Endocrinology, Vol 125, 314-320, Copyright © 1989 by Endocrine Society

ARTICLES

Regulation of rat brain/HepG2 glucose transporter gene expression by insulin and insulin-like growth factor-I in primary cultures of neuronal and glial cells

H Werner, MK Raizada, LM Mudd, HL Foyt, IA Simpson, CT Roberts Jr and D LeRoith
Section on Molecular and Cellular Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892.

We have demonstrated the expression of the rat brain/HepG2 glucose transporter gene in primary cultures of rat neuronal and glial cells by Northern blot analysis with a rat brain glucose transporter cDNA probe. Incubation of both neuronal and glial cells with insulin and insulin- like growth factor-I induced a time- and dose-dependent increase in the steady state levels of glucose transporter mRNA. The maximal response was achieved between 2-4 h and subsequently decreased. Both insulin and insulin-like growth factor-I at a dose of 1 ng/ml elicited an approximately 57% increase in glucose transporter mRNA levels in neuronal cultures after 90 min, suggesting that each peptide was acting through its own receptor. On the other hand, insulin stimulated [3H]2- deoxyglucose uptake in glial, but not neuronal, cells. These results suggest that insulin-like peptides regulate the expression of the rat brain/Hep G2 glucose transporter gene at both transcriptional and posttranscriptional levels, and that these regulatory mechanisms may be dissociated from each other. Insulin-like peptides may, therefore, participate in the control of brain energy metabolism.

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