Sodium caprate augments the hypoglycemic effect of berberine via AMPK in inhibiting hepatic gluconeogenesis

► We report the hypoglycemic effect of berberine enhanced by sodium caprate. ► We report AMPK activity increased by berberine treatment. ► We report reduced expression of PEPCK, PGC-1, HNF-4α and FOXO1 by berberine treatment. Berberine (BER), a natural product and active ingredient of genera Berberi...

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Veröffentlicht in:Molecular and cellular endocrinology 2012-11, Vol.363 (1-2), p.122-130
Hauptverfasser: Zhang, Ming, Lv, Xiaoyan, Li, Jing, Meng, Zhaojie, Wang, Qiujing, Chang, WenGuang, Li, Wei, Chen, Li, Liu, Yanjun
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container_issue 1-2
container_start_page 122
container_title Molecular and cellular endocrinology
container_volume 363
creator Zhang, Ming
Lv, Xiaoyan
Li, Jing
Meng, Zhaojie
Wang, Qiujing
Chang, WenGuang
Li, Wei
Chen, Li
Liu, Yanjun
description ► We report the hypoglycemic effect of berberine enhanced by sodium caprate. ► We report AMPK activity increased by berberine treatment. ► We report reduced expression of PEPCK, PGC-1, HNF-4α and FOXO1 by berberine treatment. Berberine (BER), a natural product and active ingredient of genera Berberis and Coptis, has been demonstrated to possess anti-diabetic activities. However, the poor bioavailability of this agent greatly limits its clinical application. In our previous study, we demonstrated that co-administration of sodium caprate, an absorption enhancer, with BER could significantly increase the bioavailability of BER without any serious mucosal damage. Here, we investigated the effects of BER on AMP-activated protein kinase (AMPK)/gluconeogenesis pathway and the effects of sodium caprate on hypoglycemic action of BER. The ability of BER co-administered with sodium caprate to reduce insulin resistance was investigated in diabetic rat model induced by high-fat diet and low dose STZ. Western blot was performed to evaluate effects of BER on AMPK signaling proteins involved in hepatic gluconeogenesis in diabetic rat and HepG2 hepatocytes. BER reduced body weight and caused a significant improvement in glucose tolerance without altering food intake in diabetic rats. Similarly, BER reduced plasma triglycerides and improved insulin action in diabetic rats. BER down-regulated the elevated expressions of gluconeogenesis key enzymes PEPCK and G6Pase, inhibited the translocation of TORC2 from cytoplasm to nucleus and increased AMPK activity in liver tissues. The effect of BER was higher when co-administered with sodium caprate. BER treatment resulted in reduced glucose production in HepG2 hepatocytes. BER increased AMPK activity, reduced the expression of PEPCK, and the nuclear transcription factors PGC-1, HNF-4α and FOXO1. The effect of BER on gluconeogenesis could be partly blocked by AMPK inhibitor, Compound C. BER could suppress hepatic gluconeogenesis in rat model of diabetes at least in part via stimulation of AMPK activity and this action of BER is augmented by sodium caprate.
doi_str_mv 10.1016/j.mce.2012.08.006
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Berberine (BER), a natural product and active ingredient of genera Berberis and Coptis, has been demonstrated to possess anti-diabetic activities. However, the poor bioavailability of this agent greatly limits its clinical application. In our previous study, we demonstrated that co-administration of sodium caprate, an absorption enhancer, with BER could significantly increase the bioavailability of BER without any serious mucosal damage. Here, we investigated the effects of BER on AMP-activated protein kinase (AMPK)/gluconeogenesis pathway and the effects of sodium caprate on hypoglycemic action of BER. The ability of BER co-administered with sodium caprate to reduce insulin resistance was investigated in diabetic rat model induced by high-fat diet and low dose STZ. Western blot was performed to evaluate effects of BER on AMPK signaling proteins involved in hepatic gluconeogenesis in diabetic rat and HepG2 hepatocytes. BER reduced body weight and caused a significant improvement in glucose tolerance without altering food intake in diabetic rats. Similarly, BER reduced plasma triglycerides and improved insulin action in diabetic rats. BER down-regulated the elevated expressions of gluconeogenesis key enzymes PEPCK and G6Pase, inhibited the translocation of TORC2 from cytoplasm to nucleus and increased AMPK activity in liver tissues. The effect of BER was higher when co-administered with sodium caprate. BER treatment resulted in reduced glucose production in HepG2 hepatocytes. BER increased AMPK activity, reduced the expression of PEPCK, and the nuclear transcription factors PGC-1, HNF-4α and FOXO1. The effect of BER on gluconeogenesis could be partly blocked by AMPK inhibitor, Compound C. BER could suppress hepatic gluconeogenesis in rat model of diabetes at least in part via stimulation of AMPK activity and this action of BER is augmented by sodium caprate.</description><identifier>ISSN: 0303-7207</identifier><identifier>EISSN: 1872-8057</identifier><identifier>DOI: 10.1016/j.mce.2012.08.006</identifier><identifier>PMID: 22922125</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>active ingredients ; Adenylate Kinase - metabolism ; AMP-activated protein kinase ; animal models ; Animals ; Area Under Curve ; Berberine ; Berberine - pharmacology ; Berberine - therapeutic use ; Berberis ; bioavailability ; Blood Glucose ; body weight ; Coptis ; cytoplasm ; Decanoic Acids - pharmacology ; Decanoic Acids - therapeutic use ; Diabetes ; Diabetes Mellitus, Experimental - drug therapy ; Diabetes Mellitus, Experimental - enzymology ; Diabetes Mellitus, Experimental - metabolism ; Drug Synergism ; Drug Therapy, Combination ; food intake ; Gene Expression - drug effects ; gluconeogenesis ; Gluconeogenesis - drug effects ; glucose ; Glucose - metabolism ; glucose tolerance ; Glucose Tolerance Test ; Glucose-6-Phosphatase - genetics ; Glucose-6-Phosphatase - metabolism ; glycemic effect ; Hep G2 Cells ; Hepatic gluconeogenesis ; hepatocytes ; high fat diet ; Humans ; Hypoglycemic Agents - pharmacology ; Hypoglycemic Agents - therapeutic use ; insulin ; insulin resistance ; Lipid Metabolism - drug effects ; liver ; Liver - drug effects ; Liver - enzymology ; Liver - metabolism ; Male ; Mechanistic Target of Rapamycin Complex 2 ; Metabolic syndrome ; Multiprotein Complexes - metabolism ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Phosphoenolpyruvate Carboxykinase (GTP) - genetics ; Phosphoenolpyruvate Carboxykinase (GTP) - metabolism ; Phosphorylation ; Protein Processing, Post-Translational ; proteins ; Rats ; Rats, Wistar ; RNA-Binding Proteins - metabolism ; Sodium caprate ; tissues ; TOR Serine-Threonine Kinases - metabolism ; transcription factors ; Transcription Factors - metabolism ; triacylglycerols ; Western blotting</subject><ispartof>Molecular and cellular endocrinology, 2012-11, Vol.363 (1-2), p.122-130</ispartof><rights>2012 Elsevier Ireland Ltd</rights><rights>Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.</rights><rights>2012 Elsevier Ireland Ltd. All rights reserved. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c574t-8e1e12bfe8a5b5d2898ad68b188b683b3fa6c0c5219275a3ec758d5fa717cbe23</citedby><cites>FETCH-LOGICAL-c574t-8e1e12bfe8a5b5d2898ad68b188b683b3fa6c0c5219275a3ec758d5fa717cbe23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0303720712003875$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22922125$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Ming</creatorcontrib><creatorcontrib>Lv, Xiaoyan</creatorcontrib><creatorcontrib>Li, Jing</creatorcontrib><creatorcontrib>Meng, Zhaojie</creatorcontrib><creatorcontrib>Wang, Qiujing</creatorcontrib><creatorcontrib>Chang, WenGuang</creatorcontrib><creatorcontrib>Li, Wei</creatorcontrib><creatorcontrib>Chen, Li</creatorcontrib><creatorcontrib>Liu, Yanjun</creatorcontrib><title>Sodium caprate augments the hypoglycemic effect of berberine via AMPK in inhibiting hepatic gluconeogenesis</title><title>Molecular and cellular endocrinology</title><addtitle>Mol Cell Endocrinol</addtitle><description>► We report the hypoglycemic effect of berberine enhanced by sodium caprate. ► We report AMPK activity increased by berberine treatment. ► We report reduced expression of PEPCK, PGC-1, HNF-4α and FOXO1 by berberine treatment. Berberine (BER), a natural product and active ingredient of genera Berberis and Coptis, has been demonstrated to possess anti-diabetic activities. However, the poor bioavailability of this agent greatly limits its clinical application. In our previous study, we demonstrated that co-administration of sodium caprate, an absorption enhancer, with BER could significantly increase the bioavailability of BER without any serious mucosal damage. Here, we investigated the effects of BER on AMP-activated protein kinase (AMPK)/gluconeogenesis pathway and the effects of sodium caprate on hypoglycemic action of BER. The ability of BER co-administered with sodium caprate to reduce insulin resistance was investigated in diabetic rat model induced by high-fat diet and low dose STZ. Western blot was performed to evaluate effects of BER on AMPK signaling proteins involved in hepatic gluconeogenesis in diabetic rat and HepG2 hepatocytes. BER reduced body weight and caused a significant improvement in glucose tolerance without altering food intake in diabetic rats. Similarly, BER reduced plasma triglycerides and improved insulin action in diabetic rats. BER down-regulated the elevated expressions of gluconeogenesis key enzymes PEPCK and G6Pase, inhibited the translocation of TORC2 from cytoplasm to nucleus and increased AMPK activity in liver tissues. The effect of BER was higher when co-administered with sodium caprate. BER treatment resulted in reduced glucose production in HepG2 hepatocytes. BER increased AMPK activity, reduced the expression of PEPCK, and the nuclear transcription factors PGC-1, HNF-4α and FOXO1. The effect of BER on gluconeogenesis could be partly blocked by AMPK inhibitor, Compound C. BER could suppress hepatic gluconeogenesis in rat model of diabetes at least in part via stimulation of AMPK activity and this action of BER is augmented by sodium caprate.</description><subject>active ingredients</subject><subject>Adenylate Kinase - metabolism</subject><subject>AMP-activated protein kinase</subject><subject>animal models</subject><subject>Animals</subject><subject>Area Under Curve</subject><subject>Berberine</subject><subject>Berberine - pharmacology</subject><subject>Berberine - therapeutic use</subject><subject>Berberis</subject><subject>bioavailability</subject><subject>Blood Glucose</subject><subject>body weight</subject><subject>Coptis</subject><subject>cytoplasm</subject><subject>Decanoic Acids - pharmacology</subject><subject>Decanoic Acids - therapeutic use</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Experimental - drug therapy</subject><subject>Diabetes Mellitus, Experimental - enzymology</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Drug Synergism</subject><subject>Drug Therapy, Combination</subject><subject>food intake</subject><subject>Gene Expression - drug effects</subject><subject>gluconeogenesis</subject><subject>Gluconeogenesis - drug effects</subject><subject>glucose</subject><subject>Glucose - metabolism</subject><subject>glucose tolerance</subject><subject>Glucose Tolerance Test</subject><subject>Glucose-6-Phosphatase - genetics</subject><subject>Glucose-6-Phosphatase - metabolism</subject><subject>glycemic effect</subject><subject>Hep G2 Cells</subject><subject>Hepatic gluconeogenesis</subject><subject>hepatocytes</subject><subject>high fat diet</subject><subject>Humans</subject><subject>Hypoglycemic Agents - pharmacology</subject><subject>Hypoglycemic Agents - therapeutic use</subject><subject>insulin</subject><subject>insulin resistance</subject><subject>Lipid Metabolism - drug effects</subject><subject>liver</subject><subject>Liver - drug effects</subject><subject>Liver - enzymology</subject><subject>Liver - metabolism</subject><subject>Male</subject><subject>Mechanistic Target of Rapamycin Complex 2</subject><subject>Metabolic syndrome</subject><subject>Multiprotein Complexes - metabolism</subject><subject>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha</subject><subject>Phosphoenolpyruvate Carboxykinase (GTP) - genetics</subject><subject>Phosphoenolpyruvate Carboxykinase (GTP) - metabolism</subject><subject>Phosphorylation</subject><subject>Protein Processing, Post-Translational</subject><subject>proteins</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>RNA-Binding Proteins - metabolism</subject><subject>Sodium caprate</subject><subject>tissues</subject><subject>TOR Serine-Threonine Kinases - metabolism</subject><subject>transcription factors</subject><subject>Transcription Factors - metabolism</subject><subject>triacylglycerols</subject><subject>Western blotting</subject><issn>0303-7207</issn><issn>1872-8057</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kV2L1TAQhoMo7nH1B3ijufSmdZI2TYogLItfuKKw7nVI02mbY9t0k_bA-fdmOeuiN8JALvLMm5k8hLxkkDNg1dt9PlnMOTCeg8oBqkdkx5TkmQIhH5MdFFBkkoM8I89i3AOAFFw9JWec15wzLnbk17Vv3TZRa5ZgVqRm6yec10jXAelwXHw_Hi1OzlLsOrQr9R1tMKRyM9KDM_Ti24-v1M2pBte41c09HXAxa2rpx836GX2PM0YXn5MnnRkjvrg_z8nNxw8_Lz9nV98_fbm8uMqskOWaKWTIeNOhMqIRLVe1Mm2lGqZUU6miKTpTWbCCs5pLYQq0UqhWdEYyaRvkxTl5f8pdtmbC1qZ9ghn1EtxkwlF74_S_N7MbdO8PupC1qJhIAW_uA4K_3TCuenLR4jiatMwWNavqslRc8DKh7ITa4GMM2D08w0DfSdJ7nSTpO0kalE6SUs-rv-d76PhjJQGvT0BnvDZ9cFHfXKcEAcAUYyUk4t2JwPSPB4dBR-twtti6kCzp1rv_DPAbW5SuPw</recordid><startdate>20121105</startdate><enddate>20121105</enddate><creator>Zhang, Ming</creator><creator>Lv, Xiaoyan</creator><creator>Li, Jing</creator><creator>Meng, Zhaojie</creator><creator>Wang, Qiujing</creator><creator>Chang, WenGuang</creator><creator>Li, Wei</creator><creator>Chen, Li</creator><creator>Liu, Yanjun</creator><general>Elsevier Ireland Ltd</general><scope>FBQ</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7S9</scope><scope>L.6</scope><scope>5PM</scope></search><sort><creationdate>20121105</creationdate><title>Sodium caprate augments the hypoglycemic effect of berberine via AMPK in inhibiting hepatic gluconeogenesis</title><author>Zhang, Ming ; Lv, Xiaoyan ; Li, Jing ; Meng, Zhaojie ; Wang, Qiujing ; Chang, WenGuang ; Li, Wei ; Chen, Li ; Liu, Yanjun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c574t-8e1e12bfe8a5b5d2898ad68b188b683b3fa6c0c5219275a3ec758d5fa717cbe23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>active ingredients</topic><topic>Adenylate Kinase - metabolism</topic><topic>AMP-activated protein kinase</topic><topic>animal models</topic><topic>Animals</topic><topic>Area Under Curve</topic><topic>Berberine</topic><topic>Berberine - pharmacology</topic><topic>Berberine - therapeutic use</topic><topic>Berberis</topic><topic>bioavailability</topic><topic>Blood Glucose</topic><topic>body weight</topic><topic>Coptis</topic><topic>cytoplasm</topic><topic>Decanoic Acids - pharmacology</topic><topic>Decanoic Acids - therapeutic use</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Experimental - drug therapy</topic><topic>Diabetes Mellitus, Experimental - enzymology</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Drug Synergism</topic><topic>Drug Therapy, Combination</topic><topic>food intake</topic><topic>Gene Expression - drug effects</topic><topic>gluconeogenesis</topic><topic>Gluconeogenesis - drug effects</topic><topic>glucose</topic><topic>Glucose - metabolism</topic><topic>glucose tolerance</topic><topic>Glucose Tolerance Test</topic><topic>Glucose-6-Phosphatase - genetics</topic><topic>Glucose-6-Phosphatase - metabolism</topic><topic>glycemic effect</topic><topic>Hep G2 Cells</topic><topic>Hepatic gluconeogenesis</topic><topic>hepatocytes</topic><topic>high fat diet</topic><topic>Humans</topic><topic>Hypoglycemic Agents - pharmacology</topic><topic>Hypoglycemic Agents - therapeutic use</topic><topic>insulin</topic><topic>insulin resistance</topic><topic>Lipid Metabolism - drug effects</topic><topic>liver</topic><topic>Liver - drug effects</topic><topic>Liver - enzymology</topic><topic>Liver - metabolism</topic><topic>Male</topic><topic>Mechanistic Target of Rapamycin Complex 2</topic><topic>Metabolic syndrome</topic><topic>Multiprotein Complexes - metabolism</topic><topic>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha</topic><topic>Phosphoenolpyruvate Carboxykinase (GTP) - genetics</topic><topic>Phosphoenolpyruvate Carboxykinase (GTP) - metabolism</topic><topic>Phosphorylation</topic><topic>Protein Processing, Post-Translational</topic><topic>proteins</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>RNA-Binding Proteins - metabolism</topic><topic>Sodium caprate</topic><topic>tissues</topic><topic>TOR Serine-Threonine Kinases - metabolism</topic><topic>transcription factors</topic><topic>Transcription Factors - metabolism</topic><topic>triacylglycerols</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Ming</creatorcontrib><creatorcontrib>Lv, Xiaoyan</creatorcontrib><creatorcontrib>Li, Jing</creatorcontrib><creatorcontrib>Meng, Zhaojie</creatorcontrib><creatorcontrib>Wang, Qiujing</creatorcontrib><creatorcontrib>Chang, WenGuang</creatorcontrib><creatorcontrib>Li, Wei</creatorcontrib><creatorcontrib>Chen, Li</creatorcontrib><creatorcontrib>Liu, Yanjun</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular and cellular endocrinology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Ming</au><au>Lv, Xiaoyan</au><au>Li, Jing</au><au>Meng, Zhaojie</au><au>Wang, Qiujing</au><au>Chang, WenGuang</au><au>Li, Wei</au><au>Chen, Li</au><au>Liu, Yanjun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sodium caprate augments the hypoglycemic effect of berberine via AMPK in inhibiting hepatic gluconeogenesis</atitle><jtitle>Molecular and cellular endocrinology</jtitle><addtitle>Mol Cell Endocrinol</addtitle><date>2012-11-05</date><risdate>2012</risdate><volume>363</volume><issue>1-2</issue><spage>122</spage><epage>130</epage><pages>122-130</pages><issn>0303-7207</issn><eissn>1872-8057</eissn><abstract>► We report the hypoglycemic effect of berberine enhanced by sodium caprate. ► We report AMPK activity increased by berberine treatment. ► We report reduced expression of PEPCK, PGC-1, HNF-4α and FOXO1 by berberine treatment. Berberine (BER), a natural product and active ingredient of genera Berberis and Coptis, has been demonstrated to possess anti-diabetic activities. However, the poor bioavailability of this agent greatly limits its clinical application. In our previous study, we demonstrated that co-administration of sodium caprate, an absorption enhancer, with BER could significantly increase the bioavailability of BER without any serious mucosal damage. Here, we investigated the effects of BER on AMP-activated protein kinase (AMPK)/gluconeogenesis pathway and the effects of sodium caprate on hypoglycemic action of BER. The ability of BER co-administered with sodium caprate to reduce insulin resistance was investigated in diabetic rat model induced by high-fat diet and low dose STZ. Western blot was performed to evaluate effects of BER on AMPK signaling proteins involved in hepatic gluconeogenesis in diabetic rat and HepG2 hepatocytes. BER reduced body weight and caused a significant improvement in glucose tolerance without altering food intake in diabetic rats. Similarly, BER reduced plasma triglycerides and improved insulin action in diabetic rats. BER down-regulated the elevated expressions of gluconeogenesis key enzymes PEPCK and G6Pase, inhibited the translocation of TORC2 from cytoplasm to nucleus and increased AMPK activity in liver tissues. The effect of BER was higher when co-administered with sodium caprate. BER treatment resulted in reduced glucose production in HepG2 hepatocytes. BER increased AMPK activity, reduced the expression of PEPCK, and the nuclear transcription factors PGC-1, HNF-4α and FOXO1. The effect of BER on gluconeogenesis could be partly blocked by AMPK inhibitor, Compound C. BER could suppress hepatic gluconeogenesis in rat model of diabetes at least in part via stimulation of AMPK activity and this action of BER is augmented by sodium caprate.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>22922125</pmid><doi>10.1016/j.mce.2012.08.006</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record>
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ispartof Molecular and cellular endocrinology, 2012-11, Vol.363 (1-2), p.122-130
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1872-8057
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source MEDLINE; Elsevier ScienceDirect Journals
subjects active ingredients
Adenylate Kinase - metabolism
AMP-activated protein kinase
animal models
Animals
Area Under Curve
Berberine
Berberine - pharmacology
Berberine - therapeutic use
Berberis
bioavailability
Blood Glucose
body weight
Coptis
cytoplasm
Decanoic Acids - pharmacology
Decanoic Acids - therapeutic use
Diabetes
Diabetes Mellitus, Experimental - drug therapy
Diabetes Mellitus, Experimental - enzymology
Diabetes Mellitus, Experimental - metabolism
Drug Synergism
Drug Therapy, Combination
food intake
Gene Expression - drug effects
gluconeogenesis
Gluconeogenesis - drug effects
glucose
Glucose - metabolism
glucose tolerance
Glucose Tolerance Test
Glucose-6-Phosphatase - genetics
Glucose-6-Phosphatase - metabolism
glycemic effect
Hep G2 Cells
Hepatic gluconeogenesis
hepatocytes
high fat diet
Humans
Hypoglycemic Agents - pharmacology
Hypoglycemic Agents - therapeutic use
insulin
insulin resistance
Lipid Metabolism - drug effects
liver
Liver - drug effects
Liver - enzymology
Liver - metabolism
Male
Mechanistic Target of Rapamycin Complex 2
Metabolic syndrome
Multiprotein Complexes - metabolism
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
Phosphoenolpyruvate Carboxykinase (GTP) - genetics
Phosphoenolpyruvate Carboxykinase (GTP) - metabolism
Phosphorylation
Protein Processing, Post-Translational
proteins
Rats
Rats, Wistar
RNA-Binding Proteins - metabolism
Sodium caprate
tissues
TOR Serine-Threonine Kinases - metabolism
transcription factors
Transcription Factors - metabolism
triacylglycerols
Western blotting
title Sodium caprate augments the hypoglycemic effect of berberine via AMPK in inhibiting hepatic gluconeogenesis
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