The effect of rapid changes in plasma sugar concentration on the brush‐border potential difference in rat jejunum

Abstract

SUMMARYThe effect of infusion (2 h) of various sugars (20 %, w/v) or early diabetes mellitus (2 h following injection of streptozotocin) on the potential difference (PD) across the brush border of rat jejunum has been studied in vitro. Infusion of glucose or galactose resulted in hyperpolarization of the brush-border PD (-55-2 and -549 mV respectively) compared with mannitol-infused animals (-47-7 mV). Infusion of fructose and ca-methyl glucoside was without effect on PD. Ion substitution experiments showed that the glucose infusion-induced hyperpolarization was due either to a decrease in Cl-conductance and/or increased K+ conductance of the brush-border membrane. Na+ conductance appeared to be unaltered in these experiments. Since galactose infusion hyperpolarized PD without elevating plasma glucose or insulin levels, it seems that neither glucose nor insulin alone is responsible for the significantly greater PD. Treatment with streptozotocin produced glycosuria and hyperglycaemia within approximately 90 min and animals were used 30-60 min later. PD in streptozotocin-treated animals (-51-8 mV) was significantly greater than that measured in diluent-injected animals (-45-3 mV, P < 0001). However, unlike the situation with sugar infusion, ion substitution experiments showed that the hyperpolarization seen in diabetic animals was due to a decreased Na+ conductance of the brush-border membrane. Since the magnitude of the brush-border PD dictates the electrochemical driving force for Na+-sugar cotransport, our data represent the first evidence for an effect of acute hyperglycaemia on the capacity for brush border sugar uptake. However, the enterocyte and systemic factors responsible for the membrane hyperpolarization are unclear.

Stimulation of fructose transport across the intestinal brush-border membrane by PMA is mediated by GLUT2 and dynamically regulated by protein kinase C

“…In the present work, vesicles were highly purified with sucrase specific activities in the range of 16-20-fold greater than the homogenate. In common with other workers using similar procedures, there was no significant enrichment of the Na + \K + -ATPase-specific activity [14] and we could not detect Na + \K + -ATPase by Western blotting [5]. Yet brush-border GLUT2 levels in i o are comparable with those in highly purified basolateral membrane vesicle preparations (Figure 6).…”

Hyperpolarization of the plasma membrane potential provokes reorganization of the actin cytoskeleton and increases the stability of adherens junctions in bovine corneal endothelial cells in culture

“…These procedures have been previously reported to provoke PMP hyperpolarization in diverse types of cells [Sharp and Debnam, 1994;Spindler et al, 1998;Schweigel et al, 1999;Hosoi et al, 2004;Petkov et al, 2005;Liang et al, 2008] In particular, in cultured BCE cells substitution of extracellular sodium by choline, in the absence of bicarbonate (as in the present study), was shown to provoke sustained hyperpolarization [Jentsch et al, 1984]. Also, in bullfrog corneal endothelium, valinomycin has been employed to produce lasting hyperpolarizations [Graves and Sachs, 1982].…”

Streptozotocin diabetes and the expression of GLUT1 at the brush border and basolateral membranes of intestinal enterocytes

“…However, enhanced membrane expression of GLUT1 in diabetes will result in greater facilitated glucose transport at the BLM and increased phlorizin-insensitive (non SGLTl-mediated) glucose uptake at the brush border, both of which are a feature of the disease [1,2,19,20]. As such, increased enterocyte GLUT1 expression in diabetes will contribute to postprandial hyperglycaemia.…”