Document Detail


Gut sensing of dietary K⁺ intake increases renal K⁺excretion.
MedLine Citation:
PMID:  21543632     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Dietary K(+) intake may increase renal K(+) excretion via increasing plasma [K(+)] and/or activating a mechanism independent of plasma [K(+)]. We evaluated these mechanisms during normal dietary K(+) intake. After an overnight fast, [K(+)] and renal K(+) excretion were measured in rats fed either 0% K(+) or the normal 1% K(+) diet. In a third group, rats were fed with the 0% K(+) diet, and KCl was infused to match plasma [K(+)] profile to that of the 1% K(+) diet group. The 1% K(+) feeding significantly increased renal K(+) excretion, associated with slight increases in plasma [K(+)], whereas the 0% K(+) diet decreased K(+) excretion, associated with decreases in plasma [K(+)]. In the KCl-infused 0% K(+) diet group, renal K(+) excretion was significantly less than that of the 1% K(+) group, despite matched plasma [K(+)] profiles. We also examined whether dietary K(+) alters plasma profiles of gut peptides, such as guanylin, uroguanylin, glucagon-like peptide 1, and glucose-dependent insulinotropic polypeptide, pituitary peptides, such as AVP, α-MSH, and γ-MSH, or aldosterone. Our data do not support a role for these hormones in the stimulation of renal K(+) excretion during normal K(+) intake. In conclusion, postprandial increases in renal K(+) excretion cannot be fully accounted for by changes in plasma [K(+)] and that gut sensing of dietary K(+) is an important component of the regulation of renal K(+) excretion. Our studies on gut and pituitary peptide hormones suggest that there may be previously unknown humoral factors that stimulate renal K(+) excretion during dietary K(+) intake.
Authors:
Ki-Sook Oh; Young Taek Oh; Sang-Wook Kim; Toshihiro Kita; Insug Kang; Jang H Youn
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-05-04
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  301     ISSN:  1522-1490     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2011 Aug 
Date Detail:
Created Date:  2011-08-03     Completed Date:  2011-10-18     Revised Date:  2013-06-30    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R421-9     Citation Subset:  IM    
Affiliation:
Department of Physiology and Biophysics, University of Southern California, Keck School of Medicine, Los Angeles, California 90089-9142, USA.
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MeSH Terms
Descriptor/Qualifier:
Aldosterone / blood,  metabolism
Amiloride / pharmacology
Animals
Blood Glucose
Gastrointestinal Tract / metabolism*
Gene Expression Regulation / physiology
Kidney / metabolism*
Male
Pituitary Hormones / genetics,  metabolism
Postprandial Period
Potassium / blood*,  metabolism*
Potassium, Dietary / metabolism*
Rats
Rats, Wistar
Sodium / blood
Sodium Channel Blockers / pharmacology
Grant Support
ID/Acronym/Agency:
DK 080233/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/Pituitary Hormones; 0/Potassium, Dietary; 0/Sodium Channel Blockers; 2609-46-3/Amiloride; 52-39-1/Aldosterone; 7440-09-7/Potassium; 7440-23-5/Sodium
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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