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Updated: Aug 15, 2026
08:03
Glucose Uptake Measurement and Response to Insulin Stimulation in In Vitro Cultured Human Primary Myotubes
Published on: June 25, 2017
The glucose sensor in HIT cells is the glucose transporter
FEBS Letters
|July 27, 1987
Summary
In HIT-T15 cells, glucose uptake, not metabolism, limits glucose utilization. The glucose transporter acts as the primary sensor for glucose-stimulated insulin release, differing from normal B-cells.
Area of Science:
- Cell Biology
- Endocrinology
- Biochemistry
Background:
- The HIT-T15 cell line is a clonal insulin-producing cell line used to study pancreatic beta-cell function.
- Understanding glucose metabolism and its regulation is crucial for comprehending insulin secretion.
Purpose of the Study:
- To investigate the rate-limiting step in glucose utilization by the HIT-T15 cell line.
- To determine the role of the glucose transporter in glucose sensing and insulin release.
Main Methods:
- Assessing glucose transport rates in HIT-T15 cells.
- Evaluating the effect of glucose transporter inhibitors on glucose utilization.
- Investigating substrate specificity of the HIT cell glucose transporter.
- Measuring glucose-stimulated insulin release in the presence of inhibitors and competitors.
Main Results:
- Glucose entry into HIT-T15 cells, not intracellular metabolism, limits glucose utilization.
- The HIT cell glucose transporter showed affinity for mannose, 2-deoxyglucose, and 3-O-methylglucose, but not L-glucose or N-acetylglucosamine.
- The Michaelis constant (Km) for glucose was 4.3 mM, aligning with half-maximal insulin release.
- Phloretin and cytochalasin B inhibited glucose-stimulated insulin release, while mannoheptulose did not.
Conclusions:
- Glucose transport rate limits glucose metabolism in HIT-T15 cells, unlike in normal islets.
- The glucose transporter in HIT-T15 cells functions as the glucose sensor, dictating the concentration-dependence and specificity of insulin release.
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