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.

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.

scholarly journals The effect of ispaghula (Fybogel and Metamucil) and guar gum on glucose tolerance in man

1984 ◽  
Vol 51 (3) ◽  
pp. 371-378 ◽  
Author(s):  
H. A. Jarjis ◽  
N. A. Blackburn ◽  
J. S. Redfern ◽  
N. W. Read
Keyword(s):  
Gastric Emptying ◽  
Glucose Tolerance ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Guar Gum ◽  
Normal Subjects ◽  
Oral Glucose ◽  
Diabetic Patients ◽  
Glucose Plasma ◽  
Insulin Responses

1. The effects of incorporating Fybogel (3·5 and 7 g doses), Metamucil (7 g) or guar gum (2·5 and 14·5 g doses) in a drink containing 50 g glucose on plasma glucose, plasma insulin and gastric emptying were studied in thirty-eight normal volunteers. In addition, the effects of Fybogel (7 g) on glucose tolerance, plasma insulin and gastric emptying were measured in fourteen non-insulin-dependent diabetics.2. Both doses of guar gum significantly lowered plasma glucose and plasma insulin responses to the oral glucose load in normal subjects, although 14·5 g guar gum did not delay the half-time for gastric emptying.3. Neither Fybogel nor Metamucil had significant effects on plasma glucose responses in normal subjects. In addition, Fybogel (at either dose) had no significant effects on plasma insulin levels, or on gastric emptying in normal subjects or on plasma glucose and insulin responses in diabetic patients.4. The viscosity of ispaghula solutions (Fybogel) was lower than that of guar gum solutions.

Studies on the mechanism of acute glucose-induced aldosterone suppression. Role of corticotrophin

1983 ◽  
Vol 103 (3) ◽  
pp. 391-399 ◽  
Author(s):  
Claudia P. Ferrier ◽  
Mario G. Bianchetti ◽  
Carlo Beretta-Piccoli ◽  
Ladislav Link ◽  
Claude Bachman ◽  
...  
Keyword(s):  
Plasma Concentrations ◽  
Plasma Potassium ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Oral Glucose ◽  
Loading Test ◽  
Glucose Loading ◽  
Group A ◽  
Group B

Abstract. A possible role of corticotrophin in mediating the acute glucose-induced suppression of plasma aldosterone was assessed in two groups of normal subjects (group A, N = 9 and group B, N = 10), by studying the effects of a standard oral glucose loading test on plasma concentrations of glucose, insulin, cortisol, potassium, aldosterone and renin activity, a) under basal conditions (groups A and B), b) after 2 days of dexamethasone (0.5 mg/6 h) (group A), c) after 8 weeks of treatment with the diuretic indapamide, 2.5 mg/day (group B) and d) after additional 2 days of combined administration of indapamide and dexamethasone (0.5 mg/6 h) (group B). In addition, the spontaneous daytime related variations of these parameters were assessed in group A in a control study without glucose loading. Under basal conditions, the acute increase in plasma glucose and insulin was accompanied by a significant decrease of plasma potassium (P < 0.01), cortisol (P < 0.01) and by a slight increase in plasma renin activity. None of these changes occurred in the control experiment without glucose loading. Dexamethasone caused a significant decrease in pre-loading plasma aldosterone. Indapamide caused a significant decrease in pre-loading plasma potassium and a marked stimulation of renin and aldosterone. After combined indapamide-dexamethasone administration, pre-loading plasma aldosterone decreased to control values. Glucose loading under dexamethasone or combined indapamide-dexamethasone administration caused a similar suppression of plasma aldosterone as observed under control conditions. These findings suggest that corticotrophin does not play an important role in mediating the acute aldosterone inhibitory effect of glucose loading. However, corticotrophin may contribute to the maintenance of the secondary hyperaldosteronism induced by diuretic treatment.

Carbohydrate ingestion before exercise: comparison of glucose, fructose, and sweet placebo

1981 ◽  
Vol 51 (4) ◽  
pp. 783-787 ◽  
Author(s):  
V. A. Koivisto ◽  
S. L. Karonen ◽  
E. A. Nikkila
Keyword(s):  
Plasma Glucose ◽  
Plasma Insulin ◽  
Cycle Ergometer ◽  
Vo2 Max ◽  
Vigorous Exercise ◽  
Carbohydrate Ingestion ◽  
Rapid Fall ◽  
Ergometer Exercise ◽  
Glucose Ingestion ◽  
Response To Exercise

To examine the effect of various carbohydrates on the metabolic and hormonal response to exercise, 75 g glucose, fructose, or placebo were given to nine well-trained males (VO2 max 60 +/- 1 ml . kg-1 . min-1) 45 min before cycle ergometer exercise performed at 75% VO2 max for 30 min. After glucose ingestion, the rise in plasma glucose was 3-fold (P less than 0.005) in plasma insulin 2.5-fold (P less than 0.01) greater than after fructose. During exercise, after glucose administration plasma glucose fell from 5.3 +/- 0.3 to 2.5 +/- 0.2 mmol/l (P less than 0.001) and after fructose from 4.5 +/- 0.1 to 3.9 +/- 0.3 mmol/l (P less than 0.05). The fall in plasma glucose was closely related to the preexercise levels of plasma insulin (r = 0.82, P less than 0.001) and glucose (r = 0.81, P less than 0.001). Both glucose and fructose ingestion decreased the FFA levels by 40–50% (P less than 0.005) and during exercise they remained 30–40% lower after carbohydrate than placebo administration (P less than 0.02). This study suggests that glucose ingestion prior to exercise results in hypoglycemia during vigorous exercise, this rapid fall in plasma glucose is mediated, at least in part, by hyperinsulinemia, and fructose ingestion is associated with a modest rise in plasma insulin and does not result in hypoglycemia during exercise.

Adrenocortical hormone secretory response to chronic NH4Cl-induced metabolic acidosis

1987 ◽  
Vol 252 (4) ◽  
pp. E454-E460 ◽  
Author(s):  
M. Schambelan ◽  
A. Sebastian ◽  
B. A. Katuna ◽  
E. Arteaga
Keyword(s):  
Metabolic Acidosis ◽  
Urinary Excretion ◽  
Potassium Concentration ◽  
Control Period ◽  
Plasma Potassium ◽  
Plasma Aldosterone ◽  
Aldosterone Secretion ◽  
Plasma Aldosterone Concentration ◽  
Hydrogen Ion Concentration ◽  
Adrenocortical Hormone

We examined the effect of chronic metabolic acidosis on adrenocortical hormone production by administering NH4Cl for 5 days to four normal subjects. Plasma aldosterone concentration, aldosterone secretion, and urinary excretion of aldosterone-18-glucuronide increased significantly, whereas there were no significant changes in the plasma concentrations of cortisol, corticosterone, or deoxycorticosterone, or in the urinary excretion of 17-hydroxycorticoids. By day 2, plasma renin activity (PRA) and concentration (PRC) were not significantly different from control, and the slope of the regression line relating plasma aldosterone concentration to PRA was significantly greater than the slope in the control period, i.e., the sensitivity of aldosterone secretion to renin stimulation was increased. By day 5, however, PRA and PRC were increased above control. Plasma potassium concentration did not change significantly. Thus chronic NH4Cl-induced acidosis induces a sustained stimulation of aldosterone secretion in the absence of a change in adrenocorticotropin-dependent adrenocortical hormone secretion. Factors other than an increase in renin secretion and plasma potassium concentration may be involved in at least the early phase of aldosterone stimulation, suggesting that plasma hydrogen ion concentration might be a separate regulator of aldosterone secretion.

Effects of acute α2-blockade on insulin action and secretion in humans

1998 ◽  
Vol 274 (1) ◽  
pp. E57-E64 ◽  
Author(s):  
Andrea Natali ◽  
Amalia Gastaldelli ◽  
Alfredo Quiñones Galvan ◽  
Anna Maria Sironi ◽  
Demetrio Ciociaro ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Energy Expenditure ◽  
Plasma Insulin ◽  
Time Course ◽  
Resting Energy Expenditure ◽  
Oral Glucose ◽  
Cardiac Work ◽  
C Peptide ◽  
Glucose Ingestion ◽  
Resting Energy

We tested whether acute α2-blockade affects insulin secretion, glucose and fat metabolism, thermogenesis, and hemodynamics in humans. During a 5-h epinephrine infusion (50 ng ⋅ min−1 ⋅ kg−1) in five volunteers, deriglidole, a selective α2-receptor inhibitor, led to a more sustained rise in plasma insulin and C-peptide levels (+59 ± 14 vs. +28 ± 6, and +273 ± 18 vs. +53 ± 14 pM, P < 0.01 vs. placebo) despite a smaller rise in plasma glucose (+0.90 ± 0.4 vs. +1.5 ± 0.3 mM, P < 0.01). Another 10 subjects were studied in the postabsorptive state and during a 4-h hyperglycemic (+4 mM) clamp, coupled with the ingestion of 75 g of glucose at 2 h. In the postabsorptive state, hepatic glucose production, resting energy expenditure, and plasma insulin, free fatty acid (FFA), and potassium concentrations were not affected by acute α2-blockade. Hyperglycemia elicited a biphasic rise in plasma insulin (to a peak of 140 ± 24 pM), C-peptide levels (1,520 ± 344 pM), and insulin secretion (to 410 ± 22 pmol/min); superimposed glucose ingestion elicited a further twofold rise in insulin and C-peptide levels, and insulin secretion. However, α2-blockade failed to change these secretory responses. Fasting blood β-hydroxybutyrate and glycerol and plasma FFA and potassium concentrations all declined with hyperglycemia; time course and extent of these changes were not affected by α2-blockade. Resting energy expenditure (+25 vs. +16%, P < 0.01) and external cardiac work (+28% vs. +19%, P < 0.01) showed larger increments after α2-blockade. We conclude that acute α2-blockade in humans 1) prevents epinephrine-induced inhibition of insulin secretion, 2) does not potentiate basal or intravenous- or oral glucose-induced insulin release, 3) enhances thermogenesis, and 4) increases cardiac work.

scholarly journals Glucose–insulin relationships and thyroid status of cockerels selected for high or low residual food consumption

2000 ◽  
Vol 83 (6) ◽  
pp. 645-651 ◽  
Author(s):  
Jean-François Gabarrou ◽  
Pierre Andre Geraert ◽  
John Williams ◽  
Laurent Ruffier ◽  
Nicole Rideau
Keyword(s):  
Food Consumption ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Plasma Concentrations ◽  
Insulin Concentration ◽  
Glucose Disposal ◽  
Oral Glucose ◽  
Thyroid Status ◽  
Plasma Insulin Concentration ◽  
Diet Induced Thermogenesis

The plasma glucose–insulin relationships and thyroid status were investigated in two lines of adult cockerels divergently selected for high (R+) or low (R-) residual food consumption (RFC). For a given body weight, R+ birds had a 74 % higher food intake than R- birds. Plasma glucose concentrations were significantly lower in the R+ line compared with the R- when fasted, whereas R+ birds exhibited a significantly lower plasma insulin concentration than R- birds either in fed or fasted state. After an overnight fast, R+ birds also exhibited a higher sensitivity to exogenous insulin in view of its more pronounced hypoglycaemic effect. After an oral glucose load, the glucose disposal of R+ cockerels was faster despite lower glucose-induced plasma insulin concentration. Whilst plasma triacylglycerol concentrations were lower in the R+ line when fed, plasma non-esterified fatty acid concentrations were higher in fasted R+ than R- cockerels (684v.522 μmol/l). Higher plasma triiodothyronine concentrations were observed in fed R+ compared with R- birds (3·0v.2·1 nmol/l respectively). The higher plasma concentrations of triiodothyronine associated with lower concentrations of insulin could account for the leanness and the elevated diet-induced thermogenesis previously observed in the R+ line.

Sensitivity of insulin secretion to feedback inhibition by hyperinsulinaemia

1981 ◽  
Vol 98 (1) ◽  
pp. 81-86 ◽  
Author(s):  
Ralph A. DeFronzo ◽  
Christian Binder ◽  
John Wahren ◽  
Philip Felig ◽  
Eleuterio Ferrannini ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Feedback Inhibition ◽  
Normal Subjects ◽  
Insulin Concentration ◽  
Plasma Insulin Concentration ◽  
C Peptide ◽  
Endogenous Insulin ◽  
Arterial Plasma

Abstract. The ability of insulin to inhibit its own secretion was examined in 15 normal subjects given an intravenous infusion of insulin in a dose of 0.25, 0.50, 1.0, 5.0 or 10.0 mU/kg/min for two hours. Arterial plasma insulin concentration achieved during the infusion segregated into three levels of hyperinsulinaemia: 35 ± 1 (mean ± sem), 87 ± 15 and 828 ± 210 μU/ml. Plasma glucose concentration was kept constant at the basal level by a variable glucose infusion. Fasting C-peptide (0.29 ± 0.02 pmol/ml) fell significantly in all subjects during hyperinsulinaemia and reached a concentration of 0.19 ± 0.03 pmol/ml at 60 min and 0.14 ± 0.03 at 120 min after the start of the insulin infusion. The C-peptide response was not related to the infusion dose nor to the steady state plasma insulin concentration. It is concluded that (a) basal insulin secretion as evaluated from C-peptide measurements is inhibited by small (24 ± 3 μU/ml) physiological elevations in plasma insulin concentration independent of changes in plasma glucose, and (b) supraphysiological or even pharmacological elevations in plasma insulin do not result in a further decrease in endogenous insulin secretion above that achieved with mild hyperinsulinaemia.

Glucose intolerance in thyrotoxicosis roles of insulin, glucagon and somatostatin

1987 ◽  
Vol 114 (2) ◽  
pp. 228-234 ◽  
Author(s):  
Karen S. L. Lam ◽  
Rose T. T. Yeung ◽  
Patricia W. M. Ho ◽  
S. K. Lam
Keyword(s):  
B Cell ◽  
Glucose Intolerance ◽  
Plasma Glucose ◽  
Insulin Response ◽  
Oral Glucose ◽  
Insulinogenic Index ◽  
C Peptide ◽  
Pancreatic B Cell ◽  
Significant Difference ◽  
Glucose Ingestion

Abstract. The responses in plasma glucose, insulin, C-peptide, glucagon and somatostatin to an oral glucose load were studied in 10 thyrotoxic patients and 10 matched euthyroid controls. The thyrotoxic patients had higher mean fasting plasma glucose (P < 0.05) and responded to oral glucose with an earlier peak at 30 min which was higher than the corresponding glucose level in the controls (P < 0.05). Impaired glucose tolerance was found in 3 patients. Fasting insulin and C-peptide levels were normal in the thyrotoxic patients when corrected for the higher glucose levels. Following glucose ingestion, there was no significant difference between the areas under the insulin or C-peptide curves in patients and controls, but Seltzer's insulinogenic index was reduced in the patients (P < 0.01) suggesting an impaired pancreatic B-cell response to oral glucose. Mean basal glucagon was normal in the thyrotoxic patients. However, while in the controls plasma glucagon became suppressed following glucose ingestion (P < 0.0001), no significant suppression was found in the patients. In the thyrotoxic patients, mean basal somatostatin was normal, but the area under the somatostatin curve following glucose ingestion was significantly increased (P < 0.02). Our findings suggest that décreased glucagon suppression and impaired insulin response after glucose ingestion are involved in glucose intolerance in thyrotoxicosis. Enhanced somatostatin responses to oral glucose in thyrotoxicosis may have contributed to the observed impairment in pancreatic B-cell responsiveness.

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