Cited by 63Potassium and Related DisordersSodium Intake and HealthIon Transport and Channel Regulation

Gut sensing of potassium intake and its role in potassium homeostasis

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Youn, Jang H.·2013·Seminars in Nephrology

Abstract

Extracellular K(+) homeostasis has been explained by feedback mechanisms in which changes in extracellular K(+) concentration drive renal K(+) excretion directly or indirectly via stimulating aldosterone secretion. However, this cannot explain meal-induced kaliuresis, which often occurs without increases in plasma K(+) or aldosterone concentrations. Recent studies have produced evidence supporting a feedforward control in which gut sensing of dietary K(+) increases renal K(+) excretion (and extrarenal K(+) uptake) independent of plasma K(+) concentrations, namely, a gut factor. This review focuses on these new findings and discusses the role of gut factor in acute and chronic regulation of extracellular K(+) as well as in the beneficial effects of high K(+) intake on the cardiovascular system.

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Crossref · 10.1016/j.semnephrol.2013.04.005

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  • K+ intake activates a feedforward control in which distal tubule K+ secretion is stimulated before changes in plasma K+ concentration or aldosterone concentration can be observed.

    “K+ intake has been shown to activate a feedforward control in which distal tubule K+ secretion is stimulated before changes in plasma K+ concentration or ALD concentration can be observed [1, 15–18].”

    From A mathematical model of potassium homeostasis: Effect of feedforward and feedback controls (2022) · cites this paper as [18]

    The “Feedforward control of K+ homeostasis” section says sensing K+ intake can increase renal K+ excretion without or before increases in plasma K+ or aldosterone. The “Gut sensing of K+ stimulates kaliuresis after a meal” section likewise reports excretion independent of those regulators. The paper does not establish that the feedforward response specifically stimulates distal-tubule K+ secretion; it describes that mechanism as a potential explanation for meal-induced excretion. (LLM, conf=0.84)

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References 65 · Cited by 63

Authors
Youn, J. H.
Affiliations
University of Southern California (US)
Corresponding author
Youn, Jang H.
Venue
Seminars in Nephrology
Publisher
Elsevier BV
Published
2013-05
Volume
33
Issue
3
Pages
248-256
ISSN
0270-9295 (ISSN-L)
OpenAlex
W2006720127
Cited by
63
References
65
Citations by year
2026: 6 · 2025: 4 · 2024: 2 · 2023: 5 · 2022: 9 · 2021: 4 · 2020: 5 · 2019: 4 · 2018: 2 · 2017: 8 · 2016: 5 · 2015: 7 · 2014: 2
FWCI
0.73
Type
journal article
Language
en
Open access
Locations
  • Seminars in Nephrology (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute of Diabetes and Digestive and Kidney Diseases (DK090749, R21DK090749)
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Potassium and Related Disorders
  • Health Sciences › Nursing › Nutrition and Dietetics › Sodium Intake and Health
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
Keywords
potassium homeostasis, potassium intake, renal potassium excretion, feedforward control, aldosterone
MeSH terms
Animals, Gastrointestinal Hormones, Homeostasis, Humans, Insulin, Potassium, Potassium, Dietary

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