Adrenergic control of plasma magnesium in man

1987 ◽  
Vol 72 (1) ◽  
pp. 135-138 ◽  
Author(s):  
Kenneth F. Whyte ◽  
George J. Addis ◽  
Robert Whitesmith ◽  
John L. Reid
Keyword(s):  
Plasma Glucose ◽  
Plasma Insulin ◽  
Plasma Potassium ◽  
Normal Subjects ◽  
Stress Tests ◽  
Adrenergic Stimulation ◽  
Insulin Levels ◽  
Plasma Insulin Levels ◽  
Adrenaline Infusion ◽  
Plasma Magnesium

1. Regulation of magnesium balance is poorly understood. However, hypomagnesaemia has been reported in patients in clinical situations where circulating catecholamines are raised including myocardial infarction, cardiac surgery and insulin-induced hypoglycaemia stress tests. 2. The effects of l-adrenaline infusions, sufficient to achieve pathophysiological levels of adrenaline, and of therapeutic intravenous infusions of salbutamol, a β2-agonist, on plasma magnesium, plasma potassium, plasma glucose and plasma insulin levels were studied in a placebo-controlled design in eight normal subjects. 3. Plasma magnesium levels fell significantly during the adrenaline infusion and also during the salbutamol infusion, though more slowly. In a 1 h period of observation after cessation of the infusions no recovery of plasma magnesium levels was seen. Significant falls in plasma potassium levels were also observed during both infusions with spontaneous recovery within 30 min after the infusions. 4. No significant changes in plasma insulin levels occurred with either salbutamol or l-adrenaline compared with control. Plasma glucose levels rose significantly during the adrenaline infusion. 5. The study suggests that both l-adrenaline and salbutamol cause shifts in plasma magnesium which are not mediated by insulin. We propose that intracellular shifts of magnesium occur as a result of β-adrenergic stimulation.

Effect of adrenaline on insulin secretion in rats treated chronically with adrenaline

1976 ◽  
Vol 54 (6) ◽  
pp. 870-875 ◽  
Author(s):  
Suzanne Rousseau-Migneron ◽  
André Nadeau ◽  
Jacques LeBlanc
Keyword(s):  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Plasma Glucose ◽  
Basal Insulin ◽  
Plasma Insulin ◽  
Intravenous Glucose ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Plasma Insulin Levels ◽  
Adrenaline Infusion

To determine whether rats could adapt to a chronic exogenous supply of adrenaline by a decrease in the well-known inhibitory effect of adrenaline on insulin secretion, plasma glucose and insulin levels were measured in unanesthetized control and adrenaline-treated rats (300 μg/kg twice a day for 28 days) during an adrenaline infusion (0.75 μg kg−1 min−1), after an acute glucose load (0.5 g/kg), and during the simultaneous administration of both agents. Chronic treatment with adrenaline did not modify the initial glucose levels but it greatly diminished the basal insulin values (21.57 ± 2.48 vs. 44.69 ± 3.3 μU/ml, p < 0.01). In the control rats, despite the elevated glucose concentrations, a significant drop in plasma insulin levels was observed within the first 15 min of adrenaline infusion, followed by a period of recovery. In the adrenaline-treated group, in which plasma glucose levels were lower than in control animals, plasma insulin levels did not drop as in control rats, but a significant increase was found after 30 min of infusion. During the intravenous glucose tolerance test, the plasma glucose and insulin responses showed similar patterns; however, during the concomitant adrenaline infusion, the treated rats showed a better glucose tolerance than their controls. These results indicate that rats chronically treated with adrenaline adapt to the diabetogenic effect of an infusion of adrenaline by having a lower inhibition of insulin release, although the lower basal insulin levels may indicate a greater sensitivity to endogenous insulin.

Alterations in body fat stores and plasma insulin levels with daily intervals of heat exposure in Holtzman rats

1993 ◽  
Vol 265 (5) ◽  
pp. R1109-R1114 ◽  
Author(s):  
C. J. De Souza ◽  
A. H. Meier
Keyword(s):  
Glucose Tolerance ◽  
Ambient Temperature ◽  
Body Fat ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Time Of Day ◽  
Light Onset ◽  
Insulin Levels ◽  
Fat Stores ◽  
Plasma Insulin Levels

The ability of timed daily increases in ambient temperature (from 22 +/- 1 degree C to 40 +/- 1 degree C for 2 h) to alter body fat stores, blood lipid levels, and insulin resistance were tested in male Holtzman rats. Of the six times of day tested only temperature pulses administered 16 h after light onset consistently decreased body weights, retroperitoneal fat stores, and plasma insulin levels. Subsequently, temperature pulses were administered either 0 (TP0) or 16 (TP16) h after light onset (light-dark 12:12 h). While no differences were observed between the TP0 group and the constant temperature (22 degrees C) controls, decreases in body weight gain, food consumption, retroperitoneal fat stores, and plasma concentrations of insulin, cholesterol, and triglycerides were consistently observed in the TP16 group. Although changes in plasma glucose during an oral glucose tolerance test were similar when the two treatment groups were compared with their respective controls, glucose tolerance was achieved with less insulin in the TP16 animals than in their respective controls. Insulin effectiveness was greater in the TP16 group as indicated by a decrease in plasma glucose, after insulin injection, that was of greater magnitude and longer duration than in controls. Hence, timed daily increases in ambient temperature may decrease obesity in part by decreasing plasma insulin levels apparently as a consequence of increased tissue sensitivity to insulin (greater glucose tolerance and less insulin intolerance). Because the treatment is effective only at a particular time of day the findings support a role for circadian neuroendocrine interactions in the regulation of these metabolic states.

Swim training alters sympathoadrenal and endocrine responses to hemorrhage in borderline hypertensive rats

1995 ◽  
Vol 269 (1) ◽  
pp. R124-R130
Author(s):  
D. E. McCoy ◽  
J. E. Steele ◽  
R. H. Cox ◽  
R. L. Wiley
Keyword(s):  
Plasma Glucose ◽  
Plasma Insulin ◽  
Rest Period ◽  
Endocrine Function ◽  
Plasma Norepinephrine ◽  
Hypertensive Rats ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Plasma Insulin Levels ◽  
Positive Correlations

Swim training alters cardiovascular, sympathoadrenal, and endocrine responses to hemorrhage in borderline hypertensive rats (BHR). The effects of 10, 20, and 30% blood volume hemorrhages on cardiovascular, sympathoadrenal, and endocrine function in swim-trained (T; 2 h/day, 5 day/wk for 10-12 wk) and age-matched, untrained, sedentary, control (UT) borderline hypertensive rats (BHR) were assessed. Heart rate (HR) in UT BHR was significantly greater during the baseline (rest) period than T BHR. HR increased slightly from baseline in both groups after 10% hemorrhage but was significantly decreased in both groups after 20 and 30% hemorrhages. The decrease was eliminated by atropine (1 mg/kg iv). Systolic (SBP) and diastolic (DBP) blood pressures decreased significantly after 20 and 30% hemorrhages in both T and UT BHR but were not different between the groups at these times. Plasma norepinephrine levels were significantly increased above baseline after 20 and 30% hemorrhages in UT BHR and were significantly greater in UT BHR than T BHR after 30% hemorrhage. Plasma glucose levels increased significantly after 30% hemorrhage in both groups but were significantly greater in UT BHR than T BHR. Both plasma norepinephrine and plasma epinephrine levels showed strong positive correlations with plasma glucose. After 20 and 30% hemorrhages, plasma insulin levels were unchanged in T BHR but were significantly decreased in UT BHR. Plasma insulin levels were significantly less in UT than T BHR after 30% hemorrhage. These results suggest that swim training alters the effect that hemorrhage exerts on endocrine and sympathoadrenal function in BHR.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of standard oral glucose loading on aldosterone secretion in primary hyperaldosteronism

1982 ◽  
Vol 101 (1) ◽  
pp. 66-71 ◽  
Author(s):  
C. Beretta-Piccoli ◽  
P. Weidmann ◽  
J. J. Brown ◽  
R. Fraser ◽  
A. F. Lever ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Plasma Insulin ◽  
Plasma Potassium ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
Primary Hyperaldosteronism ◽  
Oral Glucose ◽  
Aldosterone Secretion ◽  
Glucose Loading ◽  
Glucose Ingestion

Abstract. The effects of mild acute decreases in plasma potassium induced by standard oral glucose loading (100 g) on plasma aldosterone and renin levels were assessed in 10 patients with primary hyperaldosteronism as compared with 10 normal subjects. Following overnight fast, mean plasma glucose was identical in both groups; plasma insulin, potassium and renin levels were lower and plasma aldosterone higher in patients than in controls. Glucose loading significantly increased plasma glucose and insulin concentrations and decreased plasma potassium and aldosterone levels in both groups. The increases in plasma insulin and the decreases in plasma potassium or aldosterone tended to be blunted in primary hyperaldosteronism. Glucose-induced changes in plasma aldosterone correlated significantly (P < 0.025) with those in plasma potassium in the patients and with variations in plasma renin activity in the normal subjects. These findings suggest that the metabolic changes induced by glucose ingestion are capable of modifying aldosterone secretion in primary hyperaldosteronism. However, the glucose-induced decreases in plasma aldosterone are blunted in this disorder; this could be related to the impaired insulin response to glucose loading.

scholarly journals Plasma corticosterone, insulin and glucose changes induced by brief exposure to isoflurane, diethyl ether and CO2 in male rats

2010 ◽  
Author(s):  
H Zardooz ◽  
F Rostamkhani ◽  
J Zaringhalam ◽  
F Faraji Shahrivar
Keyword(s):  
Diethyl Ether ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Plasma Corticosterone ◽  
Male Rats ◽  
Insulin Levels ◽  
Short Term Exposure ◽  
Plasma Insulin Levels ◽  
The Impact ◽  
Fasted Rats

The impact of anesthetic agents on endocrine and metabolic factors is an important issue. The present study has compared the effects of a short-term exposure to diethyl ether, isoflurane, or CO2 on plasma corticosterone, insulin and glucose concentrations since the duration of anesthetic exposure may have an effect on those factors. Male rats were divided into fed and fasted groups. The experimental rats were briefly exposed to diethyl ether, isoflurane, or CO2 (the degree of anesthesia was identical), while a control group was not exposed to the anesthetics. In the fed rats, diethyl ether exposure increased the levels of plasma glucose. CO2 exposure decreased plasma corticosterone and increased plasma glucose levels. Isoflurane exposure caused no changes in plasma corticosterone, glucose, or insulin levels. In the fasted rats, diethyl ether exposure increased plasma corticosterone and reduced plasma insulin levels. The plasma corticosterone and insulin levels were significantly increased by CO2 exposure. Isoflurane exposure decreased plasma insulin levels. A brief exposure to either diethyl ether or CO2 changed the plasma corticosterone, glucose, and insulin levels in fed and/or fasted rats. However, isoflurane exposure had the least effect on the concentration of these factors in both the fed and fasted states.

EFFECTS OF DIPHENYLHYDANTOIN ON BLOOD GLUCOSE AND PLASMA INSULIN LEVELS IN NORMAL SUBJECTS

Abstracts ◽  
1978 ◽  
pp. 182
Author(s):  
C. Scandellari ◽  
M. Zaccaria ◽  
N. Sicolo ◽  
G. Erie ◽  
A. Basso ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Plasma Insulin ◽  
Normal Subjects ◽  
Insulin Levels ◽  
Plasma Insulin Levels

Pre- and postabsorptive insulin secretion in chronic decerebrate rats

1986 ◽  
Vol 250 (4) ◽  
pp. R539-R548 ◽  
Author(s):  
F. W. Flynn ◽  
K. C. Berridge ◽  
H. J. Grill
Keyword(s):  
Insulin Secretion ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Oral Glucose ◽  
Base Line ◽  
Intravenous Glucose ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Percent Change ◽  
Plasma Insulin Levels

Basal, taste-stimulated (preabsorptive), and postabsorptive insulin secretion and plasma glucose responses were studied in chronic decerebrate rats and their pair-fed neurologically intact controls. In experiment 1, preabsorptive insulin responses (PIR) elicited by oral infusions of glucose solution was measured in chronic decerebrate rats. Oral glucose was ingested and led to a significant short-latency elevation in plasma insulin levels. Plasma glucose levels remained constant during this time. These data show that caudal brain stem mechanisms, in isolation of the forebrain, are sufficient for the neurally mediated PIR elicited by oral glucose stimulation. In experiment 2, effects of decerebration on postabsorptive insulin secretion were measured. During the 3 h immediately after transection there was no effect of decerebration on peripheral plasma insulin or glucose levels. Thereafter, however, basal plasma insulin levels of decerebrate rats were at least twice that of control rats. Plasma glucose levels of both groups remained identical despite the hyperinsulinemia in decerebrate rats. Atropine treatment decreased, and phentolamine administration elicited a greater absolute and percent change increase in insulin levels of decerebrate rats. These data indicate that altered autonomic tone contributes to maintaining the basal hyperinsulinemia in the decerebrate rat. In response to intragastric meals and glucose and intravenous glucose administration, insulin secretion was greater in decerebrate than in control rats. Percent change in insulin levels from base line was similar in both groups after intragastric meals and intravenous glucose. In response to intragastric glucose, however, percent increase in insulin levels was greater in decerebrate rats. Decerebrate rats demonstrated mild glucose intolerance after intragastric and intravenous treatments. These results are contrasted with the known effects of ventromedial hypothalamic lesions on insulin secretion and glucose homeostasis.

Oscillations of plasma K+ and insulin during K+ infusion in awake anephric dogs

1982 ◽  
Vol 243 (1) ◽  
pp. F44-F52 ◽  
Author(s):  
R. H. Sterns
Keyword(s):  
Plasma Insulin ◽  
Average Rate ◽  
Plasma Potassium ◽  
Regulatory Control ◽  
Control Loop ◽  
K Uptake ◽  
Insulin Levels ◽  
Constant Rate ◽  
Physiological Feedback ◽  
Plasma Insulin Levels

Changes in plasma potassium ([K+]p) and insulin levels were monitored during K+ infusion in awake and anesthetized nephrectomized, splenectomized dogs. In dogs studied while anesthetized with pentobarbital, the increase in [K+]p was linear, reflecting a nearly constant rate of cellular uptake of the infused K+. In contrast, in dogs studied 18 h after nephrectomy while awake, [K+]p oscillated during infusion, reflecting an inconstant rate of cellular K+ uptake. Although these oscillations in [K+]p were associated with parallel oscillations in plasma insulin levels (suggesting the possibility of a physiological feedback control loop involving K+ and insulin), when the oscillations in insulin levels were blunted by somatostatin infusion or abolished by pancreatectomy plus insulin replacement, oscillations in [K+]p persisted and the average rate of cellular K+ uptake was not diminished. The observed oscillations of [K+]p during K+ infusion suggest the possibility of regulatory control of cellular K+ uptake within the pathophysiologic range of [K+]p. The putative control system is independent of and quantitatively more important than K+-induced insulin secretion and is obscured by pentobarbital anesthesia.

Effect of adrenal demedullation and (or) physical training on glucose tolerance in the rat

1993 ◽  
Vol 71 (12) ◽  
pp. 931-937 ◽  
Author(s):  
Christine Jean ◽  
Gilles Tancrède ◽  
André Nadeau
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Plasma Glucose ◽  
Physical Training ◽  
Plasma Insulin ◽  
Intravenous Glucose ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Basal Plasma ◽  
Plasma Insulin Levels

Physical training increases insulin sensitivity by mechanisms not yet fully understood. Because exercise also modulates adrenergic system activity, the present study was designed to ascertain whether the improved glucose homeostasis observed in trained rats is influenced by epinephrine secretion from the adrenal medullae. Male Wistar rats previously submitted to adrenal demedullation or sham operated were kept sedentary or trained on a treadmill over a 10-week period. An intravenous glucose tolerance test (IVGTT) was done 64 h after the last bout of exercise. Basal plasma glucose levels were reduced by physical training (p < 0.005) and by adrenal demedullation (p < 0.001). Adrenodemedullated rats had lower (p < 0.005) plasma glucose levels than sham-operated animals over the whole glucose tolerance curve. Trained animals had lower (p < 0.01) plasma glucose levels than sedentary rats throughout the IVGTT, except at 45 min. The glucose disappearance rate measured after the glucose bolus injection was increased by training (p < 0.05), whereas it was not modified by adrenal demedullation. Basal plasma insulin levels were reduced (p < 0.001) by physical training but unaffected by adrenal demedullation. During the IVGTT, adrenodemedullated rats had higher (p < 0.01) plasma insulin levels at 2, 4, and 6 min, whereas trained animals had lower (p < 0.05) plasma insulin levels throughout the test. Moreover, insulin in adrenodemedullated and trained rats had returned to basal levels at 30 min. The area under the curve for insulin was diminished by physical training (p < 0.001) but was not modified by adrenal demedullation. In the basal state and during the IVGTT, the sedentary adrenodemedullated rats had higher (p < 0.05) plasma glucagon levels compared with the other groups of animals. Pancreatic insulin content was not modified by adrenal demedullation but was diminished (p < 0.01) by physical training. The pancreatic glucagon content was not altered by adrenal demedullation or physical training. Because adrenal demedullation abolished the exercise-induced increase in epinephrine secretion, the results of the present study suggest that the enhanced insulin sensitivity induced by physical training is not caused by an increase in epinephrine secretion from the adrenal medullae.Key words: adrenal demedullation, physical training, glucose tolerance, insulin sensitivity, catecholamines.

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