PANCREATIC-GLUCAGON-LIKE IMMUNOREAGTIVITY AFTER INTRAVENOUS INSULIN IN NORMALS AND CHRONIC-PANCREATITIS PATIENTS

1971 ◽  
Vol 67 (2) ◽  
pp. 401-404 ◽  
Author(s):  
I. Persson ◽  
F. Gyntelberg ◽  
L. G. Heding ◽  
J. Boss-Nielsen
Keyword(s):  
Chronic Pancreatitis ◽  
Plasma Glucose ◽  
Normal Subjects ◽  
Insulin Injection ◽  
Normal Group ◽  
Pancreatic Glucagon ◽  
Intravenous Insulin ◽  
Gut Gli

Plasma glucose and pancreatic-glucagon-like immunoreactivity (GLI) were measured in normal subjects and in patients with chronic pancreatitis after an intravenous insulin injection. Both groups showed a fall of about 40 mg/100 ml in plasma glucose at from 0 to 30 minutes. In the normal group, the pancreatic GLI increased significantly above the 0-value at 30 and 60 minutes. No increase was observed in the pancreatitis patients. In all cases a decrease in gut GLI was observed during the test.

Dose-Response Relationships to Pancreozymin in Normal Subjects and Patients with Chronic Pancreatitis

1963 ◽  
Vol 45 (2) ◽  
pp. 209-214 ◽  
Author(s):  
Donald H. Hanscom ◽  
Armand Littman ◽  
Jack V. Pinto
Keyword(s):  
Chronic Pancreatitis ◽  
Dose Response ◽  
Normal Subjects

Effect of source of dietary carbohydrate on plasma glucose and insulin responses to test meals in normal subjects

1980 ◽  
Vol 33 (6) ◽  
pp. 1279-1282 ◽  
Author(s):  
A Coulston ◽  
M Greenfield ◽  
F Kraemer ◽  
T Tobey ◽  
G Reaven
Keyword(s):  
Plasma Glucose ◽  
Normal Subjects ◽  
Dietary Carbohydrate ◽  
Insulin Responses

Contribution of cortisol to glucose counterregulation in humans

1989 ◽  
Vol 257 (1) ◽  
pp. E35-E42 ◽  
Author(s):  
P. De Feo ◽  
G. Perriello ◽  
E. Torlone ◽  
M. M. Ventura ◽  
C. Fanelli ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Glucose Concentration ◽  
Glucose Utilization ◽  
Hepatic Glucose Production ◽  
Hormone Secretion ◽  
Glucose Production ◽  
Plasma Free Fatty Acid ◽  
Normal Subjects ◽  
Plasma Glucose Concentration ◽  
Cortisol Increase

To test the hypothesis that cortisol secretion plays a counterregulatory role in hypoglycemia in humans, four studies were performed in eight normal subjects. In all studies, insulin (15 mU.m-2.min-1) was infused subcutaneously (plasma insulin 27 +/- 1 microU/ml). In study 1, plasma glucose concentration and glucose fluxes [( 3-3H]glucose), substrate, and counterregulatory hormone concentrations were simply monitored, and plasma glucose decreased from 89 +/- 2 to 52 +/- 2 mg/dl for 12 h. In study 2, (pituitary-adrenal-pancreatic clamp), insulin and counterregulatory hormone secretion (except for catecholamines) was prevented by somatostatin (0.5 mg/h, iv) and metyrapone (0.5 g/4 h, per os), and glucagon, cortisol, and growth hormone were infused to reproduce the concentrations of study 1. In study 3 (lack of cortisol increase), the pituitary-adrenal-pancreatic clamp was performed with maintenance of plasma cortisol at basal levels, and glucose was infused, whenever needed, to reproduce plasma glucose concentration of study 2. Study 4 was identical to study 3, but exogenous glucose was not infused. Isolated lack of cortisol increase caused a approximately 22% decrease in hepatic glucose production (P less than 0.01) and a approximately 15% increase in peripheral glucose utilization (P less than 0.01), which resulted in greater hypoglycemia (37 +/- 2 vs. 52 +/- 2 mg/dl, P less than 0.01) despite compensatory increases in plasma epinephrine. Lack of cortisol response also reduced plasma free fatty acid, beta-hydroxybutyrate, and glycerol concentrations approximately 50%. We conclude that cortisol normally plays an important counterregulatory role during hypoglycemia by augmenting glucose production, decreasing glucose utilization, and accelerating lipolysis.

scholarly journals The effect of posture on ventilatory muscle function and lung function

1986 ◽  
Vol 42 (3) ◽  
pp. 81-84 ◽  
Author(s):  
P. Gounden
Keyword(s):  
Muscle Strength ◽  
Lung Function ◽  
Muscle Function ◽  
Normal Subjects ◽  
Normal Group ◽  
Optimum Position ◽  
Asthmatic Group

The purpose of this study was to determine the influence of posture on ventilatory muscle strength and on lung function.Maximum static inspiratory pressures (MIPS), maximum static expiratory pressures (MEPS) and lung function measurements (FVC, FEV1, PEFR) were obtained in three different body positions in 57 normal subjects and in 16 asthmatic patients.Statistical analysis of the data obtained showed that changes in position influence the ventilatory muscle function and lung function values.The sitting lean forward and the sitting erect positions were the better positions in the normal group. The findings revealed that the sitting lean forward position was the optimum position for the asthmatic group (p 0,001).

Management of Diabetes Resistant to Subcutaneous Insulin with Intravenous Insulin via an Implanted Infusion Pump

1988 ◽  
Vol 33 (2) ◽  
pp. 239-243 ◽  
Author(s):  
K.R. Paterson ◽  
I.W. Campbell ◽  
S.M. MacRury ◽  
D.G. Gilmour ◽  
A.C. MacCuish
Keyword(s):  
Treatment Option ◽  
Insulin Infusion ◽  
Rare Complication ◽  
Infusion Pump ◽  
Insulin Injection ◽  
Management Problem ◽  
Subcutaneous Insulin ◽  
Intravenous Insulin ◽  
Infusion Devices ◽  
Insulin Dependent

Diabetes resistant to conventional subcutaneous insulin injection is a rare complication of insulin-dependent diabetes which poses a major management problem. We report three cases treated for a total of over seven patient years with fully implanted insulin infusion devices. Technical difficulties with the devices and their operation have been substantial but the patients are much improved and hospitalisation has been dramatically reduced. We suggest that implanted insulin pumps are a real treatment option for patients with this unusual syndrome.

Pancreatic Secretion of Zinc and Copper in Normal Subjects and in Patients with Chronic Pancreatitis

Digestion ◽  
1991 ◽  
Vol 49 (3) ◽  
pp. 161-166 ◽  
Author(s):  
I. Gjørup ◽  
L. Petronijevic ◽  
E. Rubinstein ◽  
B. Andersen ◽  
H. Worning ◽  
...  
Keyword(s):  
Chronic Pancreatitis ◽  
Pancreatic Secretion ◽  
Normal Subjects

Plasma Glucose Levels Affect Cerebral 18F-FDG Distribution in Cognitively Normal Subjects With Diabetes

2016 ◽  
Vol 41 (6) ◽  
pp. e274-e280 ◽  
Author(s):  
Kenji Ishibashi ◽  
Airin Onishi ◽  
Yoshinori Fujiwara ◽  
Kiichi Ishiwata ◽  
Kenji Ishii
Keyword(s):  
Plasma Glucose ◽  
Normal Subjects ◽  
Cognitively Normal ◽  
Glucose Levels ◽  
18F Fdg ◽  
Cognitively Normal Subjects

Direct evidence that an increase in aortic norepinephrine level in response to insulin-induced hypoglycemia is due to increased adrenal norepinephrine output

1989 ◽  
Vol 67 (5) ◽  
pp. 499-505 ◽  
Author(s):  
Nobuharu Yamaguchi ◽  
Richard Briand ◽  
Martine Brassard
Keyword(s):  
Direct Evidence ◽  
Plasma Concentrations ◽  
Insulin Injection ◽  
Plasma Norepinephrine ◽  
Sodium Pentobarbital ◽  
Insulin Administration ◽  
Norepinephrine Level ◽  
Intravenous Insulin ◽  
Aortic Blood ◽  
Initial Control

This study reports on the major source of circulating norepinephrine that is known to increase, progressively, during sustained hypoglycemia induced by intravenous insulin administration. Plasma concentrations of epinephrine, norepinephrine, and dopamine were simultaneously determined for adrenal venous and aortic blood in dogs anesthetized with sodium pentobarbital. The model used allowed us to perform a functional adrenalectomy (ADRX), while continuously monitoring the adrenal medullary secretory function. Under basal conditions, the net output (μg/min) of adrenal epinephrine, norepinephrine, and dopamine were 0.169 ± 0.074, 0.067 ± 0.023, and 0.011 ± 0.003, respectively. Plasma concentrations (ng/mL) of aortic epinephrine, norepinephrine, and dopamine were 0.132 ± 0.047, 0.268 ± 0.034, and 0.034 ± 0.009. Following insulin injection (0.15 IU/kg, i.v.), the net output (μg/min) of adrenal epinephrine, norepinephrine, and dopamine increased gradually (p < 0.05), reaching the values of 0.918 ± 0.200, 0.365 ± 0.058, and 0.034 ± 0.007 30 min after insulin administration. Similarly, aortic epinephrine, norepinephrine, and dopamine concentrations (ng/mL) increased significantly (p < 0.05) to 0.702 ± 0.144, 0.526 ± 0.093, and 0.066 ± 0.024. The aortic glucose concentration (mg/dL) was diminished from 81.8 ± 4.1 to 36.9 ± 3.4 (p < 0.01). After taking the blood sample at 30 min following insulin administration, ADRX was immediately performed. Five minutes after the onset of ADRX, the net output (μg/min) of adrenal epinephrine, norepinephrine, and dopamine increased further to 1.707 ± 0.374 (p < 0.05), 0.668 ± 0.139 (p < 0.05), and 0.052 ± 0.017. By contrast, aortic epinephrine, norepinephrine, and dopamine concentrations rapidly diminished (p < 0.05) to their initial control levels reaching 0.051 ± 0.014, 0.252 ± 0.023, and 0.031 ± 0.005 ng/mL, 5 min after ADRX. The present results indicate that during the early phase of insulin-induced hypoglycemia, circulating norepinephrine in aortic blood significantly increases due, primarily, to the enhanced adrenal norepinephrine output.Key words: insulin, plasma norepinephrine, adrenal catecholamines, functional adrenalectomy, hypoglycemia.

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