Glucose Transport In Cultures Research Articles

Valproic Acid Enhances Glucose Transport in the Cultured Brain Astrocytes of Glucose Transporter 1 Heterozygous Mice

Glucose transporter 1 facilitates glucose transport across the blood-brain barrier. By increasing histone acetylation at the SLC2A1 promotor, valproic acid could increase SLC2A1 gene expression. This study was designed to evaluate the effects of valproic acid on glucose transport in astrocyte cultures derived from SLC2A1 heterozygous mice. Primary astrocyte cultures were prepared from the cerebral cortex of 1-day-old neonatal mice. Cultured astrocytes were incubated with valproic acid (0.05, 0.5, and 5 mM) for 48 hours. On day 3, the glucose uptake capacity of the astrocytes was measured by using (14)C-2-Deoxy-d-glucose under zero-trans conditions. The heterozygous astrocyte glucose uptake treated with valproic acid (0.05 and 0.5 mM) for 48 hours was significantly increased compared with the untreated control heterozygous astrocytes. Our findings demonstrate that valproic acid increased glucose transport capacity in SLC2A1 heterozygous cerebral astrocytes.

Analysis of insulin-stimulated insulin receptor activation and glucose transport in cultured skeletal muscle cells from obese subjects

Obesity is associated with impaired insulin-stimulated glucose disposal in the skeletal muscle, but whether this is an intrinsic or acquired factor is unknown. In many patients with type 2 diabetes mellitus (T2D) and their nondiabetic relatives, who have a genetic predisposition for diabetes, insulin resistance is maintained in cultured muscle cells. To study the association of obesity with defects in insulin action, we investigated insulin stimulation of both insulin receptor (IR) autophosphorylation and subsequent glucose transport in primary skeletal muscle cell cultures obtained from both nonobese and obese nondiabetic subjects. In these 2 groups, there was no difference in the ability of insulin to induce autophosphorylation of the IR, phosphorylation of the downstream serine kinase Akt/PKB, or stimulation of glucose transport. Moreover, there were no major differences in cultured muscle cell content of either the IR, the IR antagonist PC-1, or GLUT 1 and GLUT 4. These data therefore indicate that the insulin resistance associated with obesity is not maintained in cultured muscle cells and suggest that this insulin resistance is an acquired feature of obesity.

Stimulation of glucose transport in cultures of density-inhibited chick embryo cells.

The rate of glucose transport in sparse, rapidly growing chick-embryo fibroblasts is much greater than that in density-inhibited cells. The addition of fresh chicken serum or trypsin to the medium of density-inhibited cells causes a large increase in the rate of glucose transport that is detectable 15 min after addition. The increase in glucose transport precedes the increase in DNA synthesis by 5-6 hr. Only small changes in rates of transport are seen with nucleosides or a nonmetabolizable amino acid. The increase in glucose transport requires protein synthesis but not RNA or DNA synthesis.