Mechanism for enhanced glucose transport response to insulin in adipose cells from chronically hyperinsulinemic rats. Increased translocation of glucose transporters from an enlarged intracellular pool.
AUTOR(ES)
Kahn, B B
RESUMO
The mechanism for the increased glucose transport response to insulin in adipose cells from chronically hyperinsulinemic rats was examined. Rats were infused with insulin s.c. for 2 wk. Isolated adipose cells were incubated with and without insulin, 3-O-methylglucose transport was measured, and glucose transporters in subcellular membrane fractions were assessed by cytochalasin B binding. Adipose cells from insulin-treated rats showed no change in basal but a 55% increase in insulin-stimulated glucose transport activity compared with those from control rats (7.1 +/- 0.8 vs. 4.6 +/- 0.5 fmol/cell per min, mean +/- SEM) and a corresponding increase in the concentration of glucose transporters in the plasma membranes (44 +/- 5 vs. 32 +/- 6 pmol/mg of membrane protein). In the low-density microsomes, glucose transporter concentrations in both basal and insulin-stimulated states were the same, but the total numbers were greater in cells from the insulin-treated rats because of a 39% increase in low-density microsomal protein. Therefore, chronic experimental hyperinsulinemia in the rat enhances the stimulatory action of insulin on glucose transport in the adipose cell by increasing the concentration of glucose transporters in the plasma membranes. This results from an enlarged intracellular pool due to increased intracellular protein and enhanced glucose transporter translocation in response to insulin.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=424219Documentos Relacionados
- Differential regulation of two glucose transporters in adipose cells from diabetic and insulin-treated diabetic rats.
- Mechanism of Insulin-resistant Glucose Transport Activity in the Enlarged Adipose Cell of the Aged, Obese Rat: RELATIVE DEPLETION OF INTRACELLULAR GLUCOSE TRANSPORT SYSTEMS
- Divergent mechanisms for the insulin resistant and hyperresponsive glucose transport in adipose cells from fasted and refed rats. Alterations in both glucose transporter number and intrinsic activity.
- Evidence that insulin causes translocation of glucose transport activity to the plasma membrane from an intracellular storage site.
- Increased insulin sensitivity and responsiveness of glucose metabolism in adipocytes from female versus male rats.