Early insulin and glucagon response to subsequent pulses of arginine, glucose, and tolbutamide in normal man.

1979 ◽  
Vol 236 (2) ◽  
pp. E85
Author(s):  
A V Greco ◽  
R Manna ◽  
G Ghirlanda ◽  
L Altomonte ◽  
A G Rebuzzi ◽  
...  

To determine the dynamics of insulin and of glucagon secretion in response to several sequential stimuli administered shortly after an arginine pulse (5 g), 20 nonobese, apparently healthy volunteers were given arginine (5 g), glucose (5 g), and tolbutamide (1 g) by rapid intravenous injection. The early insulin and glucagon area 0-8 min was studied. At the intervals and with the dosages used in this study, different stimuli with and without prestimulation with arginine did not lead to changes in early secretion of insulin. There was no exhaustion of the pool of insulin released after multiple sequential pulses. These results suggest a pattern in which stimulation induces a rapid release of insulin and activates the interchange between the stored and labile insulin pool; the 8-min interval is sufficient for the rapid return of the two compartments to a state of equilibrium. Also for glucagon, subsequent different stimuli did not exhaust glucagon release; nevertheless, glucagon is immediately suppressed by a submaximal glucose pulse.

1980 ◽  
Vol 21 (362_suppl) ◽  
pp. 131-134
Author(s):  
Trygve Aakhus ◽  
S. Christian Sommerfelt ◽  
Helge Stormorken ◽  
Kamilla Dahlström

1977 ◽  
Vol 232 (5) ◽  
pp. E464
Author(s):  
E W Chideckel ◽  
C J Goodner ◽  
D J Koerker ◽  
D G Johnson ◽  
J W Ensinck

In order to separate direct effects of epinephrine on fuel metabolism from those mediated by glucagon, epinephrine (0.1 microng/kg-min) was infused for 120 min in 18- and 65-h fasted, nonanesthetized baboons with and without a concomitant somatostatin infusion. At both stages of fasting, epinephrine stimulated glucagon, secretion, and this was blocked by somatostatin. At 18 h, with epinephrine alone, glucose rose early and remained elevated throughout the infusion. In the glycogen-depleted 65-h fasted animals, there was attenuation of the early glucose rise, with glucose reaching a maximum level at 100-120 min. With somatostatin blockade of glucagon release in the 18-h fasted animals, a pattern of attenuated early glucose rise similar to that of the 65-h fasted animals occurred. Somatostatin also inhibited this early glycogenolytic response when the epinephrine dose was increased fivefold. The behavior of FFA, glycerol, and beta-hydroxybutyrate was unchanged by the addition of somatostatin to epinephrine at either stage of fasting. Thus, glucagon mediates the early glycogenolytic response to epinephrine, but not the delayed hyperglycemia and probably not the lipolysis.


1994 ◽  
Vol 267 (5) ◽  
pp. E642-E647
Author(s):  
G. B. Pidgeon ◽  
A. M. Richards ◽  
M. G. Nicholls ◽  
R. R. Bailey ◽  
K. L. Lynn ◽  
...  

To assess the effects of ouabain on pressor and vasoactive hormone responsiveness, 10 healthy volunteers were pretreated with ouabain (0.5 mg i.v. 42 and 18 h before study) or placebo before pressor challenge with angiotensin II (ANG II; 2, 4, and 8 ng.kg-1.min-1 for 30 min/dose) and norepinephrine (NE; 5, 15, and 45 ng.kg-1.min-1 for 15 min/dose). There were no differences at baseline between the two study days regarding mean arterial pressure (MAP) or heart rate. Baseline pulse pressure, however, was significantly greater after ouabain (47 +/- 3 vs. 41 +/- 1 mmHg; P < 0.05). The mean maximum increments in MAP during ANG II and NE infusions were 17.5 +/- 1.1 and 10.5 +/- 1.3 (SE) mmHg, respectively, after ouabain and 19.2 +/- 1.3 and 10.4 +/- 1.5 mmHg after placebo (not significant). The mean heart rate was lower during both infusion periods on the ouabain study day compared with control (P < 0.05). Baseline plasma levels of ANG II, aldosterone, plasma renin activity, atrial and brain natriuretic peptide, guanosine 3',5'-cyclic monophosphate, NE, and epinephrine and achieved levels during the two infusions were similar on the two study days. We conclude that short-term ouabain administration does not alter pressor responsiveness or plasma levels of vasoactive hormones in healthy volunteers.


1997 ◽  
Vol 43 (10) ◽  
pp. 1952-1957 ◽  
Author(s):  
Ronald J Elin ◽  
Michael W Fried ◽  
Maureen Sampson ◽  
Mark Ruddel ◽  
David E Kleiner ◽  
...  

Abstract The liver metabolizes lidocaine by oxidative deethylation to form monoethylglycinexylidide (MEGX), an analyte proposed as an index of liver function. We determined MEGX and lidocaine serum concentrations with the TDx (Abbott Laboratories) at baseline and 15, 30, 60, and 90 min after the intravenous administration of lidocaine (1 mg/kg), analyzing specimens from 12 apparently healthy volunteers and 40 patients with chronic viral hepatitis diagnosed by liver biopsy and serum tests. The patients were grouped on the basis of the histology activity index. The following laboratory tests were performed on serum specimens from all subjects: albumin (ALB), alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, total bilirubin, and prothrombin time. The results showed no significant difference among the four groups for the concentrations of MEGX, lidocaine, and lidocaine/MEGX at the four time points. However, the concentrations of ALB, ALT, AST, AST/ALT, and prothrombin time were substantially different among the four groups. Thus, we conclude that assay of MEGX in our patients with chronic viral hepatitis did not contribute to the assessment of liver function when compared with apparently healthy volunteers and traditional tests of liver function.


1979 ◽  
Vol 236 (2) ◽  
pp. E98
Author(s):  
V Leclercq-Meyer ◽  
J Marchand ◽  
W J Malaisse

The calcium dependency of glucagon release by the perfused rat pancreas was investigated in the presence of different nutrients: glucose, arginine, and a mixture of "fumarate + glutamate + pyruvate" (FGP, 5 mM of each salt). At a 3.3 mM glucose concentration, FGP-induced glucagon release was inhibited by the removal of calcium or addition of verapamil. At a higher glucose concentration (16.6 mM), the glucagonotropic action of FGP was again inhibited by verapamil, but the removal of extracellular calcium enhanced transiently glucagon release. Comparable results were obtained when arginine (10 mM) instead of FGP was used to stimulate the alpha cell. These findings suggest that the glucagonotropic effect of FGP or arginine depends on the availability and inward transport of calcium, whereas extracellular calcium per se may be required for glucose to be sensed by the alpha cell as an inhibitor of glucagon secretion. Thus, the nutritional environment offered to the alpha cell may condition the expression of the different mechanisms involved in the control of glucagon release by calcium.


1997 ◽  
Vol 3 (3) ◽  
pp. 174-182
Author(s):  
Alexander Kaplan ◽  
Svetlana Kaplan ◽  
Karen F. Marcoe ◽  
Lester R. Sauvage ◽  
William P. Hammond

We sought to develop a predictive method, based on the integration of blood parameters found to be significantly associated with thrombosis and progression of atherosclerosis, that would be more accurate than primary reliance on elevation of separate risk factors. The study involved 1,034 male subjects. Lipid profiles and fibrinogen levels were determined for 123 men with documented clinical atherosclerosis and 123 apparently healthy volunteers. There were significant differences between these groups for fibrinogen, triglycerides, and HDL cholesterol. An algebraic expression was then developed which combined normalized values of fibrinogen, HDL cholesterol, and triglycerides with platelet count and aggregation data to yield a numerical value, the clinical atheroscterosis predisposition (CAP) factor. We then tested this CAP factor with a validation group of 788 men, 372 of whom were patients with documented clinical atherosclerosis; the rest were apparently healthy. A 3-year prospective evaluation was done for 72 of the 123 apparently healthy volunteers. The CAP factor was 90% indicative of patient status for the 372 men with documented complications of atherosclerosis and appeared to predict severe coronary disease in the 3-year prospective evaluation. This initial study suggests that integrated analysis of thrombotic factors in white males. provides a useful estimate of an individual's risk for subsequent development of clinical atherosclerosis. Key Words: Atherosclerosis-Prevention and control-Blood-Platelets-Cholesterol-Triglycerides--Fibrinogen.


2006 ◽  
Vol 61 (6) ◽  
pp. 769-778 ◽  
Author(s):  
T van Vliet ◽  
R G J M Jacobs ◽  
E de Deckere ◽  
H van den Berg ◽  
A de Bree ◽  
...  

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