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Mol Endocrinol. 1989 Feb;3(2):273-9. doi: 10.1210/mend-3-2-273.

Developmental regulation of rat brain/Hep G2 glucose transporter gene expression.

Molecular endocrinology (Baltimore, Md.)

H Werner, M Adamo, W L Lowe, C T Roberts, D LeRoith

Affiliations

  1. Diabetes Branch, Section on Molecular and Cellular Physiology, National Institute of Diabetes, Digestive and Kidney Diseases, Bethesda, Maryland 20892.

PMID: 2710134 DOI: 10.1210/mend-3-2-273

Abstract

The developmental regulation of rat brain-derived/Hep G2 glucose transporter gene expression was studied by means of Northern blot hybridization, using a rat brain glucose transporter cDNA probe, in order to directly quantify steady state glucose transporter mRNA levels. The results obtained showed different tissue-specific patterns of glucose transporter mRNA levels during ontogenesis; while in brain there was a sustained increase in the levels of the message from 20 days embryogenesis until 50 days postnatal, other organs such as heart, lung, liver, and muscle expressed maximal levels of the glucose transporter mRNA in 20-day fetuses and 1-day neonates, decreasing subsequently to very low levels. The relative expression of the glucose transporter mRNA in the different tissues, at both fetal and adult stages, was analyzed using a solution hybridization-RNase protection assay. This approach revealed that, while the heart expresses the highest levels of glucose transporter mRNA at 20 days of fetal life, the brain shows the highest levels at the adult stage. These results indicate a tissue-specific ontogenic pattern of glucose transporter gene expression, suggesting a developmental role for this glucose transporter gene product.

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