Insulin-Sensitizing Effect of LXR Agonist T0901317 in High-Fat Fed Rats is Associated with Restored Muscle GLUT4 Expression and Insulin-Stimulated AS160 Phosphorylation

Background/Aim: Liver X receptors (LXRs) are ligand-activated transcription factors that were shown to stimulate hepatic lipogenesis leading to liver steatosis and hypertriglyceridemia. Despite their pro-lipogenic action, LXR activators normalize glycemia and improve insulin sensitivity in rodent mo...
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Autor*in:	Marcin Baranowski [verfasserIn] Piotr Zabielski [verfasserIn] Agnieszka U. Błachnio-Zabielska [verfasserIn] Ewa Harasim [verfasserIn] Adrian Chabowski [verfasserIn] Jan Górski [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2014

Schlagwörter:	Akt/PKB Insulin resistance IRS1 Lipid mediators Skeletal muscle

Übergeordnetes Werk:	In: Cellular Physiology and Biochemistry - Cell Physiol Biochem Press GmbH & Co KG, 2002, 33(2014), 4, Seite 1047-1057
Übergeordnetes Werk:	volume:33 ; year:2014 ; number:4 ; pages:1047-1057

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.1159/000358675

Katalog-ID:	DOAJ07719196X

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245	1	0	\|a Insulin-Sensitizing Effect of LXR Agonist T0901317 in High-Fat Fed Rats is Associated with Restored Muscle GLUT4 Expression and Insulin-Stimulated AS160 Phosphorylation
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520			\|a Background/Aim: Liver X receptors (LXRs) are ligand-activated transcription factors that were shown to stimulate hepatic lipogenesis leading to liver steatosis and hypertriglyceridemia. Despite their pro-lipogenic action, LXR activators normalize glycemia and improve insulin sensitivity in rodent models of type 2 diabetes. Antidiabetic action of LXR agonists is thought to result from suppression of hepatic gluconeogenesis. However, it remains unclear whether LXR activation affects muscle insulin sensitivity. In the present study we attempted to answer this question. Methods: The experiments were performed on male Wistar rats fed for 5 weeks on either standard chow or high fat diet. The latter group was further divided into two subgroups receiving either selective LXR agonist - T0901317 (10mg/kg/d) or vehicle during the last week of the experiment. All animals were then anaesthetized and samples of the soleus as well as red and white sections of the gastrocnemius muscle were excised. Results: As expected, administration of T0901317 to high-fat fed rats augmented diet-induced hyperlipidemia. Nevertheless, it also normalized glucose tolerance and improved insulin-stimulated glucose uptake in isolated soleus muscle. In addition, LXR agonist completely restored glucose transporter 4 expression and insulin-stimulated Akt substrate of 160 kDa phosphorylation in all investigated muscles. Insulin-sensitizing effect of T0901317 was not related to changes in intramuscular level of lipid mediators of insulin resistance, since neither diacylglycerols nor ceramide content was affected by the treatment. Conclusion: We conclude that improvement in muscle insulin sensitivity is one of the mechanisms underlying the antidiabetic action of LXR activators.
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allfields	10.1159/000358675 doi (DE-627)DOAJ07719196X (DE-599)DOAJb59197eb9a9c442085bdbbcdc02a2cd8 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Marcin Baranowski verfasserin aut Insulin-Sensitizing Effect of LXR Agonist T0901317 in High-Fat Fed Rats is Associated with Restored Muscle GLUT4 Expression and Insulin-Stimulated AS160 Phosphorylation 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background/Aim: Liver X receptors (LXRs) are ligand-activated transcription factors that were shown to stimulate hepatic lipogenesis leading to liver steatosis and hypertriglyceridemia. Despite their pro-lipogenic action, LXR activators normalize glycemia and improve insulin sensitivity in rodent models of type 2 diabetes. Antidiabetic action of LXR agonists is thought to result from suppression of hepatic gluconeogenesis. However, it remains unclear whether LXR activation affects muscle insulin sensitivity. In the present study we attempted to answer this question. Methods: The experiments were performed on male Wistar rats fed for 5 weeks on either standard chow or high fat diet. The latter group was further divided into two subgroups receiving either selective LXR agonist - T0901317 (10mg/kg/d) or vehicle during the last week of the experiment. All animals were then anaesthetized and samples of the soleus as well as red and white sections of the gastrocnemius muscle were excised. Results: As expected, administration of T0901317 to high-fat fed rats augmented diet-induced hyperlipidemia. Nevertheless, it also normalized glucose tolerance and improved insulin-stimulated glucose uptake in isolated soleus muscle. In addition, LXR agonist completely restored glucose transporter 4 expression and insulin-stimulated Akt substrate of 160 kDa phosphorylation in all investigated muscles. Insulin-sensitizing effect of T0901317 was not related to changes in intramuscular level of lipid mediators of insulin resistance, since neither diacylglycerols nor ceramide content was affected by the treatment. Conclusion: We conclude that improvement in muscle insulin sensitivity is one of the mechanisms underlying the antidiabetic action of LXR activators. Akt/PKB Insulin resistance IRS1 Lipid mediators Skeletal muscle Physiology Biochemistry Piotr Zabielski verfasserin aut Agnieszka U. Błachnio-Zabielska verfasserin aut Ewa Harasim verfasserin aut Adrian Chabowski verfasserin aut Jan Górski verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 33(2014), 4, Seite 1047-1057 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:33 year:2014 number:4 pages:1047-1057 https://doi.org/10.1159/000358675 kostenfrei https://doaj.org/article/b59197eb9a9c442085bdbbcdc02a2cd8 kostenfrei http://www.karger.com/Article/FullText/358675 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 33 2014 4 1047-1057
spelling	10.1159/000358675 doi (DE-627)DOAJ07719196X (DE-599)DOAJb59197eb9a9c442085bdbbcdc02a2cd8 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Marcin Baranowski verfasserin aut Insulin-Sensitizing Effect of LXR Agonist T0901317 in High-Fat Fed Rats is Associated with Restored Muscle GLUT4 Expression and Insulin-Stimulated AS160 Phosphorylation 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background/Aim: Liver X receptors (LXRs) are ligand-activated transcription factors that were shown to stimulate hepatic lipogenesis leading to liver steatosis and hypertriglyceridemia. Despite their pro-lipogenic action, LXR activators normalize glycemia and improve insulin sensitivity in rodent models of type 2 diabetes. Antidiabetic action of LXR agonists is thought to result from suppression of hepatic gluconeogenesis. However, it remains unclear whether LXR activation affects muscle insulin sensitivity. In the present study we attempted to answer this question. Methods: The experiments were performed on male Wistar rats fed for 5 weeks on either standard chow or high fat diet. The latter group was further divided into two subgroups receiving either selective LXR agonist - T0901317 (10mg/kg/d) or vehicle during the last week of the experiment. All animals were then anaesthetized and samples of the soleus as well as red and white sections of the gastrocnemius muscle were excised. Results: As expected, administration of T0901317 to high-fat fed rats augmented diet-induced hyperlipidemia. Nevertheless, it also normalized glucose tolerance and improved insulin-stimulated glucose uptake in isolated soleus muscle. In addition, LXR agonist completely restored glucose transporter 4 expression and insulin-stimulated Akt substrate of 160 kDa phosphorylation in all investigated muscles. Insulin-sensitizing effect of T0901317 was not related to changes in intramuscular level of lipid mediators of insulin resistance, since neither diacylglycerols nor ceramide content was affected by the treatment. Conclusion: We conclude that improvement in muscle insulin sensitivity is one of the mechanisms underlying the antidiabetic action of LXR activators. Akt/PKB Insulin resistance IRS1 Lipid mediators Skeletal muscle Physiology Biochemistry Piotr Zabielski verfasserin aut Agnieszka U. Błachnio-Zabielska verfasserin aut Ewa Harasim verfasserin aut Adrian Chabowski verfasserin aut Jan Górski verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 33(2014), 4, Seite 1047-1057 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:33 year:2014 number:4 pages:1047-1057 https://doi.org/10.1159/000358675 kostenfrei https://doaj.org/article/b59197eb9a9c442085bdbbcdc02a2cd8 kostenfrei http://www.karger.com/Article/FullText/358675 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 33 2014 4 1047-1057
allfields_unstemmed	10.1159/000358675 doi (DE-627)DOAJ07719196X (DE-599)DOAJb59197eb9a9c442085bdbbcdc02a2cd8 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Marcin Baranowski verfasserin aut Insulin-Sensitizing Effect of LXR Agonist T0901317 in High-Fat Fed Rats is Associated with Restored Muscle GLUT4 Expression and Insulin-Stimulated AS160 Phosphorylation 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background/Aim: Liver X receptors (LXRs) are ligand-activated transcription factors that were shown to stimulate hepatic lipogenesis leading to liver steatosis and hypertriglyceridemia. Despite their pro-lipogenic action, LXR activators normalize glycemia and improve insulin sensitivity in rodent models of type 2 diabetes. Antidiabetic action of LXR agonists is thought to result from suppression of hepatic gluconeogenesis. However, it remains unclear whether LXR activation affects muscle insulin sensitivity. In the present study we attempted to answer this question. Methods: The experiments were performed on male Wistar rats fed for 5 weeks on either standard chow or high fat diet. The latter group was further divided into two subgroups receiving either selective LXR agonist - T0901317 (10mg/kg/d) or vehicle during the last week of the experiment. All animals were then anaesthetized and samples of the soleus as well as red and white sections of the gastrocnemius muscle were excised. Results: As expected, administration of T0901317 to high-fat fed rats augmented diet-induced hyperlipidemia. Nevertheless, it also normalized glucose tolerance and improved insulin-stimulated glucose uptake in isolated soleus muscle. In addition, LXR agonist completely restored glucose transporter 4 expression and insulin-stimulated Akt substrate of 160 kDa phosphorylation in all investigated muscles. Insulin-sensitizing effect of T0901317 was not related to changes in intramuscular level of lipid mediators of insulin resistance, since neither diacylglycerols nor ceramide content was affected by the treatment. Conclusion: We conclude that improvement in muscle insulin sensitivity is one of the mechanisms underlying the antidiabetic action of LXR activators. Akt/PKB Insulin resistance IRS1 Lipid mediators Skeletal muscle Physiology Biochemistry Piotr Zabielski verfasserin aut Agnieszka U. Błachnio-Zabielska verfasserin aut Ewa Harasim verfasserin aut Adrian Chabowski verfasserin aut Jan Górski verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 33(2014), 4, Seite 1047-1057 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:33 year:2014 number:4 pages:1047-1057 https://doi.org/10.1159/000358675 kostenfrei https://doaj.org/article/b59197eb9a9c442085bdbbcdc02a2cd8 kostenfrei http://www.karger.com/Article/FullText/358675 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 33 2014 4 1047-1057
allfieldsGer	10.1159/000358675 doi (DE-627)DOAJ07719196X (DE-599)DOAJb59197eb9a9c442085bdbbcdc02a2cd8 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Marcin Baranowski verfasserin aut Insulin-Sensitizing Effect of LXR Agonist T0901317 in High-Fat Fed Rats is Associated with Restored Muscle GLUT4 Expression and Insulin-Stimulated AS160 Phosphorylation 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background/Aim: Liver X receptors (LXRs) are ligand-activated transcription factors that were shown to stimulate hepatic lipogenesis leading to liver steatosis and hypertriglyceridemia. Despite their pro-lipogenic action, LXR activators normalize glycemia and improve insulin sensitivity in rodent models of type 2 diabetes. Antidiabetic action of LXR agonists is thought to result from suppression of hepatic gluconeogenesis. However, it remains unclear whether LXR activation affects muscle insulin sensitivity. In the present study we attempted to answer this question. Methods: The experiments were performed on male Wistar rats fed for 5 weeks on either standard chow or high fat diet. The latter group was further divided into two subgroups receiving either selective LXR agonist - T0901317 (10mg/kg/d) or vehicle during the last week of the experiment. All animals were then anaesthetized and samples of the soleus as well as red and white sections of the gastrocnemius muscle were excised. Results: As expected, administration of T0901317 to high-fat fed rats augmented diet-induced hyperlipidemia. Nevertheless, it also normalized glucose tolerance and improved insulin-stimulated glucose uptake in isolated soleus muscle. In addition, LXR agonist completely restored glucose transporter 4 expression and insulin-stimulated Akt substrate of 160 kDa phosphorylation in all investigated muscles. Insulin-sensitizing effect of T0901317 was not related to changes in intramuscular level of lipid mediators of insulin resistance, since neither diacylglycerols nor ceramide content was affected by the treatment. Conclusion: We conclude that improvement in muscle insulin sensitivity is one of the mechanisms underlying the antidiabetic action of LXR activators. Akt/PKB Insulin resistance IRS1 Lipid mediators Skeletal muscle Physiology Biochemistry Piotr Zabielski verfasserin aut Agnieszka U. Błachnio-Zabielska verfasserin aut Ewa Harasim verfasserin aut Adrian Chabowski verfasserin aut Jan Górski verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 33(2014), 4, Seite 1047-1057 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:33 year:2014 number:4 pages:1047-1057 https://doi.org/10.1159/000358675 kostenfrei https://doaj.org/article/b59197eb9a9c442085bdbbcdc02a2cd8 kostenfrei http://www.karger.com/Article/FullText/358675 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 33 2014 4 1047-1057
allfieldsSound	10.1159/000358675 doi (DE-627)DOAJ07719196X (DE-599)DOAJb59197eb9a9c442085bdbbcdc02a2cd8 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Marcin Baranowski verfasserin aut Insulin-Sensitizing Effect of LXR Agonist T0901317 in High-Fat Fed Rats is Associated with Restored Muscle GLUT4 Expression and Insulin-Stimulated AS160 Phosphorylation 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background/Aim: Liver X receptors (LXRs) are ligand-activated transcription factors that were shown to stimulate hepatic lipogenesis leading to liver steatosis and hypertriglyceridemia. Despite their pro-lipogenic action, LXR activators normalize glycemia and improve insulin sensitivity in rodent models of type 2 diabetes. Antidiabetic action of LXR agonists is thought to result from suppression of hepatic gluconeogenesis. However, it remains unclear whether LXR activation affects muscle insulin sensitivity. In the present study we attempted to answer this question. Methods: The experiments were performed on male Wistar rats fed for 5 weeks on either standard chow or high fat diet. The latter group was further divided into two subgroups receiving either selective LXR agonist - T0901317 (10mg/kg/d) or vehicle during the last week of the experiment. All animals were then anaesthetized and samples of the soleus as well as red and white sections of the gastrocnemius muscle were excised. Results: As expected, administration of T0901317 to high-fat fed rats augmented diet-induced hyperlipidemia. Nevertheless, it also normalized glucose tolerance and improved insulin-stimulated glucose uptake in isolated soleus muscle. In addition, LXR agonist completely restored glucose transporter 4 expression and insulin-stimulated Akt substrate of 160 kDa phosphorylation in all investigated muscles. Insulin-sensitizing effect of T0901317 was not related to changes in intramuscular level of lipid mediators of insulin resistance, since neither diacylglycerols nor ceramide content was affected by the treatment. Conclusion: We conclude that improvement in muscle insulin sensitivity is one of the mechanisms underlying the antidiabetic action of LXR activators. Akt/PKB Insulin resistance IRS1 Lipid mediators Skeletal muscle Physiology Biochemistry Piotr Zabielski verfasserin aut Agnieszka U. Błachnio-Zabielska verfasserin aut Ewa Harasim verfasserin aut Adrian Chabowski verfasserin aut Jan Górski verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 33(2014), 4, Seite 1047-1057 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:33 year:2014 number:4 pages:1047-1057 https://doi.org/10.1159/000358675 kostenfrei https://doaj.org/article/b59197eb9a9c442085bdbbcdc02a2cd8 kostenfrei http://www.karger.com/Article/FullText/358675 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 33 2014 4 1047-1057
language	English
source	In Cellular Physiology and Biochemistry 33(2014), 4, Seite 1047-1057 volume:33 year:2014 number:4 pages:1047-1057
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topic_facet	Akt/PKB Insulin resistance IRS1 Lipid mediators Skeletal muscle Physiology Biochemistry
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container_title	Cellular Physiology and Biochemistry
authorswithroles_txt_mv	Marcin Baranowski @@aut@@ Piotr Zabielski @@aut@@ Agnieszka U. Błachnio-Zabielska @@aut@@ Ewa Harasim @@aut@@ Adrian Chabowski @@aut@@ Jan Górski @@aut@@
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spellingShingle	Marcin Baranowski misc QP1-981 misc QD415-436 misc Akt/PKB misc Insulin resistance misc IRS1 misc Lipid mediators misc Skeletal muscle misc Physiology misc Biochemistry Insulin-Sensitizing Effect of LXR Agonist T0901317 in High-Fat Fed Rats is Associated with Restored Muscle GLUT4 Expression and Insulin-Stimulated AS160 Phosphorylation
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topic_title	QP1-981 QD415-436 Insulin-Sensitizing Effect of LXR Agonist T0901317 in High-Fat Fed Rats is Associated with Restored Muscle GLUT4 Expression and Insulin-Stimulated AS160 Phosphorylation Akt/PKB Insulin resistance IRS1 Lipid mediators Skeletal muscle
topic	misc QP1-981 misc QD415-436 misc Akt/PKB misc Insulin resistance misc IRS1 misc Lipid mediators misc Skeletal muscle misc Physiology misc Biochemistry
topic_unstemmed	misc QP1-981 misc QD415-436 misc Akt/PKB misc Insulin resistance misc IRS1 misc Lipid mediators misc Skeletal muscle misc Physiology misc Biochemistry
topic_browse	misc QP1-981 misc QD415-436 misc Akt/PKB misc Insulin resistance misc IRS1 misc Lipid mediators misc Skeletal muscle misc Physiology misc Biochemistry
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title	Insulin-Sensitizing Effect of LXR Agonist T0901317 in High-Fat Fed Rats is Associated with Restored Muscle GLUT4 Expression and Insulin-Stimulated AS160 Phosphorylation
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title_full	Insulin-Sensitizing Effect of LXR Agonist T0901317 in High-Fat Fed Rats is Associated with Restored Muscle GLUT4 Expression and Insulin-Stimulated AS160 Phosphorylation
author_sort	Marcin Baranowski
journal	Cellular Physiology and Biochemistry
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author_browse	Marcin Baranowski Piotr Zabielski Agnieszka U. Błachnio-Zabielska Ewa Harasim Adrian Chabowski Jan Górski
container_volume	33
class	QP1-981 QD415-436
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author-letter	Marcin Baranowski
doi_str_mv	10.1159/000358675
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title_sort	insulin-sensitizing effect of lxr agonist t0901317 in high-fat fed rats is associated with restored muscle glut4 expression and insulin-stimulated as160 phosphorylation
callnumber	QP1-981
title_auth	Insulin-Sensitizing Effect of LXR Agonist T0901317 in High-Fat Fed Rats is Associated with Restored Muscle GLUT4 Expression and Insulin-Stimulated AS160 Phosphorylation
abstract	Background/Aim: Liver X receptors (LXRs) are ligand-activated transcription factors that were shown to stimulate hepatic lipogenesis leading to liver steatosis and hypertriglyceridemia. Despite their pro-lipogenic action, LXR activators normalize glycemia and improve insulin sensitivity in rodent models of type 2 diabetes. Antidiabetic action of LXR agonists is thought to result from suppression of hepatic gluconeogenesis. However, it remains unclear whether LXR activation affects muscle insulin sensitivity. In the present study we attempted to answer this question. Methods: The experiments were performed on male Wistar rats fed for 5 weeks on either standard chow or high fat diet. The latter group was further divided into two subgroups receiving either selective LXR agonist - T0901317 (10mg/kg/d) or vehicle during the last week of the experiment. All animals were then anaesthetized and samples of the soleus as well as red and white sections of the gastrocnemius muscle were excised. Results: As expected, administration of T0901317 to high-fat fed rats augmented diet-induced hyperlipidemia. Nevertheless, it also normalized glucose tolerance and improved insulin-stimulated glucose uptake in isolated soleus muscle. In addition, LXR agonist completely restored glucose transporter 4 expression and insulin-stimulated Akt substrate of 160 kDa phosphorylation in all investigated muscles. Insulin-sensitizing effect of T0901317 was not related to changes in intramuscular level of lipid mediators of insulin resistance, since neither diacylglycerols nor ceramide content was affected by the treatment. Conclusion: We conclude that improvement in muscle insulin sensitivity is one of the mechanisms underlying the antidiabetic action of LXR activators.
abstractGer	Background/Aim: Liver X receptors (LXRs) are ligand-activated transcription factors that were shown to stimulate hepatic lipogenesis leading to liver steatosis and hypertriglyceridemia. Despite their pro-lipogenic action, LXR activators normalize glycemia and improve insulin sensitivity in rodent models of type 2 diabetes. Antidiabetic action of LXR agonists is thought to result from suppression of hepatic gluconeogenesis. However, it remains unclear whether LXR activation affects muscle insulin sensitivity. In the present study we attempted to answer this question. Methods: The experiments were performed on male Wistar rats fed for 5 weeks on either standard chow or high fat diet. The latter group was further divided into two subgroups receiving either selective LXR agonist - T0901317 (10mg/kg/d) or vehicle during the last week of the experiment. All animals were then anaesthetized and samples of the soleus as well as red and white sections of the gastrocnemius muscle were excised. Results: As expected, administration of T0901317 to high-fat fed rats augmented diet-induced hyperlipidemia. Nevertheless, it also normalized glucose tolerance and improved insulin-stimulated glucose uptake in isolated soleus muscle. In addition, LXR agonist completely restored glucose transporter 4 expression and insulin-stimulated Akt substrate of 160 kDa phosphorylation in all investigated muscles. Insulin-sensitizing effect of T0901317 was not related to changes in intramuscular level of lipid mediators of insulin resistance, since neither diacylglycerols nor ceramide content was affected by the treatment. Conclusion: We conclude that improvement in muscle insulin sensitivity is one of the mechanisms underlying the antidiabetic action of LXR activators.
abstract_unstemmed	Background/Aim: Liver X receptors (LXRs) are ligand-activated transcription factors that were shown to stimulate hepatic lipogenesis leading to liver steatosis and hypertriglyceridemia. Despite their pro-lipogenic action, LXR activators normalize glycemia and improve insulin sensitivity in rodent models of type 2 diabetes. Antidiabetic action of LXR agonists is thought to result from suppression of hepatic gluconeogenesis. However, it remains unclear whether LXR activation affects muscle insulin sensitivity. In the present study we attempted to answer this question. Methods: The experiments were performed on male Wistar rats fed for 5 weeks on either standard chow or high fat diet. The latter group was further divided into two subgroups receiving either selective LXR agonist - T0901317 (10mg/kg/d) or vehicle during the last week of the experiment. All animals were then anaesthetized and samples of the soleus as well as red and white sections of the gastrocnemius muscle were excised. Results: As expected, administration of T0901317 to high-fat fed rats augmented diet-induced hyperlipidemia. Nevertheless, it also normalized glucose tolerance and improved insulin-stimulated glucose uptake in isolated soleus muscle. In addition, LXR agonist completely restored glucose transporter 4 expression and insulin-stimulated Akt substrate of 160 kDa phosphorylation in all investigated muscles. Insulin-sensitizing effect of T0901317 was not related to changes in intramuscular level of lipid mediators of insulin resistance, since neither diacylglycerols nor ceramide content was affected by the treatment. Conclusion: We conclude that improvement in muscle insulin sensitivity is one of the mechanisms underlying the antidiabetic action of LXR activators.
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title_short	Insulin-Sensitizing Effect of LXR Agonist T0901317 in High-Fat Fed Rats is Associated with Restored Muscle GLUT4 Expression and Insulin-Stimulated AS160 Phosphorylation
url	https://doi.org/10.1159/000358675 https://doaj.org/article/b59197eb9a9c442085bdbbcdc02a2cd8 http://www.karger.com/Article/FullText/358675 https://doaj.org/toc/1015-8987 https://doaj.org/toc/1421-9778
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author2	Piotr Zabielski Agnieszka U. Błachnio-Zabielska Ewa Harasim Adrian Chabowski Jan Górski
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up_date	2024-07-04T00:15:45.210Z
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Insulin-Sensitizing Effect of LXR Agonist T0901317 in High-Fat Fed Rats is Associated with Restored Muscle GLUT4 Expression and Insulin-Stimulated AS160 Phosphorylation

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