Postprandial Effects on ENaC-Mediated Sodium Absorption

Gregory Blass, Christine A. Klemens, Michael W Brands, Oleg Palygin, Alexander Staruschenko

Research output: Contribution to journalArticle

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Abstract

Recent studies have suggested that postprandial increases in insulin directly contribute to reduced urinary sodium excretion. An abundance of research supports the ability of insulin to augment epithelial sodium channel (ENaC) transport. This study hypothesized that ENaC contributes to the increase in renal sodium reabsorption following a meal. To test this, we used fasted or 4 hour postprandial Sprague Dawley rats to analyze ENaC expression and activity. We also assessed total expression of additional sodium transporters (Na + -Cl cotransporter (NCC), Na + -K + -2Cl cotransporter (NKCC2), and Na + -K + -ATPase (NKA)) and circulating hormones involved in the renin-angiotensin-aldosterone system (RAAS). We found that after carbohydrate stimulus, ENaC open probability increased in split-open isolated collecting duct tubules, while ENaC protein levels remained unchanged. This was supported by a lack of change in phosphorylated Nedd4-2, an E3 ubiquitin ligase protein which regulates the number of ENaCs at the plasma membrane. Additionally, we found no differences in total expression of NCC, NKCC2, or NKA in the postprandial rats. Lastly, there were no significant changes in RAAS signaling between the stimulated and fasted rats, suggesting that acute hyperinsulinemia increases ENaC activity independent of the RAAS signaling cascade. These results demonstrate that insulin regulation of ENaC is a potential mechanism to preserve sodium and volume loss following a meal, and that this regulation is distinct from classical ENaC regulation by RAAS.

Original languageEnglish (US)
Article number4296
JournalScientific Reports
Volume9
Issue number1
DOIs
StatePublished - Dec 1 2019
Externally publishedYes

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Renin-Angiotensin System
Sodium
Insulin
Meals
Member 1 Solute Carrier Family 12
Member 3 Solute Carrier Family 12
Sodium-Potassium-Chloride Symporters
Epithelial Sodium Channels
Ubiquitin-Protein Ligases
Hyperinsulinism
Sprague Dawley Rats
Carbohydrates
Cell Membrane
Hormones
Research
Proteins
sodium-translocating ATPase

ASJC Scopus subject areas

  • General

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Postprandial Effects on ENaC-Mediated Sodium Absorption. / Blass, Gregory; Klemens, Christine A.; Brands, Michael W; Palygin, Oleg; Staruschenko, Alexander.

In: Scientific Reports, Vol. 9, No. 1, 4296, 01.12.2019.

Research output: Contribution to journalArticle

Blass, G, Klemens, CA, Brands, MW, Palygin, O & Staruschenko, A 2019, 'Postprandial Effects on ENaC-Mediated Sodium Absorption', Scientific Reports, vol. 9, no. 1, 4296. https://doi.org/10.1038/s41598-019-40639-x
Blass, Gregory ; Klemens, Christine A. ; Brands, Michael W ; Palygin, Oleg ; Staruschenko, Alexander. / Postprandial Effects on ENaC-Mediated Sodium Absorption. In: Scientific Reports. 2019 ; Vol. 9, No. 1.
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