Hyperosmolarity Reduces GLUT4 Endocytosis and Increases Its Exocytosis from a VAMP2-independent Pool in L6 Muscle Cells

The intracellular traffic of the glucose transporter 4 (GLUT4) in muscle cells remains largely unexplored. Here we make use of L6 myoblasts stably expressing GLUT4 with an exofacially directed Myc-tag (GLUT4myc) to determine the exocytic and endocytic rates of the transporter. Insulin caused a rapid (t 12 = 4 min) gain, whereas hyperosmolarity (0.45m sucrose) caused a slow (t 12 = 20 min) gain in surface GLUT4myc molecules. With prior insulin stimulation followed by addition of hypertonic sucrose, the increase in surface GLUT4myc was partly additive. Unlike the effect of insulin, the GLUT4myc gain caused by hyperosmolarity was insensitive to wortmannin or to tetanus toxin cleavage of VAMP2 and VAMP3. Disappearance of GLUT4myc from the cell surface was rapid (t 12 = 1.5 min). Insulin had no effect on the initial rate of GLUT4myc internalization. In contrast, hyperosmolarity almost completely abolished GLUT4myc internalization. Surface GLUT4myc accumulation in response to hyperosmolarity was only partially blocked by inhibition of tyrosine kinases with erbstatin analog (erbstatin A) and genistein. However, neither inhibitor interfered with the ability of hyperosmolarity to block GLUT4myc internalization. We propose that hyperosmolarity increases surface GLUT4myc by preventing GLUT4 endocytosis and stimulating its exocytosis via a pathway independent of phosphatidylinositol 3-kinase activity and of VAMP2 or VAMP3. A tetanus toxin-insensitive v-SNARE such as TI-VAMP detected in these cells, might mediate membrane fusion of the hyperosmolarity-sensitive pool. The intracellular traffic of the glucose transporter 4 (GLUT4) in muscle cells remains largely unexplored. Here we make use of L6 myoblasts stably expressing GLUT4 with an exofacially directed Myc-tag (GLUT4myc) to determine the exocytic and endocytic rates of the transporter. Insulin caused a rapid (t 12 = 4 min) gain, whereas hyperosmolarity (0.45m sucrose) caused a slow (t 12 = 20 min) gain in surface GLUT4myc molecules. With prior insulin stimulation followed by addition of hypertonic sucrose, the increase in surface GLUT4myc was partly additive. Unlike the effect of insulin, the GLUT4myc gain caused by hyperosmolarity was insensitive to wortmannin or to tetanus toxin cleavage of VAMP2 and VAMP3. Disappearance of GLUT4myc from the cell surface was rapid (t 12 = 1.5 min). Insulin had no effect on the initial rate of GLUT4myc internalization. In contrast, hyperosmolarity almost completely abolished GLUT4myc internalization. Surface GLUT4myc accumulation in response to hyperosmolarity was only partially blocked by inhibition of tyrosine kinases with erbstatin analog (erbstatin A) and genistein. However, neither inhibitor interfered with the ability of hyperosmolarity to block GLUT4myc internalization. We propose that hyperosmolarity increases surface GLUT4myc by preventing GLUT4 endocytosis and stimulating its exocytosis via a pathway independent of phosphatidylinositol 3-kinase activity and of VAMP2 or VAMP3. A tetanus toxin-insensitive v-SNARE such as TI-VAMP detected in these cells, might mediate membrane fusion of the hyperosmolarity-sensitive pool. glucose transporter 4 o-phenylenediamine dihydrochloride HEPES-modified RPMI tetanus toxin phosphatidylinositol 3-kinase erbstatin analog vesicle-associated membrane protein tetanus toxin-insensitive VAMP green fluorescence protein enhanced GFP minimal essential medium phosphate-buffered saline trans-epoxysuccinyl-l-leucylamido-(4-guanidino)butane soluble NSF accessory protein SNAP receptor The glucose transporter 4 (GLUT4)1 is the predominant glucose transporter of muscle and adipose cells. In untreated adipocytes, GLUT4 the membrane and intracellular with the the and detected GLUT4 in intracellular and GLUT4 exocytic GLUT4 endocytosis via by the inhibition of via with or of GLUT4 in is the traffic of transporter in muscle cells, the that muscle the in of glucose the of GLUT4 in a a of GLUT4 the membrane of muscle adipose cells L6 muscle cells in and in that the stimulation of GLUT4 exocytosis or insulin GLUT4 endocytosis is The of exocytic and endocytic to insulin in muscle cells to to the cell surface accumulation of was that accumulation from the stimulation of GLUT4 exocytosis by from by insulin a However, the in the of exocytic from endocytic traffic of The effect of hyperosmolarity to to that hyperosmolarity GLUT4 the cell surface by GLUT4 We a of L6 myoblasts stably expressing GLUT4 with an (GLUT4myc) to GLUT4 endocytosis in response to of was to insulin and hyperosmolarity the of GLUT4 in L6 muscle cells in to the endocytic and exocytic of GLUT4 and to the of the of GLUT4 in We that insulin and hyperosmolarity the of GLUT4 from intracellular to the membrane in L6 insulin GLUT4 hyperosmolarity largely its inhibition of tyrosine kinases GLUT4 the block of GLUT4 and only partially GLUT4 accumulation the cell The that insulin GLUT4 from a that is by tetanus toxin and In contrast, the accumulation of GLUT4 the cell surface caused by hyperosmolarity from GLUT4 endocytosis and stimulating its is to GLUT4 from the an that is insensitive to inhibition by tetanus toxin and is a of insulin in muscle and cells. In the L6 muscle cell GLUT4 from myoblasts We that of GLUT4myc in L6 myoblasts to the of the protein to a insulin to glucose is on the in the intracellular GLUT4myc the of the of the and the of glucose to insulin is we in the that of the GLUT4myc a a with in cell and of the intracellular of GLUT4myc insulin or hypertonic of the GLUT4myc is to the cell surface as with in adipocytes, GLUT4myc is in the intracellular in the and is to the cell surface in response to insulin and hyperosmolarity in GLUT4 and rapid insulin of the GLUT4myc is in the of insulin, the rate of GLUT4myc is the 12 of that insulin GLUT4 in with in cells a of gain in surface GLUT4 to to inhibition of GLUT4 endocytosis The GLUT4myc in L6 myoblasts is to the or GLUT4 or in the of insulin via and hypertonic to the of by preventing the and We that hyperosmolarity by a gain in GLUT4myc the cell surface and preventing GLUT4myc the that hyperosmolarity GLUT4 the cell in inhibition of GLUT4 is a that a tyrosine pathway and tyrosine activity is the surface gain in GLUT4 in However, is that effect is to the of GLUT4 the cell an inhibitor of the tyrosine erbstatin was to the inhibition of GLUT4myc endocytosis by hyperosmolarity in muscle cells A and the GLUT4 by only A and We propose that inhibition of GLUT4 endocytosis of the GLUT4 surface and the from the stimulation of GLUT4 exocytosis in response to of GLUT4 by inhibition of tyrosine is that GLUT4 endocytosis is blocked by hyperosmolarity in and GLUT4 from the cell surface with in response to insulin and hypertonic We that an exocytic GLUT4 in L6 muscle cells, by insulin and that hyperosmolarity GLUT4 from an of GLUT4 the that insulin and hyperosmolarity GLUT4 from intracellular in L6 muscle cells is to tetanus and in muscle and cells and in GLUT4 in muscle and cells and tetanus toxin the GLUT4myc in L6 that the by the tetanus VAMP2 by the that VAMP2 is GLUT4 fusion with the membrane in response to insulin We that of tetanus toxin GLUT4myc caused by the that insulin and hyperosmolarity GLUT4 from intracellular VAMP2 and that is tetanus neither VAMP2 the v-SNARE the of GLUT4 from the is that a tetanus toxin-insensitive VAMP such as TI-VAMP mediate fusion of the with the membrane in muscle cells. TI-VAMP was detected in and its was partially from that of VAMP2 or VAMP3. The of TI-VAMP in fusion of the is of insulin and hyperosmolarity on GLUT4myc was partly additive. A to an effect in the cells with prior to to insulin We to effect we myoblasts in the The of these to the inhibition of insulin by hyperosmolarity the of as In contrast, L6 muscle cells with insulin, followed by the addition of caused a increase in the surface GLUT4myc with the effect of GLUT4myc from an GLUT4 to the of GLUT4myc the cell and as in GLUT4myc the cell hyperosmolarity a gain of GLUT4 the cell insulin and hyperosmolarity in is GLUT4 in and muscle cells In contrast, the accumulation of GLUT4 the cell surface is by the inhibitor wortmannin in inhibition was in wortmannin of or might Here we that activity is GLUT4myc caused by hyperosmolarity in L6 that in the of GLUT4 the surface in response to insulin is to of GLUT4 from a exocytic and from a that in muscle cells a effect of insulin is to GLUT4myc exocytosis from a is from the by hyperosmolarity and from the pool. the of intracellular GLUT4 traffic by the of GLUT4myc is in L6 myoblasts in the In the of insulin, of GLUT4myc and to the cell surface with a 12 of of the GLUT4myc remains and with a 12 of Insulin and hyperosmolarity GLUT4 from Insulin GLUT4 from a that the of and GLUT4 exocytosis from an the that and tetanus and the GLUT4 the cell surface by to the accumulation of GLUT4 the cell surface by The the and The glucose transporter 4 (GLUT4)1 is the predominant glucose transporter of muscle and adipose cells. In untreated adipocytes, GLUT4 the membrane and intracellular with the the and detected GLUT4 in intracellular and GLUT4 exocytic GLUT4 endocytosis via by the inhibition of via with or of GLUT4 in is the traffic of transporter in muscle cells, the that muscle the in of glucose Insulin the of GLUT4 in a a of GLUT4 the membrane of muscle adipose cells L6 muscle cells in and in that the stimulation of GLUT4 exocytosis or insulin GLUT4 endocytosis is The of exocytic and endocytic to insulin in muscle cells to to the cell surface accumulation of was that accumulation from the stimulation of GLUT4 exocytosis by from by insulin a However, the in the of exocytic from endocytic traffic of The effect of hyperosmolarity to to that hyperosmolarity GLUT4 the cell surface by GLUT4 We a of L6 myoblasts stably expressing GLUT4 with an (GLUT4myc) to GLUT4 endocytosis in response to The of was to insulin and hyperosmolarity the of GLUT4 in L6 muscle cells in to the endocytic and exocytic of GLUT4 and to the of the of GLUT4 in We that insulin and hyperosmolarity the of GLUT4 from intracellular to the membrane in L6 insulin GLUT4 hyperosmolarity largely its inhibition of tyrosine kinases GLUT4 the block of GLUT4 and only partially GLUT4 accumulation the cell The that insulin GLUT4 from a that is by tetanus toxin and In contrast, the accumulation of GLUT4 the cell surface caused by hyperosmolarity from GLUT4 endocytosis and stimulating its is to GLUT4 from the an that is insensitive to inhibition by tetanus toxin and is a of insulin in muscle and cells. In the L6 muscle cell GLUT4 from myoblasts We that of GLUT4myc in L6 myoblasts to the of the protein to a insulin to glucose is on the in the intracellular GLUT4myc the of the of the and the of glucose to insulin is we in the that of the GLUT4myc a a with in cell and of the intracellular of GLUT4myc insulin or hypertonic of the GLUT4myc is to the cell surface as with in adipocytes, GLUT4myc is in the intracellular in the and is to the cell surface in response to insulin and hyperosmolarity in GLUT4 and rapid insulin of the GLUT4myc is in the of insulin, the rate of GLUT4myc is the 12 of that insulin GLUT4 in with in cells a of gain in surface GLUT4 to to inhibition of GLUT4 endocytosis The GLUT4myc in L6 myoblasts is to the or GLUT4 or in the of insulin via and hypertonic to the of by preventing the and We that hyperosmolarity by a gain in GLUT4myc the cell surface and preventing GLUT4myc the that hyperosmolarity GLUT4 the cell in inhibition of GLUT4 is a that a tyrosine pathway and tyrosine activity is the surface gain in GLUT4 in However, is that effect is to the of GLUT4 the cell an inhibitor of the tyrosine erbstatin was to the inhibition of GLUT4myc endocytosis by hyperosmolarity in muscle cells A and the GLUT4 by only A and We propose that inhibition of GLUT4 endocytosis of the GLUT4 surface and the from the stimulation of GLUT4 exocytosis in response to of GLUT4 by inhibition of tyrosine is that GLUT4 endocytosis is blocked by hyperosmolarity in and GLUT4 from the cell surface with in response to insulin and hypertonic We that an exocytic GLUT4 in L6 muscle cells, by insulin and that hyperosmolarity GLUT4 from an of GLUT4 the that insulin and hyperosmolarity GLUT4 from intracellular in L6 muscle cells is to tetanus and in muscle and cells and in GLUT4 in muscle and cells and tetanus toxin the GLUT4myc in L6 that the by the tetanus VAMP2 by the that VAMP2 is GLUT4 fusion with the membrane in response to insulin We that of tetanus toxin GLUT4myc caused by the that insulin and hyperosmolarity GLUT4 from intracellular VAMP2 and that is tetanus neither VAMP2 the v-SNARE the of GLUT4 from the is that a tetanus toxin-insensitive VAMP such as TI-VAMP mediate fusion of the with the membrane in muscle cells. TI-VAMP was detected in and its was partially from that of VAMP2 or VAMP3. The of TI-VAMP in fusion of the is of insulin and hyperosmolarity on GLUT4myc was partly additive. A to an effect in the cells with prior to to insulin We to effect we myoblasts in the The of these to the inhibition of insulin by hyperosmolarity the of as In contrast, L6 muscle cells with insulin, followed by the addition of caused a increase in the surface GLUT4myc with the effect of GLUT4myc from an GLUT4 to the of GLUT4myc the cell and as in GLUT4myc the cell hyperosmolarity a gain of GLUT4 the cell insulin and hyperosmolarity in is GLUT4 in and muscle cells In contrast, the accumulation of GLUT4 the cell surface is by the inhibitor wortmannin in inhibition was in wortmannin of or might Here we that activity is GLUT4myc caused by hyperosmolarity in L6 that in the of GLUT4 the surface in response to insulin is to of GLUT4 from a exocytic and from a that in muscle cells a effect of insulin is to GLUT4myc exocytosis from a is from the by hyperosmolarity and from the pool. the of intracellular GLUT4 traffic by the of GLUT4myc is in L6 myoblasts in the In the of insulin, of GLUT4myc and to the cell surface with a 12 of of the GLUT4myc remains and with a 12 of Insulin and hyperosmolarity GLUT4 from Insulin GLUT4 from a that the of and GLUT4 exocytosis from an the that and tetanus and the GLUT4 the cell surface by to the accumulation of GLUT4 the cell surface by The the and GLUT4 is a of insulin in muscle and cells. In the L6 muscle cell GLUT4 from myoblasts We that of GLUT4myc in L6 myoblasts to the of the protein to a insulin to glucose is on the in the intracellular GLUT4myc the of the of the and the of glucose to insulin is we in the that of the GLUT4myc a a with in cell and of the intracellular of GLUT4myc insulin or hypertonic of the GLUT4myc is to the cell surface as with in adipocytes, GLUT4myc is in the intracellular in the and is to the cell surface in response to insulin and hyperosmolarity in Insulin GLUT4 and rapid insulin of the GLUT4myc is in the of insulin, the rate of GLUT4myc is the 12 of that insulin GLUT4 in with in cells a of gain in surface GLUT4 to to inhibition of GLUT4 endocytosis The GLUT4myc in L6 myoblasts is to the or GLUT4 or in the of insulin via and hypertonic to the of by preventing the and We that hyperosmolarity by a gain in GLUT4myc the cell surface and preventing GLUT4myc the that hyperosmolarity GLUT4 the cell in inhibition of GLUT4 is a that a tyrosine pathway and tyrosine activity is the surface gain in GLUT4 in However, is that effect is to the of GLUT4 the cell an inhibitor of the tyrosine erbstatin was to the inhibition of GLUT4myc endocytosis by hyperosmolarity in muscle cells A and the GLUT4 by only A and We propose that inhibition of GLUT4 endocytosis of the GLUT4 surface and the from the stimulation of GLUT4 exocytosis in response to of GLUT4 by inhibition of tyrosine is that GLUT4 endocytosis is blocked by hyperosmolarity in and GLUT4 from the cell surface with in response to insulin and hypertonic We that an exocytic GLUT4 in L6 muscle cells, by insulin and that hyperosmolarity GLUT4 from an of GLUT4 the that insulin and hyperosmolarity GLUT4 from intracellular in L6 muscle cells is to tetanus and in muscle and cells and in GLUT4 in muscle and cells and tetanus toxin the GLUT4myc in L6 that the by the tetanus VAMP2 by the that VAMP2 is GLUT4 fusion with the membrane in response to insulin We that of tetanus toxin GLUT4myc caused by the that insulin and hyperosmolarity GLUT4 from intracellular VAMP2 and that is tetanus neither VAMP2 the v-SNARE the of GLUT4 from the is that a tetanus toxin-insensitive VAMP such as TI-VAMP mediate fusion of the with the membrane in muscle cells. TI-VAMP was detected in and its was partially from that of VAMP2 or VAMP3. The of TI-VAMP in fusion of the is of insulin and hyperosmolarity on GLUT4myc was partly additive. A to an effect in the cells with prior to to insulin We to effect we myoblasts in the The of these to the inhibition of insulin by hyperosmolarity the of as In contrast, L6 muscle cells with insulin, followed by the addition of caused a increase in the surface GLUT4myc with the effect of GLUT4myc from an GLUT4 to the of GLUT4myc the cell and as in GLUT4myc the cell hyperosmolarity a gain of GLUT4 the cell insulin and hyperosmolarity in is GLUT4 in and muscle cells In contrast, the accumulation of GLUT4 the cell surface is by the inhibitor wortmannin in inhibition was in wortmannin of or might Here we that activity is GLUT4myc caused by hyperosmolarity in L6 that in the of GLUT4 the surface in response to insulin is to of GLUT4 from a exocytic and from a that in muscle cells a effect of insulin is to GLUT4myc exocytosis from a is from the by hyperosmolarity and from the pool. the of intracellular GLUT4 traffic by the of GLUT4myc is in L6 myoblasts in the In the of insulin, of GLUT4myc and to the cell surface with a 12 of of the GLUT4myc remains and with a 12 of Insulin and hyperosmolarity GLUT4 from Insulin GLUT4 from a that the of and GLUT4 exocytosis from an the that and tetanus and the GLUT4 the cell surface by to the accumulation of GLUT4 the cell surface by The the and Insulin GLUT4 and rapid insulin of the GLUT4myc is in the of insulin, the rate of GLUT4myc is the 12 of that insulin GLUT4 in with in cells a of gain in surface GLUT4 to to inhibition of GLUT4 endocytosis The GLUT4myc in L6 myoblasts is to the or GLUT4 or in the of insulin via and hypertonic to the of by preventing the and We that hyperosmolarity by a gain in GLUT4myc the cell surface and preventing GLUT4myc the that hyperosmolarity GLUT4 the cell in inhibition of GLUT4 is a that a tyrosine pathway and tyrosine activity is the surface gain in GLUT4 in However, is that effect is to the of GLUT4 the cell an inhibitor of the tyrosine erbstatin was to the inhibition of GLUT4myc endocytosis by hyperosmolarity in muscle cells A and the GLUT4 by only A and We propose that inhibition of GLUT4 endocytosis of the GLUT4 surface and the from the stimulation of GLUT4 exocytosis in response to of GLUT4 by inhibition of tyrosine is that GLUT4 endocytosis is blocked by hyperosmolarity in and GLUT4 from the cell surface with in response to insulin and hypertonic We that an exocytic GLUT4 in L6 muscle cells, by insulin and that hyperosmolarity GLUT4 from an of GLUT4 the that insulin and hyperosmolarity GLUT4 from intracellular in L6 muscle cells is to tetanus and in muscle and cells and in GLUT4 in muscle and cells and tetanus toxin the GLUT4myc in L6 that the by the tetanus VAMP2 by the that VAMP2 is GLUT4 fusion with the membrane in response to insulin We that of tetanus toxin GLUT4myc caused by the that insulin and hyperosmolarity GLUT4 from intracellular VAMP2 and that is tetanus neither VAMP2 the v-SNARE the of GLUT4 from the is that a tetanus toxin-insensitive VAMP such as TI-VAMP mediate fusion of the with the membrane in muscle cells. TI-VAMP was detected in and its was partially from that of VAMP2 or VAMP3. The of TI-VAMP in fusion of the is of insulin and hyperosmolarity on GLUT4myc was partly additive. A to an effect in the cells with prior to to insulin We to effect we myoblasts in the The of these to the inhibition of insulin by hyperosmolarity the of as In contrast, L6 muscle cells with insulin, followed by the addition of caused a increase in the surface GLUT4myc with the effect of GLUT4myc from an GLUT4 to the of GLUT4myc the cell and as in GLUT4myc the cell hyperosmolarity a gain of GLUT4 the cell insulin and hyperosmolarity in is GLUT4 in and muscle cells In contrast, the accumulation of GLUT4 the cell surface is by the inhibitor wortmannin in inhibition was in wortmannin of or might Here we that activity is GLUT4myc caused by hyperosmolarity in L6 that in the of GLUT4 the surface in response to insulin is to of GLUT4 from a exocytic and from a that in muscle cells a effect of insulin is to GLUT4myc exocytosis from a is from the by hyperosmolarity and from the pool. the of intracellular GLUT4 traffic by the of GLUT4myc is in L6 myoblasts in the In the of insulin, of GLUT4myc and to the cell surface with a 12 of of the GLUT4myc remains and with a 12 of Insulin and hyperosmolarity GLUT4 from Insulin GLUT4 from a that the of and GLUT4 exocytosis from an the that and tetanus and the GLUT4 the cell surface by to the accumulation of GLUT4 the cell surface by The the and Insulin GLUT4 and rapid insulin of the GLUT4myc is in the of insulin, the rate of GLUT4myc is the 12 of that insulin GLUT4 in with in cells a of gain in surface GLUT4 to to inhibition of GLUT4 endocytosis The GLUT4myc in L6 myoblasts is to the or GLUT4 or in the of insulin via and hypertonic to the of by preventing the and We that hyperosmolarity by a gain in GLUT4myc the cell surface and preventing GLUT4myc the that hyperosmolarity GLUT4 the cell in inhibition of GLUT4 is a that a tyrosine pathway and tyrosine activity is the surface gain in GLUT4 in However, is that effect is to the of GLUT4 the cell an inhibitor of the tyrosine erbstatin was to the inhibition of GLUT4myc endocytosis by hyperosmolarity in muscle cells A and the GLUT4 by only A and We propose that inhibition of GLUT4 endocytosis of the GLUT4 surface and the from the stimulation of GLUT4 exocytosis in response to of GLUT4 by inhibition of tyrosine is that GLUT4 endocytosis is blocked by hyperosmolarity in cells. GLUT4myc rapid insulin of the GLUT4myc is in the of insulin, the rate of GLUT4myc is the 12 of that insulin GLUT4 in with in cells a of gain in surface GLUT4 to to inhibition of GLUT4 endocytosis The GLUT4myc in L6 myoblasts is to the or GLUT4 or in the of insulin GLUT4 via and hypertonic to the of by preventing the and We that hyperosmolarity by a gain in GLUT4myc the cell surface and preventing GLUT4myc the that hyperosmolarity GLUT4 the cell in inhibition of GLUT4 is a that a tyrosine pathway and tyrosine activity is the surface gain in GLUT4 in However, is that effect is to the of GLUT4 the cell an inhibitor of the tyrosine erbstatin was to the inhibition of GLUT4myc endocytosis by hyperosmolarity in muscle cells A and the GLUT4 by only A and We propose that inhibition of GLUT4 endocytosis of the GLUT4 surface and the from the stimulation of GLUT4 exocytosis in response to of GLUT4 by inhibition of tyrosine is that GLUT4 endocytosis is blocked by hyperosmolarity in cells. Insulin and GLUT4 from the cell surface with in response to insulin and hypertonic We that an exocytic GLUT4 in L6 muscle cells, by insulin and that hyperosmolarity GLUT4 from an of GLUT4 the that insulin and hyperosmolarity GLUT4 from intracellular in L6 muscle cells is to tetanus and in muscle and cells and in GLUT4 in muscle and cells and tetanus toxin the GLUT4myc in L6 that the by the tetanus VAMP2 by the that VAMP2 is GLUT4 fusion with the membrane in response to insulin We that of tetanus toxin GLUT4myc caused by the that insulin and hyperosmolarity GLUT4 from intracellular VAMP2 and that is tetanus neither VAMP2 the v-SNARE the of GLUT4 from the is that a tetanus toxin-insensitive VAMP such as TI-VAMP mediate fusion of the with the membrane in muscle cells. TI-VAMP was detected in and its was partially from that of VAMP2 or VAMP3. The of TI-VAMP in fusion of the is of insulin and hyperosmolarity on GLUT4myc was partly additive. A to an effect in the cells with prior to to insulin We to effect we myoblasts in the The of these to the inhibition of insulin by hyperosmolarity the of as In contrast, L6 muscle cells with insulin, followed by the addition of caused a increase in the surface GLUT4myc with the effect of GLUT4myc from an GLUT4 to the of GLUT4myc the cell and as in GLUT4myc the cell hyperosmolarity a gain of GLUT4 the cell insulin and hyperosmolarity in is GLUT4 in and muscle cells In contrast, the accumulation of GLUT4 the cell surface is by the inhibitor wortmannin in inhibition was in wortmannin of or might Here we that activity is GLUT4myc caused by hyperosmolarity in L6 that in the of GLUT4 the surface in response to insulin is to of GLUT4 from a exocytic and from a that in muscle cells a effect of insulin is to GLUT4myc exocytosis from a is from the by hyperosmolarity and from the pool. the of intracellular GLUT4 traffic by the of GLUT4myc is in L6 myoblasts in the In the of insulin, of GLUT4myc and to the cell surface with a 12 of of the GLUT4myc remains and with a 12 of Insulin and hyperosmolarity GLUT4 from Insulin GLUT4 from a that the of and GLUT4 exocytosis from an the that and tetanus and the GLUT4 the cell surface by to the accumulation of GLUT4 the cell surface by The the and GLUT4 the cell surface with in response to insulin and hypertonic We that an exocytic GLUT4 in L6 muscle cells, by insulin and that hyperosmolarity GLUT4 from an of GLUT4 the that insulin and hyperosmolarity GLUT4 from intracellular in L6 muscle cells is to tetanus VAMP2 and in muscle and cells and in GLUT4 in muscle and cells and tetanus toxin the GLUT4myc in L6 that the by the tetanus VAMP2 by the that VAMP2 is GLUT4 fusion with the membrane in response to insulin We that of tetanus toxin GLUT4myc caused by the that insulin and hyperosmolarity GLUT4 from intracellular VAMP2 and that is tetanus neither VAMP2 the v-SNARE the of GLUT4 from the is that a tetanus toxin-insensitive VAMP such as TI-VAMP mediate fusion of the with the membrane in muscle cells. TI-VAMP was detected in and its was partially from that of VAMP2 or VAMP3. The of TI-VAMP in fusion of the is The of insulin and hyperosmolarity on GLUT4myc was partly additive. A to an effect in the cells with prior to to insulin We to effect we myoblasts in the The of these to the inhibition of insulin by hyperosmolarity the of as In contrast, L6 muscle cells with insulin, followed by the addition of caused a increase in the surface GLUT4myc with the effect of GLUT4myc from an GLUT4 to the of GLUT4myc the cell and as in GLUT4myc the cell hyperosmolarity a gain of GLUT4 the cell insulin and hyperosmolarity in is GLUT4 in and muscle cells In contrast, the accumulation of GLUT4 the cell surface is by the inhibitor wortmannin in inhibition was in wortmannin of or might Here we that activity is GLUT4myc caused by hyperosmolarity in L6 that in the of GLUT4 the surface in response to insulin is to of GLUT4 from a exocytic and from a that in muscle cells a effect of insulin is to GLUT4myc exocytosis from a is from the by hyperosmolarity and from the pool. the of intracellular GLUT4 traffic by In the of GLUT4myc is in L6 myoblasts in the In the of insulin, of GLUT4myc and to the cell surface with a 12 of of the GLUT4myc remains and with a 12 of Insulin and hyperosmolarity GLUT4 from Insulin GLUT4 from a that the of and GLUT4 exocytosis from an the that and tetanus and the GLUT4 the cell surface by to the accumulation of GLUT4 the cell surface by The the and We and and and on the

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