Transgenic mice expressing the human SLC2A1 gene under the direction of the rat Myl2 myosin light chain promoter have increased amounts of the SLC2A1 protein product in the sarcolemma of skeletal muscle. Overexpression impacts glucose homeostasis in that glucose administered orally is disposed from the blood more rapidly in transgenic animals resulting in markedly reduced blood glucose levels when compared to wildtype littermates. Although basal glucose transport is enhanced, transgenic animals exhibit impaired glucose transport in response to insulin. This strain is suitable for applications in diabetes and hypoglycemia research.

These MLC-Glut1b mice express a transgene containing the human SLC2A1 gene,
and exhibit increased amounts of the SLC2A1 protein product in the sarcolemma of skeletal muscle.

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