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Improvement of high-glucose and insulin resistance of chromium malate in 3T3-L1 adipocytes by glucose uptake and insulin sensitivity signaling pathways and its mechanism

Previous study has revealed that chromium malate could improve insulin resistance and the regulation of fasting blood glucose in type 2 diabetic rats. This study was designed to investigate the effect of chromium malate on hypoglycemic and improve insulin resistance activities in 3T3-L1 adipocytes w...

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Autores principales: Feng, Weiwei, Liu, Yongchao, Fei, Fan, Chen, Yao, Ding, Yangyang, Yan, Mengjiao, Feng, Yun, Zhao, Ting, Mao, Guanghua, Yang, Liuqing, Wu, Xiangyang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Royal Society of Chemistry 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9059288/
https://www.ncbi.nlm.nih.gov/pubmed/35521592
http://dx.doi.org/10.1039/c8ra07470d
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author Feng, Weiwei
Liu, Yongchao
Fei, Fan
Chen, Yao
Ding, Yangyang
Yan, Mengjiao
Feng, Yun
Zhao, Ting
Mao, Guanghua
Yang, Liuqing
Wu, Xiangyang
author_facet Feng, Weiwei
Liu, Yongchao
Fei, Fan
Chen, Yao
Ding, Yangyang
Yan, Mengjiao
Feng, Yun
Zhao, Ting
Mao, Guanghua
Yang, Liuqing
Wu, Xiangyang
author_sort Feng, Weiwei
collection PubMed
description Previous study has revealed that chromium malate could improve insulin resistance and the regulation of fasting blood glucose in type 2 diabetic rats. This study was designed to investigate the effect of chromium malate on hypoglycemic and improve insulin resistance activities in 3T3-L1 adipocytes with insulin resistance and investigate the acting mechanism. The result indicated that chromium malate exhibited direct hypoglycemic activity in vitro. Compared with the model group, chromium malate could significantly promote the expression levels of GLUT-4, Akt, Irs-1, PPARγ, PI3K and p38-MAPK and their mRNA, increase p-AKT/AKT level, AKT and AMPKβ1 phosphorylation and reduce Irs-1 phosphorylation and p-Irs-1/Irs-1 level in 3T3-L1 adipocytes (p < 0.05). Chromium malate is more effective in regulating the proteins and mRNA expressions than those of chromium trichloride and chromium picolinate. Compared to the model group, pretreatment with the specific p38-MAPK inhibitor completely inhibited the GLUT-4 and Irs-1 proteins and mRNA expressions induced by the chromium malate. In conclusion, chromium malate had a beneficial influence on improvement of controlling glucose levels and insulin resistance in 3T3-L1 adipocytes with insulin resistance by regulating proteins productions and genes expressions in glucose uptake and insulin sensitivity signaling pathways.
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spelling pubmed-90592882022-05-04 Improvement of high-glucose and insulin resistance of chromium malate in 3T3-L1 adipocytes by glucose uptake and insulin sensitivity signaling pathways and its mechanism Feng, Weiwei Liu, Yongchao Fei, Fan Chen, Yao Ding, Yangyang Yan, Mengjiao Feng, Yun Zhao, Ting Mao, Guanghua Yang, Liuqing Wu, Xiangyang RSC Adv Chemistry Previous study has revealed that chromium malate could improve insulin resistance and the regulation of fasting blood glucose in type 2 diabetic rats. This study was designed to investigate the effect of chromium malate on hypoglycemic and improve insulin resistance activities in 3T3-L1 adipocytes with insulin resistance and investigate the acting mechanism. The result indicated that chromium malate exhibited direct hypoglycemic activity in vitro. Compared with the model group, chromium malate could significantly promote the expression levels of GLUT-4, Akt, Irs-1, PPARγ, PI3K and p38-MAPK and their mRNA, increase p-AKT/AKT level, AKT and AMPKβ1 phosphorylation and reduce Irs-1 phosphorylation and p-Irs-1/Irs-1 level in 3T3-L1 adipocytes (p < 0.05). Chromium malate is more effective in regulating the proteins and mRNA expressions than those of chromium trichloride and chromium picolinate. Compared to the model group, pretreatment with the specific p38-MAPK inhibitor completely inhibited the GLUT-4 and Irs-1 proteins and mRNA expressions induced by the chromium malate. In conclusion, chromium malate had a beneficial influence on improvement of controlling glucose levels and insulin resistance in 3T3-L1 adipocytes with insulin resistance by regulating proteins productions and genes expressions in glucose uptake and insulin sensitivity signaling pathways. The Royal Society of Chemistry 2018-12-21 /pmc/articles/PMC9059288/ /pubmed/35521592 http://dx.doi.org/10.1039/c8ra07470d Text en This journal is © The Royal Society of Chemistry https://creativecommons.org/licenses/by-nc/3.0/
spellingShingle Chemistry
Feng, Weiwei
Liu, Yongchao
Fei, Fan
Chen, Yao
Ding, Yangyang
Yan, Mengjiao
Feng, Yun
Zhao, Ting
Mao, Guanghua
Yang, Liuqing
Wu, Xiangyang
Improvement of high-glucose and insulin resistance of chromium malate in 3T3-L1 adipocytes by glucose uptake and insulin sensitivity signaling pathways and its mechanism
title Improvement of high-glucose and insulin resistance of chromium malate in 3T3-L1 adipocytes by glucose uptake and insulin sensitivity signaling pathways and its mechanism
title_full Improvement of high-glucose and insulin resistance of chromium malate in 3T3-L1 adipocytes by glucose uptake and insulin sensitivity signaling pathways and its mechanism
title_fullStr Improvement of high-glucose and insulin resistance of chromium malate in 3T3-L1 adipocytes by glucose uptake and insulin sensitivity signaling pathways and its mechanism
title_full_unstemmed Improvement of high-glucose and insulin resistance of chromium malate in 3T3-L1 adipocytes by glucose uptake and insulin sensitivity signaling pathways and its mechanism
title_short Improvement of high-glucose and insulin resistance of chromium malate in 3T3-L1 adipocytes by glucose uptake and insulin sensitivity signaling pathways and its mechanism
title_sort improvement of high-glucose and insulin resistance of chromium malate in 3t3-l1 adipocytes by glucose uptake and insulin sensitivity signaling pathways and its mechanism
topic Chemistry
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9059288/
https://www.ncbi.nlm.nih.gov/pubmed/35521592
http://dx.doi.org/10.1039/c8ra07470d
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