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Sympathetic Activation Promotes Sodium Glucose Co-Transporter-1 Protein Expression in Rodent Skeletal Muscle. | LitMetric

Sympathetic Activation Promotes Sodium Glucose Co-Transporter-1 Protein Expression in Rodent Skeletal Muscle.

Biomedicines

Dobney Hypertension Centre, School of Biomedical Sciences-Royal Perth Hospital Unit, University of Western Australia, and Royal Perth Hospital Research Foundation, Crawley, WA 6000, Australia.

Published: July 2024

AI Article Synopsis

  • Hyperactivation of the sympathetic nervous system (SNS) is associated with obesity, hypertension, and type 2 diabetes, and leads to increased norepinephrine (NE) levels which may affect sodium-glucose transport proteins.
  • The study investigates the expression of sodium-dependent glucose cotransporters SGLT1 and SGLT2 in skeletal muscle, finding that NE significantly elevates SGLT1 levels in skeletal muscle cells.
  • Treatment with the dual inhibitor Sotagliflozin in neurogenically hypertensive mice effectively reduced blood pressure, suggesting that targeting SGLT1 could help manage conditions driven by high SNS activity, warranting further clinical studies.

Article Abstract

The hyperactivation of the sympathetic nervous system (SNS) is linked to obesity, hypertension, and type 2 diabetes, which are characterized by elevated norepinephrine (NE) levels. Previous research has shown increased sodium-dependent glucose cotransporter 1 (SGLT1) protein levels in kidneys of hypertensive rodents, prompting investigation into the expression of SGLT1 in various tissues, such as skeletal muscle. This study aimed to assess (i) whether skeletal muscle cells and tissue express SGLT1 and SGLT2 proteins; (ii) if NE increases SGLT1 levels in skeletal muscle cells, and (iii) whether the skeletal muscle of neurogenically hypertensive mice exhibits increased SGLT1 expression. We found that (i) skeletal muscle cells and tissue are a novel source of the SGLT2 protein and that (ii) NE significantly elevated SGLT1 levels in skeletal muscle cells. As SGLT2 inhibition (SGLT2i) with Empagliflozin increased SGLT1 levels, in vivo studies with the dual inhibitor SGLT1/2i, Sotagliflozin were warranted. The treatment of neurogenically hypertensive mice using Sotagliflozin significantly reduced blood pressure. Our findings suggest that SNS activity upregulates the therapeutic target, SGLT1, in skeletal muscle, potentially worsening cardiometabolic control. As clinical trial data suggest cardiorenal benefits from SGLT2i, future studies should aim to utilize SGLT1i by itself, which may offer a therapeutic strategy for conditions with heightened SNS activity, such as hypertension, diabetes, and obesity.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11275186PMC
http://dx.doi.org/10.3390/biomedicines12071456DOI Listing

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