scholarly journals Effects of cadmium on glucose transport in rat adipocytes and human erythrocytes: stimulation of GLUT1 catalytic activity

1996 ◽  
Vol 28 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Mohsen Lachaal ◽  
Hongzhi Liu ◽  
Sung-soo Kim ◽  
Chan Y Jung
Keyword(s):  
Catalytic Activity ◽  
Glucose Transport ◽  
Human Erythrocytes ◽  
Rat Adipocytes ◽  
Stimulation Of

scholarly journals Stimulation of a glycosyl-phosphatidylinositol-specific phospholipase by insulin and the sulfonylurea, glimepiride, in rat adipocytes depends on increased glucose transport.

1994 ◽  
Vol 126 (5) ◽  
pp. 1267-1276 ◽  
Author(s):  
G Müller ◽  
E A Dearey ◽  
A Korndörfer ◽  
W Bandlow
Keyword(s):  
Glucose Transport ◽  
Inositol Phosphate ◽  
Glycosyl Phosphatidylinositol ◽  
Cyclic Monophosphate ◽  
Rat Adipocytes ◽  
Residual Protein ◽  
Adipocyte Cell ◽  
Anchor Structure ◽  
Specific Insulin ◽  
Stimulation Of

Lipoprotein lipase (LPL) and glycolipid-anchored cAMP-binding ectoprotein (Gce1) are modified by glycosyl-phosphatidylinositol (GPI) in rat adipocytes, however, the linkage is potentially unstable. Incubation of the cells with either insulin (0.1-30 nM) or the sulfonylurea, glimepiride (0.5-20 microM), in the presence of glucose led to conversion of up to 35 and 20%, respectively, of the total amphiphilic LPL and Gce1 to their hydrophilic versions. Inositol-phosphate was retained in the residual protein-linked anchor structure. This suggests cleavage of the GPI anchors by an endogenous GPI-specific insulin- and glimepiride-inducible phospholipase (GPI-PL). Despite cleavage, hydrophilic LPL and Gce1 remained membrane associated and were released only if a competitor, e.g., inositol-(cyclic)monophosphate, had been added. Other constituents of the GPI anchor (glucosamine and mannose) were less efficient. This suggests peripheral interaction of lipolytically cleaved LPL and Gce1 with the adipocyte cell surface involving the terminal inositol-(cyclic)monophosphate epitope and presumably a receptor of the adipocyte plasma membrane. In rat adipocytes which were resistant toward glucose transport stimulation by insulin, the sensitivity and responsiveness of GPI-PL to stimulation by insulin was drastically reduced. In contrast, activation of both GPI-PL and glucose transport by the sulfonylurea, glimepiride, was not affected significantly. Inhibition of glucose transport or incubation of rat adipocytes in glucose-free medium completely abolished stimulation of GPI-PL by either insulin or glimepiride. The activation was partially restored by the addition of glucose or nonmetabolizable 2-deoxyglucose. These data suggest that increased glucose transport stimulates a GPI-PL in rat adipocytes.

Stimulatory effect of lithium on glucose transport in rat adipocytes is not mediated by elevation of IP1

1998 ◽  
Vol 275 (2) ◽  
pp. E272-E277 ◽  
Author(s):  
Xiaoli Chen ◽  
Ellen G. McMahon ◽  
Eric A. Gulve
Keyword(s):  
Glucose Uptake ◽  
Glucose Transport ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Transport Activity ◽  
Concentration Dependent Manner ◽  
Inositol 1 ◽  
Rat Adipocytes ◽  
Increase Glucose Uptake ◽  
Stimulation Of

Lithium has been shown to increase glucose uptake in skeletal muscle and adipose tissues. The therapeutic effect of lithium on bipolar disease is thought to be mediated by its inhibitory effect on myo-inositol-1-monophosphatase (IMPase). We tested the hypothesis that the stimulatory effect of lithium on glucose uptake results from inhibition of IMPase and the resultant accumulation of inositol monophosphates (IP1) by comparing the effects of lithium and a selective IMPase inhibitor, L-690,488, on isolated rat adipocytes. Insulin produced a concentration-dependent stimulation of 2-deoxy-d-[14C]glucose (2-DG) transport (10 μU/ml caused half-maximal activation). Acute exposure to lithium stimulated basal glucose transport activity in a concentration-dependent manner, with a threefold stimulation at 30 mM lithium. Lithium also potentiated insulin-stimulated 2-DG transport. Lithium produced a concomitant increase in IP1 accumulation. In contrast, L-690,488 increased IP1 to levels comparable to those of lithium without stimulatory effects on 2-DG transport. These results demonstrate that stimulatory effects of lithium on glucose transport are not mediated by the inhibition of IMPase and subsequent accumulation of IP1 in rat adipocytes.

Stimulation of glucose transport by guanine nucleotides in permeabilized rat adipocytes

1992 ◽  
Vol 189 (1) ◽  
pp. 572-580 ◽  
Author(s):  
Yoich Suzuki ◽  
Hiroshi Shibata ◽  
Shuji Inoue ◽  
Itaru Kojima
Keyword(s):  
Glucose Transport ◽  
Guanine Nucleotides ◽  
Rat Adipocytes ◽  
Stimulation Of
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