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Related Experiment Video

Updated: Jun 19, 2025

Measurement of Insulin- and Contraction-Stimulated Glucose Uptake in Isolated and Incubated Mature Skeletal Muscle from Mice
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Sympathetic Activation Promotes Sodium Glucose Co-Transporter-1 Protein Expression in Rodent Skeletal Muscle.

Jennifer R Matthews1, Lakshini Y Herat1, Markus P Schlaich2,3,4

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Sympathetic nervous system (SNS) overactivity increases skeletal muscle sodium-dependent glucose cotransporter 1 (SGLT1). This upregulation may worsen cardiometabolic conditions like hypertension and diabetes, suggesting SGLT1 inhibition as a potential therapy.

Keywords:
blood pressurediabetesglucosehypertensionsglt1sglt2skeletal musclesodium

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Area of Science:

  • Physiology
  • Metabolic Research
  • Cardiovascular Science

Background:

  • Sympathetic nervous system (SNS) hyperactivation is linked to obesity, hypertension, and type 2 diabetes, associated with elevated norepinephrine (NE).
  • Increased kidney sodium-dependent glucose cotransporter 1 (SGLT1) in hypertension prompted investigation into SGLT1 expression in other tissues, like skeletal muscle.

Purpose of the Study:

  • To determine if skeletal muscle cells express SGLT1 and SGLT2 proteins.
  • To investigate if NE influences SGLT1 levels in skeletal muscle cells.
  • To examine SGLT1 expression in the skeletal muscle of neurogenically hypertensive mice.

Main Methods:

  • Assessed SGLT1 and SGLT2 protein expression in skeletal muscle cells and tissue.
  • Investigated the effect of norepinephrine (NE) on SGLT1 levels in skeletal muscle cells.
  • Administered dual SGLT1/2 inhibitor (Sotagliflozin) to neurogenically hypertensive mice to assess blood pressure changes.

Main Results:

  • Skeletal muscle is identified as a novel source of SGLT2 protein.
  • Norepinephrine (NE) significantly increased SGLT1 levels in skeletal muscle cells.
  • Sotagliflozin treatment significantly reduced blood pressure in neurogenically hypertensive mice.

Conclusions:

  • SNS activity upregulates skeletal muscle SGLT1, potentially impairing cardiometabolic control.
  • SGLT1 upregulation in skeletal muscle may contribute to conditions like hypertension, diabetes, and obesity.
  • Targeting SGLT1 inhibition alone could be a therapeutic strategy for conditions with heightened SNS activity.