2003
DOI: 10.1007/s11906-003-0065-2
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The effect of aldosterone on glucose metabolism

Abstract: There is an association of glucose intolerance and diabetes with primary aldosteronism, but the frequency and mechanisms are not clear. This paper reviews the possible mechanisms of impaired glucose metabolism in primary aldosteronism. Patients with primary aldosteronism can have impaired pancreatic insulin release and reduction in insulin sensitivity. These effects may be due to hypokalemia, but the evidence suggests other factors such as a direct impact of excess aldosterone on insulin action in contributing… Show more

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Cited by 86 publications
(67 citation statements)
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“…in 20,21). It was initially thought that the cause leading to glucose intolerance in conditions characterized by increased plasma aldosterone, such as primary aldosteronism, is potassium depletion, which could modulate both pancreatic insulin secretion and insulin receptor function (22,23).…”
Section: Discussionmentioning
confidence: 99%
“…in 20,21). It was initially thought that the cause leading to glucose intolerance in conditions characterized by increased plasma aldosterone, such as primary aldosteronism, is potassium depletion, which could modulate both pancreatic insulin secretion and insulin receptor function (22,23).…”
Section: Discussionmentioning
confidence: 99%
“…In the last few years, several studies highlighted the negative effects of aldosterone excess on the heart, the blood vessels, the kidney, and the brain (4,5), as well as on the glucose metabolism and insulin sensitivity (6,7), indicating the need for a prompt diagnosis of PA and a correct therapeutic approach. While the treatment of choice for APA is unilateral adrenalectomy (8,9), medical therapy is the best treatment for idiopathic hyperaldosteronism due to adrenal hyperplasia (9)(10)(11).…”
Section: Introductionmentioning
confidence: 99%
“…It is well known that hyperaldosteronism-associated hypokalemia impairs insulin secretion 16,17 and that this defect is only partially reversible after reestablishment of normal plasma K +18 . Induction of hyperaldosteronism in mouse models of diabetes leads to worsening of glucose tolerance, decreased beta-cell mass, and increased oxidative stress markers 19,20 .…”
Section: Aldosterone Mcr and Beta-cell Functionmentioning
confidence: 99%