Werner H, Raizada M K, Mudd L M, Foyt H L, Simpson I A, Roberts C T, LeRoith D
Section on Molecular and Cellular Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892.
Endocrinology. 1989 Jul;125(1):314-20. doi: 10.1210/endo-125-1-314.
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.