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Postprandial Effects on ENaC-Mediated Sodium Absorption. Sci Rep 2019 Mar 12;9(1):4296 PMID: 30862903 PMCID: PMC6414683

Pubmed ID

30862903

DOI

10.1038/s41598-019-40639-x

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.

Author List

Blass G, Klemens CA, Brands MW, Palygin O, Staruschenko A

Author

Oleg Palygin PhD Assistant Professor in the Physiology department at Medical College of Wisconsin




Scopus

2-s2.0-85062847686
jenkins-FCD Prod-336 69ef4a6b262d135130251597d5d39873903802b5