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January 1, 1982Clinical and Experimental Hypertension Part A Theory and Practice2 citations

Effect of Oral Glucose Loading on Plasma Insulin, Potassium, Renin and Aldosterone in Normal Subjects and Patients with Primary Hyperaldosteronism

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CBC Beretta-PiccoliPWP WeidmannMBMario G. Bianchetti

Structured PICO

Does oral glucose loading affect plasma aldosterone and regulatory factors differently in patients with primary hyperaldosteronism compared to normal subjects?

P
Population
10 patients with primary hyperaldosteronism and 10 normal subjects approximately matched per age and sex, plus an additional group of 21 normal subjects.
I
Intervention
Standard oral glucose loading (100 g)
C
Comparator
Normal subjects (for the hyperaldosteronism group) and baseline pre-loading values
O
Outcome
Changes in plasma aldosterone, insulin, potassium, and renin activitysurrogate

Oral glucose loading induces complex metabolic changes that modify aldosterone secretion, with a blunted inhibitory effect in primary hyperaldosteronism potentially related to an impaired insulin response.

Abstract

The effects of standard oral glucose loading (100 g) on plasma aldosterone and some regulatory factors were assessed in patients with primary hyperaldosteronism and normal subjects. Following overnight fast, mean plasma glucose was identical (10 patients and normal subjects approximately matched per age and sex); plasma insulin, potassium and renin levels were lower and plasma aldosterone higher in the patients. Glucose loading significantly increased plasma glucose and insulin concentrations and decreased plasma potassium and aldosterone levels in both groups; plasma renin activity was significantly increased only in normal subjects. The increases in plasma insulin and the decreases in plasma potassium or aldosterone tended to be blunted in primary hyperaldosteronism. Relationships among glucose-induced changes in plasma aldosterone and other factors were assessed by multiple regression analysis in these patients and normal subjects as well as an additional group of 21 normal subjects; in the latter, plasma cortisol was also measured and found to decrease significantly after glucose loading. Changes in plasma aldosterone correlated (P less than 0.025) more closely with those in plasma potassium in the patients and with variations in plasma renin activity in the normal subjects. These findings suggest that complex metabolic changes occur following glucose ingestion which are capable of modifying aldosterone secretion in normal subjects and primary hyperaldosteronism. The aldosterone-inhibitory effect of glucose tends to be blunted in the latter disorder. This could be related at least in part to an impaired insulin response in primary hyperaldosteronism.

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Beretta-Piccoli et al. (1982) studied this question.

synapsesocial.com/papers/6a1be904ea84844e355f2aa8https://doi.org/10.3109/10641968209061624
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Potassium-Aldosterone-Renin Interrelationships1975 · 188 citations
  2. 2The Plasma Aldosterone Response to Angiotensin II Infusion in Aldosterone-Producing Adenoma and Idiopathic Hyperaldosteronism*1981 · 101 citations
  3. 3Control of Aldosterone Secretion1979 · 140 citations
  4. 4Plasma Renin Activity in Relation to Serum Sodium Concentration and Body Fluid Balance1968 · 57 citations
  5. 5Presence of Insulin-Renin-Aldosterone-Potassium Interrelationship in Normal Subjects, Disrupted in Chronic Hemodialysis Patients1978 · 9 citations