Regulatory effect of insulin on the structure, function and metabolism of Na+/K+‑ATPase (Review)
Open accessAbstract
Na+/K+‑ATPase is an ancient enzyme, the role of which is to maintain Na+ and K+ gradients across cell membranes, thus preserving intracellular ion homeostasis. The regulation of Na+/K+‑ATPase is affected by several regulatory factors through a number of pathways, with hormones serving important short‑term and long‑term regulatory functions. Na+/K+‑ATPase can also be degraded through activation of the ubiquitin proteasome and autophagy‑lysosomal pathways, thereby affecting its abundance and enzymatic activity. As regards the regulatory effect of insulin, it has been found to upregulate the relative abundance of Na+/K+‑ATPase and restore the transport efficiency in multiple in vitro and in vivo experiments. Therefore, elucidating the role of insulin in the regulation Na+/K+‑ATPase may help uncover new drug targets for the treatment of related diseases. The aim of the present study was to review the structure and function of Na+/K+‑ATPase and to discuss the possible mechanisms through which it may be regulated by insulin, in order to investigate the possibility of designing new therapies for related diseases.
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One of the principal mechanisms underlying hypokalemia in THPP is increased activity of the Na+/K+-ATPase.
“One of the principal mechanisms underlying hypokalemia in THPP is the increased activity of the Na+/K+-ATPase, a transmembrane pump that hydrolyses adenosine triphosphate (ATP) to transport three sodium ions out of the cell and two potassium ions into the cell.”
From Thyrotoxic Hypokalemic Periodic Paralysis: Pathophysiological Mechanisms (2025) · cites this paper as [28]
The Introduction (page not available) describes the pump’s ATP-driven transport of three sodium ions out of the cell and two potassium ions in. Section 6, under “Skeletal muscle” (page not available), says increased Na+/K+-ATPase activity reduces extracellular potassium. The review does not identify this as a principal mechanism of hypokalemia in THPP. (LLM, conf=0.86)
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- Authors
- Wen, X.-P., & Wan, Q.-Q.
- Affiliations
- Central South University (CN)
- Transplantation Center, The Third Xiangya Hospital, Central South University, Changsha, Hunan 410013, P.R. China
- Venue
- Experimental and Therapeutic Medicine
- Publisher
- Spandidos Publications
- Published
- 2021-09-01
- Volume
- 22
- Issue
- 5
- Pages
- 1243-1243
- ISSN
- 1792-0981 (ISSN-L)
- 1792-1015
- PMC
- PMC8438676
- OpenAlex
- W3198457702
- Cited by
- 11
- References
- 69
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 2 · 2023: 1
- FWCI
- 0.08
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Licence
- cc-by-nc-nd
- Locations
- Experimental and Therapeutic Medicine (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › ATP Synthase and ATPases Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Keywords
- Na+/K+-ATPase, insulin, enzyme regulation, ion homeostasis, ubiquitin-proteasome degradation, autophagy-lysosome pathway, hormonal regulation, therapeutic target
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