Hepatic carboxylesterase 1 is induced by glucose and regulates postprandial glucose levels
Metabolic syndrome, characterized by obesity, hyperglycemia, dyslipidemia and hypertension, increases the risks for cardiovascular disease, diabetes and stroke. Carboxylesterase 1 (CES1) is an enzyme that hydrolyzes triglycerides and cholesterol esters, and is important for lipid metabolism. Our pre...
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| creator | Xu, Jiesi Yin, Liya Xu, Yang Li, Yuanyuan Zalzala, Munaf Cheng, Gang Zhang, Yanqiao |
| description | Metabolic syndrome, characterized by obesity, hyperglycemia, dyslipidemia and hypertension, increases the risks for cardiovascular disease, diabetes and stroke. Carboxylesterase 1 (CES1) is an enzyme that hydrolyzes triglycerides and cholesterol esters, and is important for lipid metabolism. Our previous data show that over-expression of mouse hepatic CES1 lowers plasma glucose levels and improves insulin sensitivity in diabetic ob/ob mice. In the present study, we determined the physiological role of hepatic CES1 in glucose homeostasis. Hepatic CES1 expression was reduced by fasting but increased in diabetic mice. Treatment of mice with glucose induced hepatic CES1 expression. Consistent with the in vivo study, glucose stimulated CES1 promoter activity and increased acetylation of histone 3 and histone 4 in the CES1 chromatin. Knockdown of ATP-citrate lyase (ACL), an enzyme that regulates histone acetylation, abolished glucose-mediated histone acetylation in the CES1 chromatin and glucose-induced hepatic CES1 expression. Finally, knockdown of hepatic CES1 significantly increased postprandial blood glucose levels. In conclusion, the present study uncovers a novel glucose-CES1-glucose pathway which may play an important role in regulating postprandial blood glucose levels. |
| doi_str_mv | 10.1371/journal.pone.0109663 |
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Carboxylesterase 1 (CES1) is an enzyme that hydrolyzes triglycerides and cholesterol esters, and is important for lipid metabolism. Our previous data show that over-expression of mouse hepatic CES1 lowers plasma glucose levels and improves insulin sensitivity in diabetic ob/ob mice. In the present study, we determined the physiological role of hepatic CES1 in glucose homeostasis. Hepatic CES1 expression was reduced by fasting but increased in diabetic mice. Treatment of mice with glucose induced hepatic CES1 expression. Consistent with the in vivo study, glucose stimulated CES1 promoter activity and increased acetylation of histone 3 and histone 4 in the CES1 chromatin. Knockdown of ATP-citrate lyase (ACL), an enzyme that regulates histone acetylation, abolished glucose-mediated histone acetylation in the CES1 chromatin and glucose-induced hepatic CES1 expression. Finally, knockdown of hepatic CES1 significantly increased postprandial blood glucose levels. In conclusion, the present study uncovers a novel glucose-CES1-glucose pathway which may play an important role in regulating postprandial blood glucose levels.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0109663</identifier><identifier>PMID: 25285996</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Acetylation ; Acetylation - drug effects ; Animal models ; Animals ; ATP Citrate (pro-S)-Lyase - metabolism ; ATP citrate lyase ; Biology and Life Sciences ; Blood ; Blood glucose ; Blood Glucose - metabolism ; Blood lipids ; Carboxylesterase ; Carboxylic Ester Hydrolases - metabolism ; Cardiovascular disease ; Cardiovascular diseases ; Cholesterol ; Chromatin ; Chromatin - metabolism ; Diabetes ; Diabetes mellitus ; Diet ; Dyslipidemia ; Enzymes ; Epigenetics ; Esters ; Fatty acids ; Gene expression ; Gene Expression Regulation, Enzymologic - drug effects ; Glucose ; Glucose - pharmacology ; Health risks ; Histones - metabolism ; Homeostasis ; Hyperglycemia ; Hypertension ; In vivo methods and tests ; Insulin ; Insulin resistance ; Kinases ; Lipid metabolism ; Lipids ; Liver ; Liver - enzymology ; Male ; Medicine and Health Sciences ; Metabolic disorders ; Metabolic syndrome ; Metabolism ; Mice ; Mice, Inbred C57BL ; Nutritional Status ; Obesity ; Overexpression ; Postprandial Period ; Rodents ; Triglycerides</subject><ispartof>PloS one, 2014-10, Vol.9 (10), p.e109663</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Xu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Xu et al 2014 Xu et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-3e2597d9941a2b84f9ed4d6a0e8067fb10cf744862c78560912a3b73aee59b3e3</citedby><cites>FETCH-LOGICAL-c692t-3e2597d9941a2b84f9ed4d6a0e8067fb10cf744862c78560912a3b73aee59b3e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4186840/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4186840/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,2096,2915,23847,27905,27906,53772,53774,79349,79350</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25285996$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Jin, Tianru</contributor><creatorcontrib>Xu, Jiesi</creatorcontrib><creatorcontrib>Yin, Liya</creatorcontrib><creatorcontrib>Xu, Yang</creatorcontrib><creatorcontrib>Li, Yuanyuan</creatorcontrib><creatorcontrib>Zalzala, Munaf</creatorcontrib><creatorcontrib>Cheng, Gang</creatorcontrib><creatorcontrib>Zhang, Yanqiao</creatorcontrib><title>Hepatic carboxylesterase 1 is induced by glucose and regulates postprandial glucose levels</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Metabolic syndrome, characterized by obesity, hyperglycemia, dyslipidemia and hypertension, increases the risks for cardiovascular disease, diabetes and stroke. Carboxylesterase 1 (CES1) is an enzyme that hydrolyzes triglycerides and cholesterol esters, and is important for lipid metabolism. Our previous data show that over-expression of mouse hepatic CES1 lowers plasma glucose levels and improves insulin sensitivity in diabetic ob/ob mice. In the present study, we determined the physiological role of hepatic CES1 in glucose homeostasis. Hepatic CES1 expression was reduced by fasting but increased in diabetic mice. Treatment of mice with glucose induced hepatic CES1 expression. Consistent with the in vivo study, glucose stimulated CES1 promoter activity and increased acetylation of histone 3 and histone 4 in the CES1 chromatin. Knockdown of ATP-citrate lyase (ACL), an enzyme that regulates histone acetylation, abolished glucose-mediated histone acetylation in the CES1 chromatin and glucose-induced hepatic CES1 expression. Finally, knockdown of hepatic CES1 significantly increased postprandial blood glucose levels. In conclusion, the present study uncovers a novel glucose-CES1-glucose pathway which may play an important role in regulating postprandial blood glucose levels.</description><subject>Acetylation</subject><subject>Acetylation - drug effects</subject><subject>Animal models</subject><subject>Animals</subject><subject>ATP Citrate (pro-S)-Lyase - metabolism</subject><subject>ATP citrate lyase</subject><subject>Biology and Life Sciences</subject><subject>Blood</subject><subject>Blood glucose</subject><subject>Blood Glucose - metabolism</subject><subject>Blood lipids</subject><subject>Carboxylesterase</subject><subject>Carboxylic Ester Hydrolases - metabolism</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular diseases</subject><subject>Cholesterol</subject><subject>Chromatin</subject><subject>Chromatin - metabolism</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diet</subject><subject>Dyslipidemia</subject><subject>Enzymes</subject><subject>Epigenetics</subject><subject>Esters</subject><subject>Fatty acids</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Enzymologic - 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Carboxylesterase 1 (CES1) is an enzyme that hydrolyzes triglycerides and cholesterol esters, and is important for lipid metabolism. Our previous data show that over-expression of mouse hepatic CES1 lowers plasma glucose levels and improves insulin sensitivity in diabetic ob/ob mice. In the present study, we determined the physiological role of hepatic CES1 in glucose homeostasis. Hepatic CES1 expression was reduced by fasting but increased in diabetic mice. Treatment of mice with glucose induced hepatic CES1 expression. Consistent with the in vivo study, glucose stimulated CES1 promoter activity and increased acetylation of histone 3 and histone 4 in the CES1 chromatin. Knockdown of ATP-citrate lyase (ACL), an enzyme that regulates histone acetylation, abolished glucose-mediated histone acetylation in the CES1 chromatin and glucose-induced hepatic CES1 expression. Finally, knockdown of hepatic CES1 significantly increased postprandial blood glucose levels. In conclusion, the present study uncovers a novel glucose-CES1-glucose pathway which may play an important role in regulating postprandial blood glucose levels.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25285996</pmid><doi>10.1371/journal.pone.0109663</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Acetylation Acetylation - drug effects Animal models Animals ATP Citrate (pro-S)-Lyase - metabolism ATP citrate lyase Biology and Life Sciences Blood Blood glucose Blood Glucose - metabolism Blood lipids Carboxylesterase Carboxylic Ester Hydrolases - metabolism Cardiovascular disease Cardiovascular diseases Cholesterol Chromatin Chromatin - metabolism Diabetes Diabetes mellitus Diet Dyslipidemia Enzymes Epigenetics Esters Fatty acids Gene expression Gene Expression Regulation, Enzymologic - drug effects Glucose Glucose - pharmacology Health risks Histones - metabolism Homeostasis Hyperglycemia Hypertension In vivo methods and tests Insulin Insulin resistance Kinases Lipid metabolism Lipids Liver Liver - enzymology Male Medicine and Health Sciences Metabolic disorders Metabolic syndrome Metabolism Mice Mice, Inbred C57BL Nutritional Status Obesity Overexpression Postprandial Period Rodents Triglycerides |
| title | Hepatic carboxylesterase 1 is induced by glucose and regulates postprandial glucose levels |
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