Insulin-induced translocation of GLUT 4 in skeletal muscle of insulin-resistant Zucker rats
Summary The genetically obese Zucker rat (fa/fa) is an animal model with severe insulin resistance of the skeletal muscle. We investigated whether a defect of insulin-dependent glucose transporter (GLUT 4) translocation might contribute to the pathogenesis of the insulin-resistant state. fa/fa rats,...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
1994 |
|---|
| Umfang: |
7 |
|---|
| Reproduktion: |
Springer Online Journal Archives 1860-2002 |
|---|---|
| Übergeordnetes Werk: |
in: Diabetologia - 1965, 37(1994) vom: Jan., Seite 3-9 |
| Übergeordnetes Werk: |
volume:37 ; year:1994 ; month:01 ; pages:3-9 ; extent:7 |
| Links: |
|---|
| Katalog-ID: |
NLEJ199927073 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLEJ199927073 | ||
| 003 | DE-627 | ||
| 005 | 20210706034412.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 070527s1994 xx |||||o 00| ||eng c | ||
| 035 | |a (DE-627)NLEJ199927073 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 245 | 1 | 0 | |a Insulin-induced translocation of GLUT 4 in skeletal muscle of insulin-resistant Zucker rats |
| 264 | 1 | |c 1994 | |
| 300 | |a 7 | ||
| 336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
| 337 | |a nicht spezifiziert |b z |2 rdamedia | ||
| 338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
| 520 | |a Summary The genetically obese Zucker rat (fa/fa) is an animal model with severe insulin resistance of the skeletal muscle. We investigated whether a defect of insulin-dependent glucose transporter (GLUT 4) translocation might contribute to the pathogenesis of the insulin-resistant state. fa/fa rats, lean controls (Fa/Fa) as well as normal Wistar rats were injected intraperitoneally with insulin and were killed after 2 or 20 min, respectively. Subcellular fractions were prepared from-hind-limb skeletal muscle and were characterized by determination of marker-enzyme activities and immunoblotting applying antibodies against α1 Na+/K+ AT Pase. The relative amounts of GLUT 1 and GLUT 4 were determined in the fractions by immunoblotting with the respective antibodies. Insulin induced an approximately two-fold increase of GLUT 4 in a plasma membrane and transverse tubule enriched fraction and a decrease in the low density enriched membrane fraction in all three groups of rats. There was a high individual variation in GLUT 4 translocation efficiency within the groups. However, no statistically significant difference was noted between the groups. No effect of insulin was detectable on the distribution of GLUT 1 or α1 Na+K+ ATPase. The data suggest that skeletal muscle insulin resistance of obese Zucker rats is not associated with a lack of GLUT 4 translocation. | ||
| 533 | |f Springer Online Journal Archives 1860-2002 | ||
| 700 | 1 | |a Galante, P. |4 oth | |
| 700 | 1 | |a Maerker, E. |4 oth | |
| 700 | 1 | |a Scholz, R. |4 oth | |
| 700 | 1 | |a Rett, K. |4 oth | |
| 700 | 1 | |a Herberg, L. |4 oth | |
| 700 | 1 | |a Mosthaf, L. |4 oth | |
| 700 | 1 | |a Häring, H. U. |4 oth | |
| 773 | 0 | 8 | |i in |t Diabetologia |d 1965 |g 37(1994) vom: Jan., Seite 3-9 |w (DE-627)NLEJ188984526 |w (DE-600)1458993-x |x 1432-0428 |7 nnns |
| 773 | 1 | 8 | |g volume:37 |g year:1994 |g month:01 |g pages:3-9 |g extent:7 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1007/BF00428770 |
| 912 | |a GBV_USEFLAG_U | ||
| 912 | |a ZDB-1-SOJ | ||
| 912 | |a GBV_NL_ARTICLE | ||
| 951 | |a AR | ||
| 952 | |d 37 |j 1994 |c 1 |h 3-9 |g 7 | ||
| matchkey_str |
article:14320428:1994----::nuiidcdrnlctoogu4nkltlucefnu |
|---|---|
| hierarchy_sort_str |
1994 |
| publishDate |
1994 |
| allfields |
(DE-627)NLEJ199927073 DE-627 ger DE-627 rakwb eng Insulin-induced translocation of GLUT 4 in skeletal muscle of insulin-resistant Zucker rats 1994 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary The genetically obese Zucker rat (fa/fa) is an animal model with severe insulin resistance of the skeletal muscle. We investigated whether a defect of insulin-dependent glucose transporter (GLUT 4) translocation might contribute to the pathogenesis of the insulin-resistant state. fa/fa rats, lean controls (Fa/Fa) as well as normal Wistar rats were injected intraperitoneally with insulin and were killed after 2 or 20 min, respectively. Subcellular fractions were prepared from-hind-limb skeletal muscle and were characterized by determination of marker-enzyme activities and immunoblotting applying antibodies against α1 Na+/K+ AT Pase. The relative amounts of GLUT 1 and GLUT 4 were determined in the fractions by immunoblotting with the respective antibodies. Insulin induced an approximately two-fold increase of GLUT 4 in a plasma membrane and transverse tubule enriched fraction and a decrease in the low density enriched membrane fraction in all three groups of rats. There was a high individual variation in GLUT 4 translocation efficiency within the groups. However, no statistically significant difference was noted between the groups. No effect of insulin was detectable on the distribution of GLUT 1 or α1 Na+K+ ATPase. The data suggest that skeletal muscle insulin resistance of obese Zucker rats is not associated with a lack of GLUT 4 translocation. Springer Online Journal Archives 1860-2002 Galante, P. oth Maerker, E. oth Scholz, R. oth Rett, K. oth Herberg, L. oth Mosthaf, L. oth Häring, H. U. oth in Diabetologia 1965 37(1994) vom: Jan., Seite 3-9 (DE-627)NLEJ188984526 (DE-600)1458993-x 1432-0428 nnns volume:37 year:1994 month:01 pages:3-9 extent:7 http://dx.doi.org/10.1007/BF00428770 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 37 1994 1 3-9 7 |
| spelling |
(DE-627)NLEJ199927073 DE-627 ger DE-627 rakwb eng Insulin-induced translocation of GLUT 4 in skeletal muscle of insulin-resistant Zucker rats 1994 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary The genetically obese Zucker rat (fa/fa) is an animal model with severe insulin resistance of the skeletal muscle. We investigated whether a defect of insulin-dependent glucose transporter (GLUT 4) translocation might contribute to the pathogenesis of the insulin-resistant state. fa/fa rats, lean controls (Fa/Fa) as well as normal Wistar rats were injected intraperitoneally with insulin and were killed after 2 or 20 min, respectively. Subcellular fractions were prepared from-hind-limb skeletal muscle and were characterized by determination of marker-enzyme activities and immunoblotting applying antibodies against α1 Na+/K+ AT Pase. The relative amounts of GLUT 1 and GLUT 4 were determined in the fractions by immunoblotting with the respective antibodies. Insulin induced an approximately two-fold increase of GLUT 4 in a plasma membrane and transverse tubule enriched fraction and a decrease in the low density enriched membrane fraction in all three groups of rats. There was a high individual variation in GLUT 4 translocation efficiency within the groups. However, no statistically significant difference was noted between the groups. No effect of insulin was detectable on the distribution of GLUT 1 or α1 Na+K+ ATPase. The data suggest that skeletal muscle insulin resistance of obese Zucker rats is not associated with a lack of GLUT 4 translocation. Springer Online Journal Archives 1860-2002 Galante, P. oth Maerker, E. oth Scholz, R. oth Rett, K. oth Herberg, L. oth Mosthaf, L. oth Häring, H. U. oth in Diabetologia 1965 37(1994) vom: Jan., Seite 3-9 (DE-627)NLEJ188984526 (DE-600)1458993-x 1432-0428 nnns volume:37 year:1994 month:01 pages:3-9 extent:7 http://dx.doi.org/10.1007/BF00428770 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 37 1994 1 3-9 7 |
| allfields_unstemmed |
(DE-627)NLEJ199927073 DE-627 ger DE-627 rakwb eng Insulin-induced translocation of GLUT 4 in skeletal muscle of insulin-resistant Zucker rats 1994 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary The genetically obese Zucker rat (fa/fa) is an animal model with severe insulin resistance of the skeletal muscle. We investigated whether a defect of insulin-dependent glucose transporter (GLUT 4) translocation might contribute to the pathogenesis of the insulin-resistant state. fa/fa rats, lean controls (Fa/Fa) as well as normal Wistar rats were injected intraperitoneally with insulin and were killed after 2 or 20 min, respectively. Subcellular fractions were prepared from-hind-limb skeletal muscle and were characterized by determination of marker-enzyme activities and immunoblotting applying antibodies against α1 Na+/K+ AT Pase. The relative amounts of GLUT 1 and GLUT 4 were determined in the fractions by immunoblotting with the respective antibodies. Insulin induced an approximately two-fold increase of GLUT 4 in a plasma membrane and transverse tubule enriched fraction and a decrease in the low density enriched membrane fraction in all three groups of rats. There was a high individual variation in GLUT 4 translocation efficiency within the groups. However, no statistically significant difference was noted between the groups. No effect of insulin was detectable on the distribution of GLUT 1 or α1 Na+K+ ATPase. The data suggest that skeletal muscle insulin resistance of obese Zucker rats is not associated with a lack of GLUT 4 translocation. Springer Online Journal Archives 1860-2002 Galante, P. oth Maerker, E. oth Scholz, R. oth Rett, K. oth Herberg, L. oth Mosthaf, L. oth Häring, H. U. oth in Diabetologia 1965 37(1994) vom: Jan., Seite 3-9 (DE-627)NLEJ188984526 (DE-600)1458993-x 1432-0428 nnns volume:37 year:1994 month:01 pages:3-9 extent:7 http://dx.doi.org/10.1007/BF00428770 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 37 1994 1 3-9 7 |
| allfieldsGer |
(DE-627)NLEJ199927073 DE-627 ger DE-627 rakwb eng Insulin-induced translocation of GLUT 4 in skeletal muscle of insulin-resistant Zucker rats 1994 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary The genetically obese Zucker rat (fa/fa) is an animal model with severe insulin resistance of the skeletal muscle. We investigated whether a defect of insulin-dependent glucose transporter (GLUT 4) translocation might contribute to the pathogenesis of the insulin-resistant state. fa/fa rats, lean controls (Fa/Fa) as well as normal Wistar rats were injected intraperitoneally with insulin and were killed after 2 or 20 min, respectively. Subcellular fractions were prepared from-hind-limb skeletal muscle and were characterized by determination of marker-enzyme activities and immunoblotting applying antibodies against α1 Na+/K+ AT Pase. The relative amounts of GLUT 1 and GLUT 4 were determined in the fractions by immunoblotting with the respective antibodies. Insulin induced an approximately two-fold increase of GLUT 4 in a plasma membrane and transverse tubule enriched fraction and a decrease in the low density enriched membrane fraction in all three groups of rats. There was a high individual variation in GLUT 4 translocation efficiency within the groups. However, no statistically significant difference was noted between the groups. No effect of insulin was detectable on the distribution of GLUT 1 or α1 Na+K+ ATPase. The data suggest that skeletal muscle insulin resistance of obese Zucker rats is not associated with a lack of GLUT 4 translocation. Springer Online Journal Archives 1860-2002 Galante, P. oth Maerker, E. oth Scholz, R. oth Rett, K. oth Herberg, L. oth Mosthaf, L. oth Häring, H. U. oth in Diabetologia 1965 37(1994) vom: Jan., Seite 3-9 (DE-627)NLEJ188984526 (DE-600)1458993-x 1432-0428 nnns volume:37 year:1994 month:01 pages:3-9 extent:7 http://dx.doi.org/10.1007/BF00428770 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 37 1994 1 3-9 7 |
| allfieldsSound |
(DE-627)NLEJ199927073 DE-627 ger DE-627 rakwb eng Insulin-induced translocation of GLUT 4 in skeletal muscle of insulin-resistant Zucker rats 1994 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary The genetically obese Zucker rat (fa/fa) is an animal model with severe insulin resistance of the skeletal muscle. We investigated whether a defect of insulin-dependent glucose transporter (GLUT 4) translocation might contribute to the pathogenesis of the insulin-resistant state. fa/fa rats, lean controls (Fa/Fa) as well as normal Wistar rats were injected intraperitoneally with insulin and were killed after 2 or 20 min, respectively. Subcellular fractions were prepared from-hind-limb skeletal muscle and were characterized by determination of marker-enzyme activities and immunoblotting applying antibodies against α1 Na+/K+ AT Pase. The relative amounts of GLUT 1 and GLUT 4 were determined in the fractions by immunoblotting with the respective antibodies. Insulin induced an approximately two-fold increase of GLUT 4 in a plasma membrane and transverse tubule enriched fraction and a decrease in the low density enriched membrane fraction in all three groups of rats. There was a high individual variation in GLUT 4 translocation efficiency within the groups. However, no statistically significant difference was noted between the groups. No effect of insulin was detectable on the distribution of GLUT 1 or α1 Na+K+ ATPase. The data suggest that skeletal muscle insulin resistance of obese Zucker rats is not associated with a lack of GLUT 4 translocation. Springer Online Journal Archives 1860-2002 Galante, P. oth Maerker, E. oth Scholz, R. oth Rett, K. oth Herberg, L. oth Mosthaf, L. oth Häring, H. U. oth in Diabetologia 1965 37(1994) vom: Jan., Seite 3-9 (DE-627)NLEJ188984526 (DE-600)1458993-x 1432-0428 nnns volume:37 year:1994 month:01 pages:3-9 extent:7 http://dx.doi.org/10.1007/BF00428770 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 37 1994 1 3-9 7 |
| language |
English |
| source |
in Diabetologia 37(1994) vom: Jan., Seite 3-9 volume:37 year:1994 month:01 pages:3-9 extent:7 |
| sourceStr |
in Diabetologia 37(1994) vom: Jan., Seite 3-9 volume:37 year:1994 month:01 pages:3-9 extent:7 |
| format_phy_str_mv |
Article |
| institution |
findex.gbv.de |
| isfreeaccess_bool |
false |
| container_title |
Diabetologia |
| authorswithroles_txt_mv |
Galante, P. @@oth@@ Maerker, E. @@oth@@ Scholz, R. @@oth@@ Rett, K. @@oth@@ Herberg, L. @@oth@@ Mosthaf, L. @@oth@@ Häring, H. U. @@oth@@ |
| publishDateDaySort_date |
1994-01-01T00:00:00Z |
| hierarchy_top_id |
NLEJ188984526 |
| id |
NLEJ199927073 |
| language_de |
englisch |
| fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ199927073</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210706034412.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070527s1994 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ199927073</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Insulin-induced translocation of GLUT 4 in skeletal muscle of insulin-resistant Zucker rats</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1994</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">7</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Summary The genetically obese Zucker rat (fa/fa) is an animal model with severe insulin resistance of the skeletal muscle. We investigated whether a defect of insulin-dependent glucose transporter (GLUT 4) translocation might contribute to the pathogenesis of the insulin-resistant state. fa/fa rats, lean controls (Fa/Fa) as well as normal Wistar rats were injected intraperitoneally with insulin and were killed after 2 or 20 min, respectively. Subcellular fractions were prepared from-hind-limb skeletal muscle and were characterized by determination of marker-enzyme activities and immunoblotting applying antibodies against α1 Na+/K+ AT Pase. The relative amounts of GLUT 1 and GLUT 4 were determined in the fractions by immunoblotting with the respective antibodies. Insulin induced an approximately two-fold increase of GLUT 4 in a plasma membrane and transverse tubule enriched fraction and a decrease in the low density enriched membrane fraction in all three groups of rats. There was a high individual variation in GLUT 4 translocation efficiency within the groups. However, no statistically significant difference was noted between the groups. No effect of insulin was detectable on the distribution of GLUT 1 or α1 Na+K+ ATPase. The data suggest that skeletal muscle insulin resistance of obese Zucker rats is not associated with a lack of GLUT 4 translocation.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="f">Springer Online Journal Archives 1860-2002</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Galante, P.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Maerker, E.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Scholz, R.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Rett, K.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Herberg, L.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Mosthaf, L.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Häring, H. U.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Diabetologia</subfield><subfield code="d">1965</subfield><subfield code="g">37(1994) vom: Jan., Seite 3-9</subfield><subfield code="w">(DE-627)NLEJ188984526</subfield><subfield code="w">(DE-600)1458993-x</subfield><subfield code="x">1432-0428</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:37</subfield><subfield code="g">year:1994</subfield><subfield code="g">month:01</subfield><subfield code="g">pages:3-9</subfield><subfield code="g">extent:7</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1007/BF00428770</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-SOJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">37</subfield><subfield code="j">1994</subfield><subfield code="c">1</subfield><subfield code="h">3-9</subfield><subfield code="g">7</subfield></datafield></record></collection>
|
| series2 |
Springer Online Journal Archives 1860-2002 |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)NLEJ188984526 |
| format |
electronic Article |
| delete_txt_mv |
keep |
| collection |
NL |
| remote_str |
true |
| illustrated |
Not Illustrated |
| issn |
1432-0428 |
| topic_title |
Insulin-induced translocation of GLUT 4 in skeletal muscle of insulin-resistant Zucker rats |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| author2_variant |
p g pg e m em r s rs k r kr l h lh l m lm h u h hu huh |
| hierarchy_parent_title |
Diabetologia |
| hierarchy_parent_id |
NLEJ188984526 |
| hierarchy_top_title |
Diabetologia |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)NLEJ188984526 (DE-600)1458993-x |
| title |
Insulin-induced translocation of GLUT 4 in skeletal muscle of insulin-resistant Zucker rats |
| spellingShingle |
Insulin-induced translocation of GLUT 4 in skeletal muscle of insulin-resistant Zucker rats |
| ctrlnum |
(DE-627)NLEJ199927073 |
| title_full |
Insulin-induced translocation of GLUT 4 in skeletal muscle of insulin-resistant Zucker rats |
| journal |
Diabetologia |
| journalStr |
Diabetologia |
| lang_code |
eng |
| isOA_bool |
false |
| recordtype |
marc |
| publishDateSort |
1994 |
| contenttype_str_mv |
zzz |
| container_start_page |
3 |
| container_volume |
37 |
| physical |
7 |
| format_se |
Elektronische Aufsätze |
| title_sort |
insulin-induced translocation of glut 4 in skeletal muscle of insulin-resistant zucker rats |
| title_auth |
Insulin-induced translocation of GLUT 4 in skeletal muscle of insulin-resistant Zucker rats |
| abstract |
Summary The genetically obese Zucker rat (fa/fa) is an animal model with severe insulin resistance of the skeletal muscle. We investigated whether a defect of insulin-dependent glucose transporter (GLUT 4) translocation might contribute to the pathogenesis of the insulin-resistant state. fa/fa rats, lean controls (Fa/Fa) as well as normal Wistar rats were injected intraperitoneally with insulin and were killed after 2 or 20 min, respectively. Subcellular fractions were prepared from-hind-limb skeletal muscle and were characterized by determination of marker-enzyme activities and immunoblotting applying antibodies against α1 Na+/K+ AT Pase. The relative amounts of GLUT 1 and GLUT 4 were determined in the fractions by immunoblotting with the respective antibodies. Insulin induced an approximately two-fold increase of GLUT 4 in a plasma membrane and transverse tubule enriched fraction and a decrease in the low density enriched membrane fraction in all three groups of rats. There was a high individual variation in GLUT 4 translocation efficiency within the groups. However, no statistically significant difference was noted between the groups. No effect of insulin was detectable on the distribution of GLUT 1 or α1 Na+K+ ATPase. The data suggest that skeletal muscle insulin resistance of obese Zucker rats is not associated with a lack of GLUT 4 translocation. |
| abstractGer |
Summary The genetically obese Zucker rat (fa/fa) is an animal model with severe insulin resistance of the skeletal muscle. We investigated whether a defect of insulin-dependent glucose transporter (GLUT 4) translocation might contribute to the pathogenesis of the insulin-resistant state. fa/fa rats, lean controls (Fa/Fa) as well as normal Wistar rats were injected intraperitoneally with insulin and were killed after 2 or 20 min, respectively. Subcellular fractions were prepared from-hind-limb skeletal muscle and were characterized by determination of marker-enzyme activities and immunoblotting applying antibodies against α1 Na+/K+ AT Pase. The relative amounts of GLUT 1 and GLUT 4 were determined in the fractions by immunoblotting with the respective antibodies. Insulin induced an approximately two-fold increase of GLUT 4 in a plasma membrane and transverse tubule enriched fraction and a decrease in the low density enriched membrane fraction in all three groups of rats. There was a high individual variation in GLUT 4 translocation efficiency within the groups. However, no statistically significant difference was noted between the groups. No effect of insulin was detectable on the distribution of GLUT 1 or α1 Na+K+ ATPase. The data suggest that skeletal muscle insulin resistance of obese Zucker rats is not associated with a lack of GLUT 4 translocation. |
| abstract_unstemmed |
Summary The genetically obese Zucker rat (fa/fa) is an animal model with severe insulin resistance of the skeletal muscle. We investigated whether a defect of insulin-dependent glucose transporter (GLUT 4) translocation might contribute to the pathogenesis of the insulin-resistant state. fa/fa rats, lean controls (Fa/Fa) as well as normal Wistar rats were injected intraperitoneally with insulin and were killed after 2 or 20 min, respectively. Subcellular fractions were prepared from-hind-limb skeletal muscle and were characterized by determination of marker-enzyme activities and immunoblotting applying antibodies against α1 Na+/K+ AT Pase. The relative amounts of GLUT 1 and GLUT 4 were determined in the fractions by immunoblotting with the respective antibodies. Insulin induced an approximately two-fold increase of GLUT 4 in a plasma membrane and transverse tubule enriched fraction and a decrease in the low density enriched membrane fraction in all three groups of rats. There was a high individual variation in GLUT 4 translocation efficiency within the groups. However, no statistically significant difference was noted between the groups. No effect of insulin was detectable on the distribution of GLUT 1 or α1 Na+K+ ATPase. The data suggest that skeletal muscle insulin resistance of obese Zucker rats is not associated with a lack of GLUT 4 translocation. |
| collection_details |
GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE |
| title_short |
Insulin-induced translocation of GLUT 4 in skeletal muscle of insulin-resistant Zucker rats |
| url |
http://dx.doi.org/10.1007/BF00428770 |
| remote_bool |
true |
| author2 |
Galante, P. Maerker, E. Scholz, R. Rett, K. Herberg, L. Mosthaf, L. Häring, H. U. |
| author2Str |
Galante, P. Maerker, E. Scholz, R. Rett, K. Herberg, L. Mosthaf, L. Häring, H. U. |
| ppnlink |
NLEJ188984526 |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| author2_role |
oth oth oth oth oth oth oth |
| up_date |
2024-07-06T01:22:57.690Z |
| _version_ |
1803790820511318016 |
| fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ199927073</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210706034412.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070527s1994 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ199927073</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Insulin-induced translocation of GLUT 4 in skeletal muscle of insulin-resistant Zucker rats</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1994</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">7</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Summary The genetically obese Zucker rat (fa/fa) is an animal model with severe insulin resistance of the skeletal muscle. We investigated whether a defect of insulin-dependent glucose transporter (GLUT 4) translocation might contribute to the pathogenesis of the insulin-resistant state. fa/fa rats, lean controls (Fa/Fa) as well as normal Wistar rats were injected intraperitoneally with insulin and were killed after 2 or 20 min, respectively. Subcellular fractions were prepared from-hind-limb skeletal muscle and were characterized by determination of marker-enzyme activities and immunoblotting applying antibodies against α1 Na+/K+ AT Pase. The relative amounts of GLUT 1 and GLUT 4 were determined in the fractions by immunoblotting with the respective antibodies. Insulin induced an approximately two-fold increase of GLUT 4 in a plasma membrane and transverse tubule enriched fraction and a decrease in the low density enriched membrane fraction in all three groups of rats. There was a high individual variation in GLUT 4 translocation efficiency within the groups. However, no statistically significant difference was noted between the groups. No effect of insulin was detectable on the distribution of GLUT 1 or α1 Na+K+ ATPase. The data suggest that skeletal muscle insulin resistance of obese Zucker rats is not associated with a lack of GLUT 4 translocation.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="f">Springer Online Journal Archives 1860-2002</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Galante, P.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Maerker, E.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Scholz, R.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Rett, K.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Herberg, L.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Mosthaf, L.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Häring, H. U.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Diabetologia</subfield><subfield code="d">1965</subfield><subfield code="g">37(1994) vom: Jan., Seite 3-9</subfield><subfield code="w">(DE-627)NLEJ188984526</subfield><subfield code="w">(DE-600)1458993-x</subfield><subfield code="x">1432-0428</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:37</subfield><subfield code="g">year:1994</subfield><subfield code="g">month:01</subfield><subfield code="g">pages:3-9</subfield><subfield code="g">extent:7</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1007/BF00428770</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-SOJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">37</subfield><subfield code="j">1994</subfield><subfield code="c">1</subfield><subfield code="h">3-9</subfield><subfield code="g">7</subfield></datafield></record></collection>
|
| score |
7.398777 |