Insulin sensitization via partial agonism of PPARγ and glucose uptake through translocation and activation of GLUT4 in PI3K/p-Akt signaling pathway by embelin in type 2 diabetic rats
The present study was aimed at isolating an antidiabetic molecule from a herbal source and assessing its mechanism of action. Embelin, isolated from Embelia ribes Burm. (Myrsinaceae) fruit, was evaluated for its potential to regulate insulin resistance, alter β-cell dysfunction and modulate key mark...
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| Published in | Biochimica et biophysica acta Vol. 1830; no. 1; pp. 2243 - 2255 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Netherlands
Elsevier B.V
01.01.2013
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0304-4165 0006-3002 1872-8006 |
| DOI | 10.1016/j.bbagen.2012.10.016 |
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| Abstract | The present study was aimed at isolating an antidiabetic molecule from a herbal source and assessing its mechanism of action.
Embelin, isolated from Embelia ribes Burm. (Myrsinaceae) fruit, was evaluated for its potential to regulate insulin resistance, alter β-cell dysfunction and modulate key markers involved in insulin sensitivity and glucose transport using high-fat diet (HFD) fed-streptozotocin (STZ) (40mg/kg)-induced type 2 diabetic rats. Molecular-dockings were performed to investigate the binding modes of embelin into PPARγ, PI3K, p-Akt and GLUT4 active sites.
Embelin (50mg/kg b wt.) reduced body weight gain, blood glucose and plasma insulin in treated diabetic rats. It further modulated the altered lipid profiles and antioxidant enzymes with cytoprotective action on β-cell. Embelin significantly increased the PPARγ expression in epididymal adipose tissue compared to diabetic control group; it also inhibited adipogenic activity; it mildly activated PPARγ levels in the liver and skeletal muscle. It also regulated insulin mediated glucose uptake in epididymal adipose tissue through translocation and activation of GLUT4 in PI3K/p-Akt signaling cascade. Embelin bound to PPARγ; it disclosed stable binding affinities to the active sites of PI3K, p-Akt and GLUT4.
These findings show that embelin could improve adipose tissue insulin sensitivity without increasing weight gain, enhance glycemic control, protect β-cell from damage and maintain glucose homeostasis in adipose tissue.
Embelin can be used in the prevention and treatment of type 2 diabetes mellitus caused due to obesity.
[Display omitted]
► Embelin was isolated from Embelia ribes Burm. fruit. ► Embelin suppressed the body weight gain in type 2 diabetic rats. ► Embelin increased the PPARγ expression in epididymal adipose tissue. ► Embelin regulated glucose uptake through GLUT4 in PI3K/ p-Akt signaling. ► Embelin docked with PPARγ, PI3K, p-Akt and GLUT4. |
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| AbstractList | The present study was aimed at isolating an antidiabetic molecule from a herbal source and assessing its mechanism of action.
Embelin, isolated from Embelia ribes Burm. (Myrsinaceae) fruit, was evaluated for its potential to regulate insulin resistance, alter β-cell dysfunction and modulate key markers involved in insulin sensitivity and glucose transport using high-fat diet (HFD) fed-streptozotocin (STZ) (40mg/kg)-induced type 2 diabetic rats. Molecular-dockings were performed to investigate the binding modes of embelin into PPARγ, PI3K, p-Akt and GLUT4 active sites.
Embelin (50mg/kg b wt.) reduced body weight gain, blood glucose and plasma insulin in treated diabetic rats. It further modulated the altered lipid profiles and antioxidant enzymes with cytoprotective action on β-cell. Embelin significantly increased the PPARγ expression in epididymal adipose tissue compared to diabetic control group; it also inhibited adipogenic activity; it mildly activated PPARγ levels in the liver and skeletal muscle. It also regulated insulin mediated glucose uptake in epididymal adipose tissue through translocation and activation of GLUT4 in PI3K/p-Akt signaling cascade. Embelin bound to PPARγ; it disclosed stable binding affinities to the active sites of PI3K, p-Akt and GLUT4.
These findings show that embelin could improve adipose tissue insulin sensitivity without increasing weight gain, enhance glycemic control, protect β-cell from damage and maintain glucose homeostasis in adipose tissue.
Embelin can be used in the prevention and treatment of type 2 diabetes mellitus caused due to obesity. The present study was aimed at isolating an antidiabetic molecule from a herbal source and assessing its mechanism of action.Embelin, isolated from Embelia ribes Burm. (Myrsinaceae) fruit, was evaluated for its potential to regulate insulin resistance, alter β-cell dysfunction and modulate key markers involved in insulin sensitivity and glucose transport using high-fat diet (HFD) fed-streptozotocin (STZ) (40mg/kg)-induced type 2 diabetic rats. Molecular-dockings were performed to investigate the binding modes of embelin into PPARγ, PI3K, p-Akt and GLUT4 active sites.Embelin (50mg/kg b wt.) reduced body weight gain, blood glucose and plasma insulin in treated diabetic rats. It further modulated the altered lipid profiles and antioxidant enzymes with cytoprotective action on β-cell. Embelin significantly increased the PPARγ expression in epididymal adipose tissue compared to diabetic control group; it also inhibited adipogenic activity; it mildly activated PPARγ levels in the liver and skeletal muscle. It also regulated insulin mediated glucose uptake in epididymal adipose tissue through translocation and activation of GLUT4 in PI3K/p-Akt signaling cascade. Embelin bound to PPARγ; it disclosed stable binding affinities to the active sites of PI3K, p-Akt and GLUT4.These findings show that embelin could improve adipose tissue insulin sensitivity without increasing weight gain, enhance glycemic control, protect β-cell from damage and maintain glucose homeostasis in adipose tissue.Embelin can be used in the prevention and treatment of type 2 diabetes mellitus caused due to obesity. The present study was aimed at isolating an antidiabetic molecule from a herbal source and assessing its mechanism of action.BACKGROUNDThe present study was aimed at isolating an antidiabetic molecule from a herbal source and assessing its mechanism of action.Embelin, isolated from Embelia ribes Burm. (Myrsinaceae) fruit, was evaluated for its potential to regulate insulin resistance, alter β-cell dysfunction and modulate key markers involved in insulin sensitivity and glucose transport using high-fat diet (HFD) fed-streptozotocin (STZ) (40mg/kg)-induced type 2 diabetic rats. Molecular-dockings were performed to investigate the binding modes of embelin into PPARγ, PI3K, p-Akt and GLUT4 active sites.METHODSEmbelin, isolated from Embelia ribes Burm. (Myrsinaceae) fruit, was evaluated for its potential to regulate insulin resistance, alter β-cell dysfunction and modulate key markers involved in insulin sensitivity and glucose transport using high-fat diet (HFD) fed-streptozotocin (STZ) (40mg/kg)-induced type 2 diabetic rats. Molecular-dockings were performed to investigate the binding modes of embelin into PPARγ, PI3K, p-Akt and GLUT4 active sites.Embelin (50mg/kg b wt.) reduced body weight gain, blood glucose and plasma insulin in treated diabetic rats. It further modulated the altered lipid profiles and antioxidant enzymes with cytoprotective action on β-cell. Embelin significantly increased the PPARγ expression in epididymal adipose tissue compared to diabetic control group; it also inhibited adipogenic activity; it mildly activated PPARγ levels in the liver and skeletal muscle. It also regulated insulin mediated glucose uptake in epididymal adipose tissue through translocation and activation of GLUT4 in PI3K/p-Akt signaling cascade. Embelin bound to PPARγ; it disclosed stable binding affinities to the active sites of PI3K, p-Akt and GLUT4.RESULTSEmbelin (50mg/kg b wt.) reduced body weight gain, blood glucose and plasma insulin in treated diabetic rats. It further modulated the altered lipid profiles and antioxidant enzymes with cytoprotective action on β-cell. Embelin significantly increased the PPARγ expression in epididymal adipose tissue compared to diabetic control group; it also inhibited adipogenic activity; it mildly activated PPARγ levels in the liver and skeletal muscle. It also regulated insulin mediated glucose uptake in epididymal adipose tissue through translocation and activation of GLUT4 in PI3K/p-Akt signaling cascade. Embelin bound to PPARγ; it disclosed stable binding affinities to the active sites of PI3K, p-Akt and GLUT4.These findings show that embelin could improve adipose tissue insulin sensitivity without increasing weight gain, enhance glycemic control, protect β-cell from damage and maintain glucose homeostasis in adipose tissue.CONCLUSIONSThese findings show that embelin could improve adipose tissue insulin sensitivity without increasing weight gain, enhance glycemic control, protect β-cell from damage and maintain glucose homeostasis in adipose tissue.Embelin can be used in the prevention and treatment of type 2 diabetes mellitus caused due to obesity.GENERAL SIGNIFICANCEEmbelin can be used in the prevention and treatment of type 2 diabetes mellitus caused due to obesity. The present study was aimed at isolating an antidiabetic molecule from a herbal source and assessing its mechanism of action. Embelin, isolated from Embelia ribes Burm. (Myrsinaceae) fruit, was evaluated for its potential to regulate insulin resistance, alter β-cell dysfunction and modulate key markers involved in insulin sensitivity and glucose transport using high-fat diet (HFD) fed-streptozotocin (STZ) (40mg/kg)-induced type 2 diabetic rats. Molecular-dockings were performed to investigate the binding modes of embelin into PPARγ, PI3K, p-Akt and GLUT4 active sites. Embelin (50mg/kg b wt.) reduced body weight gain, blood glucose and plasma insulin in treated diabetic rats. It further modulated the altered lipid profiles and antioxidant enzymes with cytoprotective action on β-cell. Embelin significantly increased the PPARγ expression in epididymal adipose tissue compared to diabetic control group; it also inhibited adipogenic activity; it mildly activated PPARγ levels in the liver and skeletal muscle. It also regulated insulin mediated glucose uptake in epididymal adipose tissue through translocation and activation of GLUT4 in PI3K/p-Akt signaling cascade. Embelin bound to PPARγ; it disclosed stable binding affinities to the active sites of PI3K, p-Akt and GLUT4. These findings show that embelin could improve adipose tissue insulin sensitivity without increasing weight gain, enhance glycemic control, protect β-cell from damage and maintain glucose homeostasis in adipose tissue. Embelin can be used in the prevention and treatment of type 2 diabetes mellitus caused due to obesity. [Display omitted] ► Embelin was isolated from Embelia ribes Burm. fruit. ► Embelin suppressed the body weight gain in type 2 diabetic rats. ► Embelin increased the PPARγ expression in epididymal adipose tissue. ► Embelin regulated glucose uptake through GLUT4 in PI3K/ p-Akt signaling. ► Embelin docked with PPARγ, PI3K, p-Akt and GLUT4. |
| Author | Balakrishna, Kedike Stalin, Antony Vishal, Rajagopal Gandhi, Gopalsamy Rajiv Ignacimuthu, Savarimuthu Paulraj, Michael Gabriel |
| Author_xml | – sequence: 1 givenname: Gopalsamy Rajiv surname: Gandhi fullname: Gandhi, Gopalsamy Rajiv organization: Division of Ethnopharmacology, Entomology Research Institute, Loyola College, Chennai 600034, India – sequence: 2 givenname: Antony surname: Stalin fullname: Stalin, Antony organization: Division of Bioinformatics, Entomology Research Institute, Loyola College, Chennai 600034, India – sequence: 3 givenname: Kedike surname: Balakrishna fullname: Balakrishna, Kedike organization: Division of Ethnopharmacology, Entomology Research Institute, Loyola College, Chennai 600034, India – sequence: 4 givenname: Savarimuthu surname: Ignacimuthu fullname: Ignacimuthu, Savarimuthu email: entolc@hotmail.com organization: Division of Ethnopharmacology, Entomology Research Institute, Loyola College, Chennai 600034, India – sequence: 5 givenname: Michael Gabriel surname: Paulraj fullname: Paulraj, Michael Gabriel organization: Division of Ethnopharmacology, Entomology Research Institute, Loyola College, Chennai 600034, India – sequence: 6 givenname: Rajagopal surname: Vishal fullname: Vishal, Rajagopal organization: Department of Biochemistry, University of Madras, Guindy campus, Chennai 600021, India |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23104384$$D View this record in MEDLINE/PubMed |
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| Copyright | 2012 Elsevier B.V. Copyright © 2012 Elsevier B.V. All rights reserved. |
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| Keywords | FFA PBS T2DM Embelin HFD SOD FBG MW Type 2 diabetes mellitus GPx PPARγ TC TZDs Molecular-docking TG b wt PI3K/p-Akt CAT STZ OGTT GLUT4 |
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| Snippet | The present study was aimed at isolating an antidiabetic molecule from a herbal source and assessing its mechanism of action.
Embelin, isolated from Embelia... The present study was aimed at isolating an antidiabetic molecule from a herbal source and assessing its mechanism of action.BACKGROUNDThe present study was... The present study was aimed at isolating an antidiabetic molecule from a herbal source and assessing its mechanism of action.Embelin, isolated from Embelia... |
| SourceID | proquest pubmed crossref elsevier |
| SourceType | Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 2243 |
| SubjectTerms | active sites adipose tissue Adipose Tissue - metabolism Adipose Tissue - pathology agonistic behavior animal disease models Animals antioxidants Benzoquinones - chemistry Benzoquinones - pharmacology binding capacity blood glucose body weight changes Diabetes Mellitus, Experimental - drug therapy Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Experimental - pathology Diabetes Mellitus, Type 2 - drug therapy Diabetes Mellitus, Type 2 - metabolism Diabetes Mellitus, Type 2 - pathology Embelia - chemistry Embelia ribes Embelin Fruit - chemistry Gene Expression Regulation - drug effects glucose Glucose - metabolism Glucose Transporter Type 4 - metabolism glucose transporters GLUT4 glycemic control high fat diet homeostasis Homeostasis - drug effects Hypoglycemic Agents - chemistry Hypoglycemic Agents - pharmacology insulin Insulin Resistance Insulin-Secreting Cells - metabolism Insulin-Secreting Cells - pathology islets of Langerhans liver Male mechanism of action Molecular-docking noninsulin-dependent diabetes mellitus obesity Obesity - drug therapy Obesity - metabolism Obesity - pathology phosphatidylinositol 3-kinase Phosphatidylinositol 3-Kinases - metabolism PI3K/p-Akt PPAR gamma - agonists PPAR gamma - metabolism PPARγ Protein Transport - drug effects Proto-Oncogene Proteins c-akt - metabolism Rats Rats, Wistar signal transduction Signal Transduction - drug effects skeletal muscle Type 2 diabetes mellitus weight gain |
| Title | Insulin sensitization via partial agonism of PPARγ and glucose uptake through translocation and activation of GLUT4 in PI3K/p-Akt signaling pathway by embelin in type 2 diabetic rats |
| URI | https://dx.doi.org/10.1016/j.bbagen.2012.10.016 https://www.ncbi.nlm.nih.gov/pubmed/23104384 https://www.proquest.com/docview/1220362483 https://www.proquest.com/docview/2000083453 |
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