The ginsenoside metabolite compound K stimulates glucagon-like peptide-1 secretion in NCI–H716 cells by regulating the RhoA/ROCKs/YAP signaling pathway and cytoskeleton formation
Ginsenoside Rb1 has been shown to have antidiabetic and anti-inflammatory effects. Its major metabolite, compound K (CK), can stimulate the secretion of glucagon-like peptide-1 (GLP1), a gastrointestinal hormone that plays a vital role in regulating glucose metabolism. However, the mechanism underly...
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Elsevier
2021-01-01
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Online Access: | http://www.sciencedirect.com/science/article/pii/S1347861320301110 |
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author | Fengyuan Tian Xi Wang Haixiang Ni Xiaohong Feng Xiao Yuan Qi Huang |
author_facet | Fengyuan Tian Xi Wang Haixiang Ni Xiaohong Feng Xiao Yuan Qi Huang |
author_sort | Fengyuan Tian |
collection | DOAJ |
description | Ginsenoside Rb1 has been shown to have antidiabetic and anti-inflammatory effects. Its major metabolite, compound K (CK), can stimulate the secretion of glucagon-like peptide-1 (GLP1), a gastrointestinal hormone that plays a vital role in regulating glucose metabolism. However, the mechanism underlying the regulation of GLP1 secretion by compound K has not been fully explored. This study was designed to investigate whether CK ameliorates incretin impairment by regulating the RhoA/ROCKs/YAP signaling pathway and cytoskeleton formation in NCI–H716 cells. Using NCI–H716 cells as a model cell line for GLP1 secretion, we analyzed the effect of CK on the expression of RhoA/ROCK/YAP pathway components. Our results suggest that the effect of CK on GLP1 secretion depends on the anti-inflammatory effect of CK. We also demonstrated that CK can affect the RhoA/ROCK/YAP pathway, which is downstream of transforming growth factor β1 (TGFβ1), by maintaining the capacity of intestinal differentiation. In addition, this effect was mediated by regulating F/G-actin dynamics. These results provide not only the mechanistic insight for the effect of CK on intestinal L cells but also the molecular basis for the further development of CK as a potential therapeutic agent to treat type 2 diabetes mellitus (T2D). |
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issn | 1347-8613 |
language | English |
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spelling | doaj.art-170cb06c877e4d35b78a828f9508a2f72022-12-21T23:19:19ZengElsevierJournal of Pharmacological Sciences1347-86132021-01-0114518896The ginsenoside metabolite compound K stimulates glucagon-like peptide-1 secretion in NCI–H716 cells by regulating the RhoA/ROCKs/YAP signaling pathway and cytoskeleton formationFengyuan Tian0Xi Wang1Haixiang Ni2Xiaohong Feng3Xiao Yuan4Qi Huang5Department of Endocrinology, The First Affiliated Hospital of Zhejiang Chinese Medicine University, Hangzhou, 310006, PR ChinaCentral Laboratory, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310006, PR ChinaDepartment of Endocrinology, The First Affiliated Hospital of Zhejiang Chinese Medicine University, Hangzhou, 310006, PR ChinaDepartment of Endocrinology, The First Affiliated Hospital of Zhejiang Chinese Medicine University, Hangzhou, 310006, PR ChinaDepartment of Endocrinology, The First Affiliated Hospital of Zhejiang Chinese Medicine University, Hangzhou, 310006, PR ChinaDepartment of Endocrinology, The First Affiliated Hospital of Zhejiang Chinese Medicine University, Hangzhou, 310006, PR China; Corresponding author. Fax: +86 574 87068200.Ginsenoside Rb1 has been shown to have antidiabetic and anti-inflammatory effects. Its major metabolite, compound K (CK), can stimulate the secretion of glucagon-like peptide-1 (GLP1), a gastrointestinal hormone that plays a vital role in regulating glucose metabolism. However, the mechanism underlying the regulation of GLP1 secretion by compound K has not been fully explored. This study was designed to investigate whether CK ameliorates incretin impairment by regulating the RhoA/ROCKs/YAP signaling pathway and cytoskeleton formation in NCI–H716 cells. Using NCI–H716 cells as a model cell line for GLP1 secretion, we analyzed the effect of CK on the expression of RhoA/ROCK/YAP pathway components. Our results suggest that the effect of CK on GLP1 secretion depends on the anti-inflammatory effect of CK. We also demonstrated that CK can affect the RhoA/ROCK/YAP pathway, which is downstream of transforming growth factor β1 (TGFβ1), by maintaining the capacity of intestinal differentiation. In addition, this effect was mediated by regulating F/G-actin dynamics. These results provide not only the mechanistic insight for the effect of CK on intestinal L cells but also the molecular basis for the further development of CK as a potential therapeutic agent to treat type 2 diabetes mellitus (T2D).http://www.sciencedirect.com/science/article/pii/S1347861320301110Compound KGlucagon-like peptide-1 (GLP1)NCI–H716 cell lineCytoskeletonDiabetes |
spellingShingle | Fengyuan Tian Xi Wang Haixiang Ni Xiaohong Feng Xiao Yuan Qi Huang The ginsenoside metabolite compound K stimulates glucagon-like peptide-1 secretion in NCI–H716 cells by regulating the RhoA/ROCKs/YAP signaling pathway and cytoskeleton formation Journal of Pharmacological Sciences Compound K Glucagon-like peptide-1 (GLP1) NCI–H716 cell line Cytoskeleton Diabetes |
title | The ginsenoside metabolite compound K stimulates glucagon-like peptide-1 secretion in NCI–H716 cells by regulating the RhoA/ROCKs/YAP signaling pathway and cytoskeleton formation |
title_full | The ginsenoside metabolite compound K stimulates glucagon-like peptide-1 secretion in NCI–H716 cells by regulating the RhoA/ROCKs/YAP signaling pathway and cytoskeleton formation |
title_fullStr | The ginsenoside metabolite compound K stimulates glucagon-like peptide-1 secretion in NCI–H716 cells by regulating the RhoA/ROCKs/YAP signaling pathway and cytoskeleton formation |
title_full_unstemmed | The ginsenoside metabolite compound K stimulates glucagon-like peptide-1 secretion in NCI–H716 cells by regulating the RhoA/ROCKs/YAP signaling pathway and cytoskeleton formation |
title_short | The ginsenoside metabolite compound K stimulates glucagon-like peptide-1 secretion in NCI–H716 cells by regulating the RhoA/ROCKs/YAP signaling pathway and cytoskeleton formation |
title_sort | ginsenoside metabolite compound k stimulates glucagon like peptide 1 secretion in nci h716 cells by regulating the rhoa rocks yap signaling pathway and cytoskeleton formation |
topic | Compound K Glucagon-like peptide-1 (GLP1) NCI–H716 cell line Cytoskeleton Diabetes |
url | http://www.sciencedirect.com/science/article/pii/S1347861320301110 |
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