Trans-Fatty Acids Aggravate Obesity, Insulin Resistance and Hepatic Steatosis in C57BL/6 Mice, Possibly by Suppressing the IRS1 Dependent Pathway

Trans-fatty acid consumption has been reported as a risk factor for metabolic disorders and targeted organ damages. Nonetheless, little is known about the roles and mechanisms of trans-fatty acids in obesity, insulin resistance (IR) and hepatic steatosis. Adult C57BL/6 male mice were fed with four d...
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Autor*in:	Xiaona Zhao [verfasserIn] Cheng Shen [verfasserIn] Hong Zhu [verfasserIn] Cong Wang [verfasserIn] Xiangwei Liu [verfasserIn] Xiaolei Sun [verfasserIn] Shasha Han [verfasserIn] Peng Wang [verfasserIn] Zhen Dong [verfasserIn] Xin Ma [verfasserIn] Kai Hu [verfasserIn] Aijun Sun [verfasserIn] Junbo Ge [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2016

Schlagwörter:	trans-fatty acid obesity insulin resistance hepatic steatosis

Übergeordnetes Werk:	In: Molecules - MDPI AG, 2003, 21(2016), 6, p 705
Übergeordnetes Werk:	volume:21 ; year:2016 ; number:6, p 705

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/molecules21060705

Katalog-ID:	DOAJ078144086

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allfields	10.3390/molecules21060705 doi (DE-627)DOAJ078144086 (DE-599)DOAJ4f8e1b9761f346f79c4cdf1219caab2e DE-627 ger DE-627 rakwb eng QD241-441 Xiaona Zhao verfasserin aut Trans-Fatty Acids Aggravate Obesity, Insulin Resistance and Hepatic Steatosis in C57BL/6 Mice, Possibly by Suppressing the IRS1 Dependent Pathway 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Trans-fatty acid consumption has been reported as a risk factor for metabolic disorders and targeted organ damages. Nonetheless, little is known about the roles and mechanisms of trans-fatty acids in obesity, insulin resistance (IR) and hepatic steatosis. Adult C57BL/6 male mice were fed with four different diets for 20 weeks: normal diet (ND), high fat diet (HFD), low trans-fatty acids diet (LTD) and high trans-fatty acid diet (HTD). The diet-induced metabolic disorders were assessed by evaluating body weight, glucose tolerance test, hepatic steatosis and plasma lipid profiles post 20-week diet. Histological (H&E, Oil-Red-O) staining and western blot analysis were employed to assess liver steatosis and potential signaling pathways. After 20-weeks of diet, the body weights of the four groups were 29.61 ± 1.89 g (ND), 39.04 ± 4.27 g (HFD), 34.09 ± 2.62 g (LTD) and 43.78 ± 4.27 g (HTD) (p < 0.05), respectively. HFD intake significantly impaired glucose tolerance, which was impaired further in the mice consuming the HTD diet. The effect was further exacerbated by HTD diet. Moreover, the HTD group exhibited significantly more severe liver steatosis compared with HFD group possibly through regulating adipose triglyceride lipase. The group consuming the HTD also exhibited significantly reduced levels of IRS1, phosphor-PKC and phosphor-AKT. These results support our hypothesis that consumption of a diet high in trans-fatty acids induces higher rates of obesity, IR and hepatic steatosis in male C57BL/6 mice, possibly by suppressing the IRS1dependent pathway. trans-fatty acid obesity insulin resistance hepatic steatosis Organic chemistry Cheng Shen verfasserin aut Hong Zhu verfasserin aut Cong Wang verfasserin aut Xiangwei Liu verfasserin aut Xiaolei Sun verfasserin aut Shasha Han verfasserin aut Peng Wang verfasserin aut Zhen Dong verfasserin aut Xin Ma verfasserin aut Kai Hu verfasserin aut Aijun Sun verfasserin aut Junbo Ge verfasserin aut In Molecules MDPI AG, 2003 21(2016), 6, p 705 (DE-627)311313132 (DE-600)2008644-1 14203049 nnns volume:21 year:2016 number:6, p 705 https://doi.org/10.3390/molecules21060705 kostenfrei https://doaj.org/article/4f8e1b9761f346f79c4cdf1219caab2e kostenfrei http://www.mdpi.com/1420-3049/21/6/705 kostenfrei https://doaj.org/toc/1420-3049 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 21 2016 6, p 705
spelling	10.3390/molecules21060705 doi (DE-627)DOAJ078144086 (DE-599)DOAJ4f8e1b9761f346f79c4cdf1219caab2e DE-627 ger DE-627 rakwb eng QD241-441 Xiaona Zhao verfasserin aut Trans-Fatty Acids Aggravate Obesity, Insulin Resistance and Hepatic Steatosis in C57BL/6 Mice, Possibly by Suppressing the IRS1 Dependent Pathway 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Trans-fatty acid consumption has been reported as a risk factor for metabolic disorders and targeted organ damages. Nonetheless, little is known about the roles and mechanisms of trans-fatty acids in obesity, insulin resistance (IR) and hepatic steatosis. Adult C57BL/6 male mice were fed with four different diets for 20 weeks: normal diet (ND), high fat diet (HFD), low trans-fatty acids diet (LTD) and high trans-fatty acid diet (HTD). The diet-induced metabolic disorders were assessed by evaluating body weight, glucose tolerance test, hepatic steatosis and plasma lipid profiles post 20-week diet. Histological (H&E, Oil-Red-O) staining and western blot analysis were employed to assess liver steatosis and potential signaling pathways. After 20-weeks of diet, the body weights of the four groups were 29.61 ± 1.89 g (ND), 39.04 ± 4.27 g (HFD), 34.09 ± 2.62 g (LTD) and 43.78 ± 4.27 g (HTD) (p < 0.05), respectively. HFD intake significantly impaired glucose tolerance, which was impaired further in the mice consuming the HTD diet. The effect was further exacerbated by HTD diet. Moreover, the HTD group exhibited significantly more severe liver steatosis compared with HFD group possibly through regulating adipose triglyceride lipase. The group consuming the HTD also exhibited significantly reduced levels of IRS1, phosphor-PKC and phosphor-AKT. These results support our hypothesis that consumption of a diet high in trans-fatty acids induces higher rates of obesity, IR and hepatic steatosis in male C57BL/6 mice, possibly by suppressing the IRS1dependent pathway. trans-fatty acid obesity insulin resistance hepatic steatosis Organic chemistry Cheng Shen verfasserin aut Hong Zhu verfasserin aut Cong Wang verfasserin aut Xiangwei Liu verfasserin aut Xiaolei Sun verfasserin aut Shasha Han verfasserin aut Peng Wang verfasserin aut Zhen Dong verfasserin aut Xin Ma verfasserin aut Kai Hu verfasserin aut Aijun Sun verfasserin aut Junbo Ge verfasserin aut In Molecules MDPI AG, 2003 21(2016), 6, p 705 (DE-627)311313132 (DE-600)2008644-1 14203049 nnns volume:21 year:2016 number:6, p 705 https://doi.org/10.3390/molecules21060705 kostenfrei https://doaj.org/article/4f8e1b9761f346f79c4cdf1219caab2e kostenfrei http://www.mdpi.com/1420-3049/21/6/705 kostenfrei https://doaj.org/toc/1420-3049 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 21 2016 6, p 705
allfields_unstemmed	10.3390/molecules21060705 doi (DE-627)DOAJ078144086 (DE-599)DOAJ4f8e1b9761f346f79c4cdf1219caab2e DE-627 ger DE-627 rakwb eng QD241-441 Xiaona Zhao verfasserin aut Trans-Fatty Acids Aggravate Obesity, Insulin Resistance and Hepatic Steatosis in C57BL/6 Mice, Possibly by Suppressing the IRS1 Dependent Pathway 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Trans-fatty acid consumption has been reported as a risk factor for metabolic disorders and targeted organ damages. Nonetheless, little is known about the roles and mechanisms of trans-fatty acids in obesity, insulin resistance (IR) and hepatic steatosis. Adult C57BL/6 male mice were fed with four different diets for 20 weeks: normal diet (ND), high fat diet (HFD), low trans-fatty acids diet (LTD) and high trans-fatty acid diet (HTD). The diet-induced metabolic disorders were assessed by evaluating body weight, glucose tolerance test, hepatic steatosis and plasma lipid profiles post 20-week diet. Histological (H&E, Oil-Red-O) staining and western blot analysis were employed to assess liver steatosis and potential signaling pathways. After 20-weeks of diet, the body weights of the four groups were 29.61 ± 1.89 g (ND), 39.04 ± 4.27 g (HFD), 34.09 ± 2.62 g (LTD) and 43.78 ± 4.27 g (HTD) (p < 0.05), respectively. HFD intake significantly impaired glucose tolerance, which was impaired further in the mice consuming the HTD diet. The effect was further exacerbated by HTD diet. Moreover, the HTD group exhibited significantly more severe liver steatosis compared with HFD group possibly through regulating adipose triglyceride lipase. The group consuming the HTD also exhibited significantly reduced levels of IRS1, phosphor-PKC and phosphor-AKT. These results support our hypothesis that consumption of a diet high in trans-fatty acids induces higher rates of obesity, IR and hepatic steatosis in male C57BL/6 mice, possibly by suppressing the IRS1dependent pathway. trans-fatty acid obesity insulin resistance hepatic steatosis Organic chemistry Cheng Shen verfasserin aut Hong Zhu verfasserin aut Cong Wang verfasserin aut Xiangwei Liu verfasserin aut Xiaolei Sun verfasserin aut Shasha Han verfasserin aut Peng Wang verfasserin aut Zhen Dong verfasserin aut Xin Ma verfasserin aut Kai Hu verfasserin aut Aijun Sun verfasserin aut Junbo Ge verfasserin aut In Molecules MDPI AG, 2003 21(2016), 6, p 705 (DE-627)311313132 (DE-600)2008644-1 14203049 nnns volume:21 year:2016 number:6, p 705 https://doi.org/10.3390/molecules21060705 kostenfrei https://doaj.org/article/4f8e1b9761f346f79c4cdf1219caab2e kostenfrei http://www.mdpi.com/1420-3049/21/6/705 kostenfrei https://doaj.org/toc/1420-3049 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 21 2016 6, p 705
allfieldsGer	10.3390/molecules21060705 doi (DE-627)DOAJ078144086 (DE-599)DOAJ4f8e1b9761f346f79c4cdf1219caab2e DE-627 ger DE-627 rakwb eng QD241-441 Xiaona Zhao verfasserin aut Trans-Fatty Acids Aggravate Obesity, Insulin Resistance and Hepatic Steatosis in C57BL/6 Mice, Possibly by Suppressing the IRS1 Dependent Pathway 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Trans-fatty acid consumption has been reported as a risk factor for metabolic disorders and targeted organ damages. Nonetheless, little is known about the roles and mechanisms of trans-fatty acids in obesity, insulin resistance (IR) and hepatic steatosis. Adult C57BL/6 male mice were fed with four different diets for 20 weeks: normal diet (ND), high fat diet (HFD), low trans-fatty acids diet (LTD) and high trans-fatty acid diet (HTD). The diet-induced metabolic disorders were assessed by evaluating body weight, glucose tolerance test, hepatic steatosis and plasma lipid profiles post 20-week diet. Histological (H&E, Oil-Red-O) staining and western blot analysis were employed to assess liver steatosis and potential signaling pathways. After 20-weeks of diet, the body weights of the four groups were 29.61 ± 1.89 g (ND), 39.04 ± 4.27 g (HFD), 34.09 ± 2.62 g (LTD) and 43.78 ± 4.27 g (HTD) (p < 0.05), respectively. HFD intake significantly impaired glucose tolerance, which was impaired further in the mice consuming the HTD diet. The effect was further exacerbated by HTD diet. Moreover, the HTD group exhibited significantly more severe liver steatosis compared with HFD group possibly through regulating adipose triglyceride lipase. The group consuming the HTD also exhibited significantly reduced levels of IRS1, phosphor-PKC and phosphor-AKT. These results support our hypothesis that consumption of a diet high in trans-fatty acids induces higher rates of obesity, IR and hepatic steatosis in male C57BL/6 mice, possibly by suppressing the IRS1dependent pathway. trans-fatty acid obesity insulin resistance hepatic steatosis Organic chemistry Cheng Shen verfasserin aut Hong Zhu verfasserin aut Cong Wang verfasserin aut Xiangwei Liu verfasserin aut Xiaolei Sun verfasserin aut Shasha Han verfasserin aut Peng Wang verfasserin aut Zhen Dong verfasserin aut Xin Ma verfasserin aut Kai Hu verfasserin aut Aijun Sun verfasserin aut Junbo Ge verfasserin aut In Molecules MDPI AG, 2003 21(2016), 6, p 705 (DE-627)311313132 (DE-600)2008644-1 14203049 nnns volume:21 year:2016 number:6, p 705 https://doi.org/10.3390/molecules21060705 kostenfrei https://doaj.org/article/4f8e1b9761f346f79c4cdf1219caab2e kostenfrei http://www.mdpi.com/1420-3049/21/6/705 kostenfrei https://doaj.org/toc/1420-3049 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 21 2016 6, p 705
allfieldsSound	10.3390/molecules21060705 doi (DE-627)DOAJ078144086 (DE-599)DOAJ4f8e1b9761f346f79c4cdf1219caab2e DE-627 ger DE-627 rakwb eng QD241-441 Xiaona Zhao verfasserin aut Trans-Fatty Acids Aggravate Obesity, Insulin Resistance and Hepatic Steatosis in C57BL/6 Mice, Possibly by Suppressing the IRS1 Dependent Pathway 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Trans-fatty acid consumption has been reported as a risk factor for metabolic disorders and targeted organ damages. Nonetheless, little is known about the roles and mechanisms of trans-fatty acids in obesity, insulin resistance (IR) and hepatic steatosis. Adult C57BL/6 male mice were fed with four different diets for 20 weeks: normal diet (ND), high fat diet (HFD), low trans-fatty acids diet (LTD) and high trans-fatty acid diet (HTD). The diet-induced metabolic disorders were assessed by evaluating body weight, glucose tolerance test, hepatic steatosis and plasma lipid profiles post 20-week diet. Histological (H&E, Oil-Red-O) staining and western blot analysis were employed to assess liver steatosis and potential signaling pathways. After 20-weeks of diet, the body weights of the four groups were 29.61 ± 1.89 g (ND), 39.04 ± 4.27 g (HFD), 34.09 ± 2.62 g (LTD) and 43.78 ± 4.27 g (HTD) (p < 0.05), respectively. HFD intake significantly impaired glucose tolerance, which was impaired further in the mice consuming the HTD diet. The effect was further exacerbated by HTD diet. Moreover, the HTD group exhibited significantly more severe liver steatosis compared with HFD group possibly through regulating adipose triglyceride lipase. The group consuming the HTD also exhibited significantly reduced levels of IRS1, phosphor-PKC and phosphor-AKT. These results support our hypothesis that consumption of a diet high in trans-fatty acids induces higher rates of obesity, IR and hepatic steatosis in male C57BL/6 mice, possibly by suppressing the IRS1dependent pathway. trans-fatty acid obesity insulin resistance hepatic steatosis Organic chemistry Cheng Shen verfasserin aut Hong Zhu verfasserin aut Cong Wang verfasserin aut Xiangwei Liu verfasserin aut Xiaolei Sun verfasserin aut Shasha Han verfasserin aut Peng Wang verfasserin aut Zhen Dong verfasserin aut Xin Ma verfasserin aut Kai Hu verfasserin aut Aijun Sun verfasserin aut Junbo Ge verfasserin aut In Molecules MDPI AG, 2003 21(2016), 6, p 705 (DE-627)311313132 (DE-600)2008644-1 14203049 nnns volume:21 year:2016 number:6, p 705 https://doi.org/10.3390/molecules21060705 kostenfrei https://doaj.org/article/4f8e1b9761f346f79c4cdf1219caab2e kostenfrei http://www.mdpi.com/1420-3049/21/6/705 kostenfrei https://doaj.org/toc/1420-3049 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 21 2016 6, p 705
language	English
source	In Molecules 21(2016), 6, p 705 volume:21 year:2016 number:6, p 705
sourceStr	In Molecules 21(2016), 6, p 705 volume:21 year:2016 number:6, p 705
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	trans-fatty acid obesity insulin resistance hepatic steatosis Organic chemistry
isfreeaccess_bool	true
container_title	Molecules
authorswithroles_txt_mv	Xiaona Zhao @@aut@@ Cheng Shen @@aut@@ Hong Zhu @@aut@@ Cong Wang @@aut@@ Xiangwei Liu @@aut@@ Xiaolei Sun @@aut@@ Shasha Han @@aut@@ Peng Wang @@aut@@ Zhen Dong @@aut@@ Xin Ma @@aut@@ Kai Hu @@aut@@ Aijun Sun @@aut@@ Junbo Ge @@aut@@
publishDateDaySort_date	2016-01-01T00:00:00Z
hierarchy_top_id	311313132
id	DOAJ078144086
language_de	englisch
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callnumber-first	Q - Science
author	Xiaona Zhao
spellingShingle	Xiaona Zhao misc QD241-441 misc trans-fatty acid misc obesity misc insulin resistance misc hepatic steatosis misc Organic chemistry Trans-Fatty Acids Aggravate Obesity, Insulin Resistance and Hepatic Steatosis in C57BL/6 Mice, Possibly by Suppressing the IRS1 Dependent Pathway
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topic_title	QD241-441 Trans-Fatty Acids Aggravate Obesity, Insulin Resistance and Hepatic Steatosis in C57BL/6 Mice, Possibly by Suppressing the IRS1 Dependent Pathway trans-fatty acid obesity insulin resistance hepatic steatosis
topic	misc QD241-441 misc trans-fatty acid misc obesity misc insulin resistance misc hepatic steatosis misc Organic chemistry
topic_unstemmed	misc QD241-441 misc trans-fatty acid misc obesity misc insulin resistance misc hepatic steatosis misc Organic chemistry
topic_browse	misc QD241-441 misc trans-fatty acid misc obesity misc insulin resistance misc hepatic steatosis misc Organic chemistry
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title	Trans-Fatty Acids Aggravate Obesity, Insulin Resistance and Hepatic Steatosis in C57BL/6 Mice, Possibly by Suppressing the IRS1 Dependent Pathway
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title_full	Trans-Fatty Acids Aggravate Obesity, Insulin Resistance and Hepatic Steatosis in C57BL/6 Mice, Possibly by Suppressing the IRS1 Dependent Pathway
author_sort	Xiaona Zhao
journal	Molecules
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author_browse	Xiaona Zhao Cheng Shen Hong Zhu Cong Wang Xiangwei Liu Xiaolei Sun Shasha Han Peng Wang Zhen Dong Xin Ma Kai Hu Aijun Sun Junbo Ge
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title_sort	trans-fatty acids aggravate obesity, insulin resistance and hepatic steatosis in c57bl/6 mice, possibly by suppressing the irs1 dependent pathway
callnumber	QD241-441
title_auth	Trans-Fatty Acids Aggravate Obesity, Insulin Resistance and Hepatic Steatosis in C57BL/6 Mice, Possibly by Suppressing the IRS1 Dependent Pathway
abstract	Trans-fatty acid consumption has been reported as a risk factor for metabolic disorders and targeted organ damages. Nonetheless, little is known about the roles and mechanisms of trans-fatty acids in obesity, insulin resistance (IR) and hepatic steatosis. Adult C57BL/6 male mice were fed with four different diets for 20 weeks: normal diet (ND), high fat diet (HFD), low trans-fatty acids diet (LTD) and high trans-fatty acid diet (HTD). The diet-induced metabolic disorders were assessed by evaluating body weight, glucose tolerance test, hepatic steatosis and plasma lipid profiles post 20-week diet. Histological (H&E, Oil-Red-O) staining and western blot analysis were employed to assess liver steatosis and potential signaling pathways. After 20-weeks of diet, the body weights of the four groups were 29.61 ± 1.89 g (ND), 39.04 ± 4.27 g (HFD), 34.09 ± 2.62 g (LTD) and 43.78 ± 4.27 g (HTD) (p < 0.05), respectively. HFD intake significantly impaired glucose tolerance, which was impaired further in the mice consuming the HTD diet. The effect was further exacerbated by HTD diet. Moreover, the HTD group exhibited significantly more severe liver steatosis compared with HFD group possibly through regulating adipose triglyceride lipase. The group consuming the HTD also exhibited significantly reduced levels of IRS1, phosphor-PKC and phosphor-AKT. These results support our hypothesis that consumption of a diet high in trans-fatty acids induces higher rates of obesity, IR and hepatic steatosis in male C57BL/6 mice, possibly by suppressing the IRS1dependent pathway.
abstractGer	Trans-fatty acid consumption has been reported as a risk factor for metabolic disorders and targeted organ damages. Nonetheless, little is known about the roles and mechanisms of trans-fatty acids in obesity, insulin resistance (IR) and hepatic steatosis. Adult C57BL/6 male mice were fed with four different diets for 20 weeks: normal diet (ND), high fat diet (HFD), low trans-fatty acids diet (LTD) and high trans-fatty acid diet (HTD). The diet-induced metabolic disorders were assessed by evaluating body weight, glucose tolerance test, hepatic steatosis and plasma lipid profiles post 20-week diet. Histological (H&E, Oil-Red-O) staining and western blot analysis were employed to assess liver steatosis and potential signaling pathways. After 20-weeks of diet, the body weights of the four groups were 29.61 ± 1.89 g (ND), 39.04 ± 4.27 g (HFD), 34.09 ± 2.62 g (LTD) and 43.78 ± 4.27 g (HTD) (p < 0.05), respectively. HFD intake significantly impaired glucose tolerance, which was impaired further in the mice consuming the HTD diet. The effect was further exacerbated by HTD diet. Moreover, the HTD group exhibited significantly more severe liver steatosis compared with HFD group possibly through regulating adipose triglyceride lipase. The group consuming the HTD also exhibited significantly reduced levels of IRS1, phosphor-PKC and phosphor-AKT. These results support our hypothesis that consumption of a diet high in trans-fatty acids induces higher rates of obesity, IR and hepatic steatosis in male C57BL/6 mice, possibly by suppressing the IRS1dependent pathway.
abstract_unstemmed	Trans-fatty acid consumption has been reported as a risk factor for metabolic disorders and targeted organ damages. Nonetheless, little is known about the roles and mechanisms of trans-fatty acids in obesity, insulin resistance (IR) and hepatic steatosis. Adult C57BL/6 male mice were fed with four different diets for 20 weeks: normal diet (ND), high fat diet (HFD), low trans-fatty acids diet (LTD) and high trans-fatty acid diet (HTD). The diet-induced metabolic disorders were assessed by evaluating body weight, glucose tolerance test, hepatic steatosis and plasma lipid profiles post 20-week diet. Histological (H&E, Oil-Red-O) staining and western blot analysis were employed to assess liver steatosis and potential signaling pathways. After 20-weeks of diet, the body weights of the four groups were 29.61 ± 1.89 g (ND), 39.04 ± 4.27 g (HFD), 34.09 ± 2.62 g (LTD) and 43.78 ± 4.27 g (HTD) (p < 0.05), respectively. HFD intake significantly impaired glucose tolerance, which was impaired further in the mice consuming the HTD diet. The effect was further exacerbated by HTD diet. Moreover, the HTD group exhibited significantly more severe liver steatosis compared with HFD group possibly through regulating adipose triglyceride lipase. The group consuming the HTD also exhibited significantly reduced levels of IRS1, phosphor-PKC and phosphor-AKT. These results support our hypothesis that consumption of a diet high in trans-fatty acids induces higher rates of obesity, IR and hepatic steatosis in male C57BL/6 mice, possibly by suppressing the IRS1dependent pathway.
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container_issue	6, p 705
title_short	Trans-Fatty Acids Aggravate Obesity, Insulin Resistance and Hepatic Steatosis in C57BL/6 Mice, Possibly by Suppressing the IRS1 Dependent Pathway
url	https://doi.org/10.3390/molecules21060705 https://doaj.org/article/4f8e1b9761f346f79c4cdf1219caab2e http://www.mdpi.com/1420-3049/21/6/705 https://doaj.org/toc/1420-3049
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author2	Cheng Shen Hong Zhu Cong Wang Xiangwei Liu Xiaolei Sun Shasha Han Peng Wang Zhen Dong Xin Ma Kai Hu Aijun Sun Junbo Ge
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up_date	2024-07-03T16:12:37.502Z
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