Dihydromyricetin Attenuates Metabolic Syndrome And Improves Insulin Sensitivity By Upregulating Insulin Receptor Substrate-1 (Y612) Tyrosine Phosphorylation In db/db Mice

Jidong He,1 Junpeng Zhang,1 Lijuan Dong,1 Xuefeng Dang,1 Li Wang,2 Long Cheng,3 Yunxiang Huang4 1Department of Gastroenterology, Baoji People’s Hospital, Baoji, Shanxi 721000, People’s Republic of China; 2Department of Diabetic Nephropathy, Baoji Central Hospital, Baoji, Shanxi 7...

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Autores principales: He J, Zhang J, Dong L, Dang X, Wang L, Cheng L, Huang Y
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Publicado: Dove Medical Press 2019
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spelling oai:doaj.org-article:d9bf8c42350f41c18f734c2703824aaf2021-12-02T09:17:34ZDihydromyricetin Attenuates Metabolic Syndrome And Improves Insulin Sensitivity By Upregulating Insulin Receptor Substrate-1 (Y612) Tyrosine Phosphorylation In db/db Mice1178-7007https://doaj.org/article/d9bf8c42350f41c18f734c2703824aaf2019-11-01T00:00:00Zhttps://www.dovepress.com/dihydromyricetin-attenuates-metabolic-syndrome-and-improves-insulin-se-peer-reviewed-article-DMSOhttps://doaj.org/toc/1178-7007Jidong He,1 Junpeng Zhang,1 Lijuan Dong,1 Xuefeng Dang,1 Li Wang,2 Long Cheng,3 Yunxiang Huang4 1Department of Gastroenterology, Baoji People’s Hospital, Baoji, Shanxi 721000, People’s Republic of China; 2Department of Diabetic Nephropathy, Baoji Central Hospital, Baoji, Shanxi 721008, People’s Republic of China; 3Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100193, People’s Republic of China; 4Department of R&D, Asparagus Engineering Research Center of Hebei Province, Qinhuangdao 066008, People’s Republic of ChinaCorrespondence: Li WangBaoji Central Hospital, No. 8, Jiangtan Road, Baoji, Shanxi 721008, People’s Republic of ChinaEmail 53080690@qq.comLong ChengInstitute of Medicinal Plant Development, Chinese Academy of Medical Sciences, Peking Union Medical College, No. 151, Malianwa North Road Haidian District, Beijing 100094, People’s Republic of ChinaTel/Fax +86 10 57833013Email 13581972102@139.comPurpose: Dihydromyricetin (DHM), the main bioactive flavonoid in vine tea, exerts multiple health beneficial effects. This work aimed to identify whether a naturally derived flavonoid product, DHM, can significantly attenuate metabolic syndrome and improve insulin sensitivity.Methods: 10-week-old db/db mice were randomly assigned to receive the antidiabetic agent metformin (Met, 50 mg/kg BW), DHM (1.0 g and 0.5 g/kg BW) or placebo and were simultaneously fed a high-fat diet for 8 weeks. The general status of the animals was observed and recorded daily, body weight and blood glucose levels were measured weekly, during the experimental period. On day 55, the oral glucose tolerance test (OGTT) was performed. After OGTT, all animals were anesthetized and sacrificed by cervical decapitation. Blood samples were collected in tubes to detect plasma insulin and the biochemical parameters of lipid metabolism. Pancreas histological changes and islet fibrosis were demonstrated by H&E staining and Masson staining, respectively. Moreover, the expression of insulin receptor substrate-1 and phosphorylated insulin receptor substrate-1 in the insulin signaling pathway was detected by Western blot assay.Results: The oral administration of DHM (1.0 g and 0.5 g/kg BW) reduced the fasting blood glucose, serum insulin, and glycated hemoglobin levels and the insulin resistance (HOMA-IR) index. Furthermore, DHM intervention decreased body weight and the serum lipid profile. In addition, DHM treatment also markedly decreased the relative abdominal fat weight. Western blot analysis indicated that DHM upregulated the IRS-1 (Y612) tyrosine phosphorylation, improving insulin resistance. Treatment with dihydromyricetin attenuated the progression of insulin resistance and pancreatic fibrosis in fatty db/db mice.Conclusion: In summary, we determined the antimetabolic syndrome effect of DHM in db/db obese mice. DHM upregulates the IRS-1 (Y612) tyrosine phosphorylation, improving insulin resistance. Therefore, DHM is a promising therapeutic candidate for the control of metabolic syndrome.Keywords: dihydromyricetin, metabolic syndrome, hypoglycemic function, insulin resistance, insulin receptor substrate-1He JZhang JDong LDang XWang LCheng LHuang YDove Medical Pressarticledihydromyricetinmetabolic syndromehypoglycemic functioninsulin resistanceinsulin receptor substrate-1Specialties of internal medicineRC581-951ENDiabetes, Metabolic Syndrome and Obesity: Targets and Therapy, Vol Volume 12, Pp 2237-2249 (2019)
institution DOAJ
collection DOAJ
language EN
topic dihydromyricetin
metabolic syndrome
hypoglycemic function
insulin resistance
insulin receptor substrate-1
Specialties of internal medicine
RC581-951
spellingShingle dihydromyricetin
metabolic syndrome
hypoglycemic function
insulin resistance
insulin receptor substrate-1
Specialties of internal medicine
RC581-951
He J
Zhang J
Dong L
Dang X
Wang L
Cheng L
Huang Y
Dihydromyricetin Attenuates Metabolic Syndrome And Improves Insulin Sensitivity By Upregulating Insulin Receptor Substrate-1 (Y612) Tyrosine Phosphorylation In db/db Mice
description Jidong He,1 Junpeng Zhang,1 Lijuan Dong,1 Xuefeng Dang,1 Li Wang,2 Long Cheng,3 Yunxiang Huang4 1Department of Gastroenterology, Baoji People’s Hospital, Baoji, Shanxi 721000, People’s Republic of China; 2Department of Diabetic Nephropathy, Baoji Central Hospital, Baoji, Shanxi 721008, People’s Republic of China; 3Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100193, People’s Republic of China; 4Department of R&D, Asparagus Engineering Research Center of Hebei Province, Qinhuangdao 066008, People’s Republic of ChinaCorrespondence: Li WangBaoji Central Hospital, No. 8, Jiangtan Road, Baoji, Shanxi 721008, People’s Republic of ChinaEmail 53080690@qq.comLong ChengInstitute of Medicinal Plant Development, Chinese Academy of Medical Sciences, Peking Union Medical College, No. 151, Malianwa North Road Haidian District, Beijing 100094, People’s Republic of ChinaTel/Fax +86 10 57833013Email 13581972102@139.comPurpose: Dihydromyricetin (DHM), the main bioactive flavonoid in vine tea, exerts multiple health beneficial effects. This work aimed to identify whether a naturally derived flavonoid product, DHM, can significantly attenuate metabolic syndrome and improve insulin sensitivity.Methods: 10-week-old db/db mice were randomly assigned to receive the antidiabetic agent metformin (Met, 50 mg/kg BW), DHM (1.0 g and 0.5 g/kg BW) or placebo and were simultaneously fed a high-fat diet for 8 weeks. The general status of the animals was observed and recorded daily, body weight and blood glucose levels were measured weekly, during the experimental period. On day 55, the oral glucose tolerance test (OGTT) was performed. After OGTT, all animals were anesthetized and sacrificed by cervical decapitation. Blood samples were collected in tubes to detect plasma insulin and the biochemical parameters of lipid metabolism. Pancreas histological changes and islet fibrosis were demonstrated by H&E staining and Masson staining, respectively. Moreover, the expression of insulin receptor substrate-1 and phosphorylated insulin receptor substrate-1 in the insulin signaling pathway was detected by Western blot assay.Results: The oral administration of DHM (1.0 g and 0.5 g/kg BW) reduced the fasting blood glucose, serum insulin, and glycated hemoglobin levels and the insulin resistance (HOMA-IR) index. Furthermore, DHM intervention decreased body weight and the serum lipid profile. In addition, DHM treatment also markedly decreased the relative abdominal fat weight. Western blot analysis indicated that DHM upregulated the IRS-1 (Y612) tyrosine phosphorylation, improving insulin resistance. Treatment with dihydromyricetin attenuated the progression of insulin resistance and pancreatic fibrosis in fatty db/db mice.Conclusion: In summary, we determined the antimetabolic syndrome effect of DHM in db/db obese mice. DHM upregulates the IRS-1 (Y612) tyrosine phosphorylation, improving insulin resistance. Therefore, DHM is a promising therapeutic candidate for the control of metabolic syndrome.Keywords: dihydromyricetin, metabolic syndrome, hypoglycemic function, insulin resistance, insulin receptor substrate-1
format article
author He J
Zhang J
Dong L
Dang X
Wang L
Cheng L
Huang Y
author_facet He J
Zhang J
Dong L
Dang X
Wang L
Cheng L
Huang Y
author_sort He J
title Dihydromyricetin Attenuates Metabolic Syndrome And Improves Insulin Sensitivity By Upregulating Insulin Receptor Substrate-1 (Y612) Tyrosine Phosphorylation In db/db Mice
title_short Dihydromyricetin Attenuates Metabolic Syndrome And Improves Insulin Sensitivity By Upregulating Insulin Receptor Substrate-1 (Y612) Tyrosine Phosphorylation In db/db Mice
title_full Dihydromyricetin Attenuates Metabolic Syndrome And Improves Insulin Sensitivity By Upregulating Insulin Receptor Substrate-1 (Y612) Tyrosine Phosphorylation In db/db Mice
title_fullStr Dihydromyricetin Attenuates Metabolic Syndrome And Improves Insulin Sensitivity By Upregulating Insulin Receptor Substrate-1 (Y612) Tyrosine Phosphorylation In db/db Mice
title_full_unstemmed Dihydromyricetin Attenuates Metabolic Syndrome And Improves Insulin Sensitivity By Upregulating Insulin Receptor Substrate-1 (Y612) Tyrosine Phosphorylation In db/db Mice
title_sort dihydromyricetin attenuates metabolic syndrome and improves insulin sensitivity by upregulating insulin receptor substrate-1 (y612) tyrosine phosphorylation in db/db mice
publisher Dove Medical Press
publishDate 2019
url https://doaj.org/article/d9bf8c42350f41c18f734c2703824aaf
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