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Abdominal obesity is associated with potassium depletion and changes in glucose homeostasis during diuretic therapy.

Published on Jun 1, 2008in Journal of Clinical Hypertension2.444
· DOI :10.1111/j.1751-7176.2008.07817.x
Lydia Sebba Souza Mariosa2
Estimated H-index: 2
(UNIFESP: Federal University of São Paulo),
Fernando Flexa Ribeiro-Filho10
Estimated H-index: 10
(UNIFESP: Federal University of São Paulo)
+ 4 AuthorsMaria Teresa Zanella19
Estimated H-index: 19
(UNIFESP: Federal University of São Paulo)
Abstract
The activation of the renin-angiotensin system (RAS) is an important mechanism that contributes to hypertension in obese individuals. Thiazide diuretics also activate the RAS in response to volume contraction and can lead to a decrease in serum potassium values and glucose metabolism abnormalities. To evaluate the impact of abdominal obesity on potassium depletion and glucose homeostasis in hypertensive patients receiving thiazide therapy, the authors studied 329 hypertensive patients without known diabetes or impaired renal function. Patients were stratified into 2 major groups according to whether they used thiazide diuretic therapy, and each group was further divided in 2 subgroups according to the presence of abdominal obesity. The authors demonstrated that obese patients receiving diuretic therapy had lower plasma potassium levels and higher glucose values compared with nonobese patients receiving diuretic therapy. In conclusion, abdominal obesity predisposes to potassium depletion during diuretic therapy in association with effects on glucose homeostasis.
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