147-155 ◽  
Author(s):  
A. Kautzky-Willer ◽  
G. Pacinl ◽  
B. Niederle ◽  
G. Schernthaner ◽  
R. Prager
Keyword(s):  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Primary Hyperparathyroidism ◽  
Before And After ◽  
Hepatic Insulin Extraction

scholarly journals Insulin Secretion and Insulin Sensitivity Before and After Surgical Treatment of Pheochromocytoma or Paraganglioma

2017 ◽  
Vol 102 (9) ◽  
pp. 3400-3405 ◽  
Author(s):  
Hisako Komada ◽  
Yushi Hirota ◽  
Anna So ◽  
Tomoaki Nakamura ◽  
Yoko Okuno ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Surgical Treatment ◽  
Insulin Sensitivity ◽  
Before And After

scholarly journals Influence of Tacrolimus on Glucose Metabolism before and after Renal Transplantation: A Prospective Study

2001 ◽  
Vol 12 (3) ◽  
pp. 583-588 ◽  
Author(s):  
ELLY M. VAN DUIJNHOVEN ◽  
JOHANNES M. M. BOOTS ◽  
MAARTEN H. L. CHRISTIAANS ◽  
BRUCE H. R. WOLFFENBUTTEL ◽  
JOHANNES P. VAN HOOFF
Keyword(s):  
Insulin Resistance ◽  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
Sensitivity Index ◽  
Intravenous Glucose ◽  
Prospective Longitudinal Study ◽  
C Peptide ◽  
Before And After ◽  
Prospective Longitudinal

Abstract. Most studies concerning the influence of tacrolimus on glucose metabolism have been performed either in animals or after organ transplantation. These clinical studies have largely been transversal with patients who were using steroids. Therefore, this prospective, longitudinal study investigated the influence of tacrolimus on glucose metabolism before and after transplantation. Eighteen Caucasian dialysis patients underwent an intravenous glucose tolerance test before and 5 d after the start of tacrolimus. Insulin sensitivity index (kG), insulin resistance (insulin/glucose ratio and homeostasis model assessment), and C-peptide and insulin secretion were calculated. Trough levels of tacrolimus were measured. After transplantation, the occurrence of posttransplantation diabetes mellitus (PTDM) was prospectively monitored. Statistical analysis was performed using the Wilcoxon signed ranks test and Spearman's rho for correlation. Before tacrolimus, kG was indeterminate in three patients. During tacrolimus, kG decreased in 16 of 18 patients, from a median of 1.74 mmol/L per min to 1.08 mmol/L per min (P < 0.0001). The correlation between C-peptide and insulin data was excellent. Insulin secretion decreased from 851.0 mU × min/L to 558.0 mU × min/L (P = 0.014), whereas insulin resistance did not change. Insulin sensitivity correlated negatively with tacrolimus trough level. After transplantation, three patients developed PTDM; before tacrolimus, two had an indeterminate and one a low normal kG. During tacrolimus administration, kG decreased in almost all patients as a result of a diminished insulin secretion response to a glucose load, whereas insulin resistance did not change. Patients with an abnormal or indeterminate kG seem to be at risk of developing PTDM while on tacrolimus.

β-Cell “rest” accompanies reduced first-pass hepatic insulin extraction in the insulin-resistant, fat-fed canine model

2007 ◽  
Vol 292 (6) ◽  
pp. E1581-E1589 ◽  
Author(s):  
Stella P. Kim ◽  
Martin Ellmerer ◽  
Erlinda L. Kirkman ◽  
Richard N. Bergman
Keyword(s):  
Insulin Resistance ◽  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Cell Function ◽  
Physiological Mechanism ◽  
Initial Increase ◽  
Β Cell ◽  
Euglycemic Hyperinsulinemic Clamp ◽  
First Pass ◽  
Hepatic Insulin Extraction

During insulin resistance, glucose homeostasis is maintained by an increase in plasma insulin via increased secretion and/or decreased first-pass hepatic insulin extraction. However, the relative importance of insulin secretion vs. clearance to compensate for insulin resistance in obesity has yet to be determined. This study utilizes the fat-fed dog model to examine longitudinal changes in insulin secretion and first-pass hepatic insulin extraction during development of obesity and insulin resistance. Six dogs were fed an isocaloric diet with an ∼8% increase in fat calories for 12 wk and evaluated at weeks 0, 6, and 12 for changes in 1) insulin sensitivity by euglycemic-hyperinsulinemic clamp, 2) first-pass hepatic insulin extraction by direct assessment, and 3) glucose-stimulated insulin secretory response by hyperglycemic clamp. We found that 12 wk of a fat diet increased subcutaneous and visceral fat as assessed by MR imaging. Consistent with increased body fat, the dogs exhibited a ∼30% decrease in insulin sensitivity and fasting hyperinsulinemia. Although insulin secretion was substantially increased at week 6, β-cell sensitivity returned to prediet levels by week 12. However, peripheral hyperinsulinemia was maintained because of a significant decrease in first-pass hepatic insulin extraction, thus maintaining hyperinsulinemia, despite changes in insulin release. Our results indicate that when obesity and insulin resistance are induced by an isocaloric, increased-fat diet, an initial increase in insulin secretion by the β-cells is followed by a decrease in first-pass hepatic insulin extraction. This may provide a secondary physiological mechanism to preserve pancreatic β-cell function during insulin resistance.

scholarly journals Obesity is associated with increased basal and postprandial β-cell insulin secretion even in the absence of insulin resistance

2020 ◽  
Author(s):  
Ada Admin ◽  
Stephan van Vliet ◽  
Han-Chow E. Koh ◽  
Bruce W. Patterson ◽  
Mihoko Yoshino ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Weight Loss ◽  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Glucose Production ◽  
Compensatory Response ◽  
Insulin Kinetics ◽  
Positron Emission ◽  
Glucose Ingestion ◽  
Before And After

We tested the hypothesis that obesity, independent of insulin resistance, is associated with increased insulin secretion. We compared insulin kinetics before and after glucose ingestion in lean healthy people and people with obesity who were matched on multi-organ insulin sensitivity (inhibition of adipose tissue lipolysis and glucose production and stimulation of muscle glucose uptake), assessed by using a two-stage hyperinsulinemic-euglycemic pancreatic clamp procedure in conjunction with glucose and palmitate tracer infusions and positron emission tomography. We also evaluated the effect of diet-induced weight loss on insulin secretion in people with obesity who did not improve insulin sensitivity despite marked (~20%) weight loss. Basal and postprandial insulin secretion rates were more than 50% greater in people with obesity than lean people even though insulin sensitivity was not different between groups. Weight loss in people with obesity decreased insulin secretion by 35% even though insulin sensitivity did not change. These results demonstrate that increased insulin secretion in people with obesity is associated with excess adiposity itself and is not simply a compensatory response to insulin resistance. These findings have important implications regarding the pathogenesis of diabetes, because hyperinsulinemia causes insulin resistance and insulin hypersecretion is an independent risk factor for developing diabetes.

Insulin Sensitivity in Patients with Primary Hyperparathyroidism Before and After Parathyroidectomy:

1991 ◽  
Vol 23 (06) ◽  
pp. 288-289 ◽  
Author(s):  
D. Micic ◽  
A. Kendereski ◽  
V. Popovic ◽  
D. Manojlovic ◽  
J. Micic
Keyword(s):  
Insulin Sensitivity ◽  
Primary Hyperparathyroidism ◽  
Before And After

We-P11:68 Insulin sensitivity in pateints with primary hyperparathyroidism before and after surgical treatment

2006 ◽  
Vol 7 (3) ◽  
pp. 361
Author(s):  
D. Micic ◽  
G. Cvijovic ◽  
A. Kendereski ◽  
M. Sumarac-Dumanovic ◽  
S. Zoric ◽  
...  
Keyword(s):  
Surgical Treatment ◽  
Insulin Sensitivity ◽  
Primary Hyperparathyroidism ◽  
Before And After

INCREASED INSULIN SENSITIVITY AND CELLULAR INSULIN BINDING IN OBESE DIABETICS FOLLOWING TREATMENT WITH GLIBENCLAMIDE

1979 ◽  
Vol 90 (3) ◽  
pp. 451-462 ◽  
Author(s):  
Henning Beck-Nielsen ◽  
Oluf Pedersen ◽  
Hans Otto Lindskov
Keyword(s):  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Binding Affinity ◽  
Insulin Receptors ◽  
Insulin Binding ◽  
Significant Alteration ◽  
Diabetic State ◽  
Before And After ◽  
Secretory Pattern

ABSTRACT The aim of the present study was to examine the effect of glibenclamide on the insulin receptors, the insulin sensitivity and the insulin secretion in obese non-ketotic diabetics. Two groups of 9 obese diabetics were studied before and after 10 days' treatment with a 1200 Kcal's diet and a 1200 kcal's diet + 10 mg/day of glibenclamide, respectively. In the group treated with diet alone we found no significant alteration of the insulin secretion pattern (P > 0.1). However, the insulin sensitivity increased 37 % (P < 0.01). Furthermore, the insulin binding to monocytes increased (P < 0.01) due to a 36% rise of the binding affinity. In the group treated with glibenclamide and diet the insulin secretory pattern was unchanged, too (P > 0.1). The insulin sensitivity, however, increased 83% (P < 0.01). Moreover, the insulin binding was raised (P < 0.01) as a result of a 80 % rise of the number of insulin receptors. In 4 patients who were treated with diet (1200 kcal/day) plus glibenclamide and in 5 patients who were treated with diet alone (1200 kcal/day) the insulin binding to monocytes was studied during treatment for 1 year. After 1 year we found a significantly (P < 0.05) higher cellular insulin binding in the glibenclamide treated patients compared to the patients who got diet alone. We conclude that 1) the augmentation of the insulin sensitivity is of great importance for the normalization of the diabetic state in obese, 2) the increase in insulin binding may be of importance for the increase in insulin sensitivity, 3) glibenclamide appears to enhance the insulin sensitivity through an increase in the number of insulin receptors.

scholarly journals Obesity is associated with increased basal and postprandial β-cell insulin secretion even in the absence of insulin resistance

2020 ◽  
Author(s):  
Ada Admin ◽  
Stephan van Vliet ◽  
Han-Chow E. Koh ◽  
Bruce W. Patterson ◽  
Mihoko Yoshino ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Weight Loss ◽  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Glucose Production ◽  
Compensatory Response ◽  
Insulin Kinetics ◽  
Positron Emission ◽  
Glucose Ingestion ◽  
Before And After

We tested the hypothesis that obesity, independent of insulin resistance, is associated with increased insulin secretion. We compared insulin kinetics before and after glucose ingestion in lean healthy people and people with obesity who were matched on multi-organ insulin sensitivity (inhibition of adipose tissue lipolysis and glucose production and stimulation of muscle glucose uptake), assessed by using a two-stage hyperinsulinemic-euglycemic pancreatic clamp procedure in conjunction with glucose and palmitate tracer infusions and positron emission tomography. We also evaluated the effect of diet-induced weight loss on insulin secretion in people with obesity who did not improve insulin sensitivity despite marked (~20%) weight loss. Basal and postprandial insulin secretion rates were more than 50% greater in people with obesity than lean people even though insulin sensitivity was not different between groups. Weight loss in people with obesity decreased insulin secretion by 35% even though insulin sensitivity did not change. These results demonstrate that increased insulin secretion in people with obesity is associated with excess adiposity itself and is not simply a compensatory response to insulin resistance. These findings have important implications regarding the pathogenesis of diabetes, because hyperinsulinemia causes insulin resistance and insulin hypersecretion is an independent risk factor for developing diabetes.

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