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Measurement of Insulin- and Contraction-Stimulated Glucose Uptake in Isolated and Incubated Mature Skeletal Muscle from Mice
Published on: May 16, 2021
Glucose transport in the equine hoof
K E Asplin1, J D Curlewis, C M McGowan
1School of Veterinary Science, The University of Queensland, Australia. asplin@nottingham.ac.uk
Equine Veterinary Journal
|May 20, 2011
Summary
Equine laminitis is not caused by impaired glucose uptake due to insulin resistance. Hoof lamellae utilize an insulin-independent glucose transport system, primarily GLUT1, not GLUT4.
Area of Science:
- Equine physiology
- Metabolic disorders
- Glucose transport mechanisms
Background:
- Insulin resistance is linked to laminitis in horses, potentially involving impaired glucose uptake.
- Glucose starvation in the hoof is a hypothesized mechanism for laminitis, but its uptake pathways are unclear.
Purpose of the Study:
- To investigate insulin-dependency of glucose uptake in equine lamellae.
- To characterize glucose transport mechanisms in healthy and laminitic ponies.
- To compare glucose transport in healthy versus laminitic equine hoof tissues.
Main Methods:
- In vitro analysis of 2-deoxy-D-[2,6-(3)H] glucose uptake in hoof lamellar explants with varying insulin and glucose concentrations.
- Quantitative PCR to measure mRNA expression of glucose transporter 1 (GLUT1) and glucose transporter 4 (GLUT4) in coronary band and lamellar tissues.
Main Results:
- Insulin did not affect glucose uptake in equine lamellar explants.
- Glucose uptake demonstrated an insulin-independent transport system.
- GLUT1 mRNA was highly expressed in lamellar and coronary band tissues, while GLUT4 mRNA was minimally detected.
Conclusions:
- The findings do not support a glucose deprivation model for laminitis linked to insulin resistance.
- Equine hoof lamellae utilize a GLUT1-mediated glucose transport system.
- GLUT4 likely plays a minor role in glucose transport in equine lamellae.
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