Glucagon-Like Peptide-1 Receptor Agonist Prevented the Progression of Hepatocellular Carcinoma in a Mouse Model of Nonalcoholic Steatohepatitis
Glucagon-like peptide-1 (GLP-1) receptor agonists are used to treat diabetes, but their effects on nonalcoholic steatohepatitis (NASH) and the development of hepatocellular carcinoma (HCC) remain unclear. In this study, mice with streptozotocin- and high-fat diet-induced diabetes and NASH were subcu...
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| Veröffentlicht in: | International journal of molecular sciences 2020-08, Vol.21 (16), p.5722 |
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| creator | Kojima, Motoyasu Takahashi, Hirokazu Kuwashiro, Takuya Tanaka, Kenichi Mori, Hitoe Ozaki, Iwata Kitajima, Yoichiro Matsuda, Yayoi Ashida, Kenji Eguchi, Yuichiro Anzai, Keizo |
| description | Glucagon-like peptide-1 (GLP-1) receptor agonists are used to treat diabetes, but their effects on nonalcoholic steatohepatitis (NASH) and the development of hepatocellular carcinoma (HCC) remain unclear. In this study, mice with streptozotocin- and high-fat diet-induced diabetes and NASH were subcutaneously treated with liraglutide or saline (control) for 14 weeks. Glycemic control, hepatocarcinogenesis, and liver histology were compared between the groups. Fasting blood glucose levels were significantly lower in the liraglutide group than in the control group (210.0 ± 17.3 mg/dL vs. 601.8 ± 123.6 mg/dL), and fasting insulin levels were significantly increased by liraglutide (0.18 ± 0.06 ng/mL vs. 0.09 ± 0.03 ng/mL). Liraglutide completely suppressed hepatocarcinogenesis, whereas HCC was observed in all control mice (average tumor count, 5.5 ± 3.87; average tumor size, 8.1 ± 5.0 mm). Liraglutide significantly ameliorated steatosis, inflammation, and hepatocyte ballooning of non-tumorous lesions in the liver compared with the control findings, and insulin-positive β-cells were observed in the pancreas in liraglutide-treated mice but not in control mice. In conclusion, liraglutide ameliorated NASH and suppressed hepatocarcinogenesis in diabetic mice. GLP-1 receptor agonists can be used to improve the hepatic outcome of diabetes. |
| doi_str_mv | 10.3390/ijms21165722 |
| format | Article |
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In this study, mice with streptozotocin- and high-fat diet-induced diabetes and NASH were subcutaneously treated with liraglutide or saline (control) for 14 weeks. Glycemic control, hepatocarcinogenesis, and liver histology were compared between the groups. Fasting blood glucose levels were significantly lower in the liraglutide group than in the control group (210.0 ± 17.3 mg/dL vs. 601.8 ± 123.6 mg/dL), and fasting insulin levels were significantly increased by liraglutide (0.18 ± 0.06 ng/mL vs. 0.09 ± 0.03 ng/mL). Liraglutide completely suppressed hepatocarcinogenesis, whereas HCC was observed in all control mice (average tumor count, 5.5 ± 3.87; average tumor size, 8.1 ± 5.0 mm). Liraglutide significantly ameliorated steatosis, inflammation, and hepatocyte ballooning of non-tumorous lesions in the liver compared with the control findings, and insulin-positive β-cells were observed in the pancreas in liraglutide-treated mice but not in control mice. In conclusion, liraglutide ameliorated NASH and suppressed hepatocarcinogenesis in diabetic mice. GLP-1 receptor agonists can be used to improve the hepatic outcome of diabetes.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms21165722</identifier><identifier>PMID: 32785012</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Agonists ; Animals ; Beta cells ; Blood glucose ; Blood Glucose - analysis ; Carcinogenesis - drug effects ; Carcinoma, Hepatocellular - prevention & control ; Diabetes mellitus ; Diabetes Mellitus, Experimental - chemically induced ; Diabetes Mellitus, Experimental - complications ; Diabetes Mellitus, Experimental - drug therapy ; Diet, High-Fat - adverse effects ; Disease Models, Animal ; Fasting ; GLP-1 receptor agonists ; Glucagon ; Glucagon-like peptide 1 ; Glucagon-Like Peptide-1 Receptor - agonists ; Hepatocellular carcinoma ; High fat diet ; Histology ; Hypoglycemic Agents - administration & dosage ; Insulin ; Insulin - blood ; Insulin resistance ; Kinases ; Liraglutide - administration & dosage ; Liver ; Liver cancer ; Liver Neoplasms - prevention & control ; Male ; Mice ; Mice, Inbred C57BL ; Non-alcoholic Fatty Liver Disease - complications ; Non-alcoholic Fatty Liver Disease - drug therapy ; Non-alcoholic Fatty Liver Disease - etiology ; Obesity ; Pancreas ; Steatosis ; Streptozocin ; Streptozocin - adverse effects ; Treatment Outcome ; Tumors</subject><ispartof>International journal of molecular sciences, 2020-08, Vol.21 (16), p.5722</ispartof><rights>2020. This work is licensed under http://creativecommons.org/licenses/by/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2020 by the authors. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c478t-2e7bf082c07e73f80a5c6a8c51bb3d5de55cf479ab2615a4a24e735c430aec73</citedby><cites>FETCH-LOGICAL-c478t-2e7bf082c07e73f80a5c6a8c51bb3d5de55cf479ab2615a4a24e735c430aec73</cites><orcidid>0000-0001-8542-1434 ; 0000-0001-8753-6016 ; 0000-0002-6263-1436</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7460814/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7460814/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32785012$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kojima, Motoyasu</creatorcontrib><creatorcontrib>Takahashi, Hirokazu</creatorcontrib><creatorcontrib>Kuwashiro, Takuya</creatorcontrib><creatorcontrib>Tanaka, Kenichi</creatorcontrib><creatorcontrib>Mori, Hitoe</creatorcontrib><creatorcontrib>Ozaki, Iwata</creatorcontrib><creatorcontrib>Kitajima, Yoichiro</creatorcontrib><creatorcontrib>Matsuda, Yayoi</creatorcontrib><creatorcontrib>Ashida, Kenji</creatorcontrib><creatorcontrib>Eguchi, Yuichiro</creatorcontrib><creatorcontrib>Anzai, Keizo</creatorcontrib><title>Glucagon-Like Peptide-1 Receptor Agonist Prevented the Progression of Hepatocellular Carcinoma in a Mouse Model of Nonalcoholic Steatohepatitis</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Glucagon-like peptide-1 (GLP-1) receptor agonists are used to treat diabetes, but their effects on nonalcoholic steatohepatitis (NASH) and the development of hepatocellular carcinoma (HCC) remain unclear. In this study, mice with streptozotocin- and high-fat diet-induced diabetes and NASH were subcutaneously treated with liraglutide or saline (control) for 14 weeks. Glycemic control, hepatocarcinogenesis, and liver histology were compared between the groups. Fasting blood glucose levels were significantly lower in the liraglutide group than in the control group (210.0 ± 17.3 mg/dL vs. 601.8 ± 123.6 mg/dL), and fasting insulin levels were significantly increased by liraglutide (0.18 ± 0.06 ng/mL vs. 0.09 ± 0.03 ng/mL). Liraglutide completely suppressed hepatocarcinogenesis, whereas HCC was observed in all control mice (average tumor count, 5.5 ± 3.87; average tumor size, 8.1 ± 5.0 mm). Liraglutide significantly ameliorated steatosis, inflammation, and hepatocyte ballooning of non-tumorous lesions in the liver compared with the control findings, and insulin-positive β-cells were observed in the pancreas in liraglutide-treated mice but not in control mice. In conclusion, liraglutide ameliorated NASH and suppressed hepatocarcinogenesis in diabetic mice. GLP-1 receptor agonists can be used to improve the hepatic outcome of diabetes.</description><subject>Agonists</subject><subject>Animals</subject><subject>Beta cells</subject><subject>Blood glucose</subject><subject>Blood Glucose - analysis</subject><subject>Carcinogenesis - drug effects</subject><subject>Carcinoma, Hepatocellular - prevention & control</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Experimental - chemically induced</subject><subject>Diabetes Mellitus, Experimental - complications</subject><subject>Diabetes Mellitus, Experimental - drug therapy</subject><subject>Diet, High-Fat - adverse effects</subject><subject>Disease Models, Animal</subject><subject>Fasting</subject><subject>GLP-1 receptor agonists</subject><subject>Glucagon</subject><subject>Glucagon-like peptide 1</subject><subject>Glucagon-Like Peptide-1 Receptor - agonists</subject><subject>Hepatocellular carcinoma</subject><subject>High fat diet</subject><subject>Histology</subject><subject>Hypoglycemic Agents - 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In this study, mice with streptozotocin- and high-fat diet-induced diabetes and NASH were subcutaneously treated with liraglutide or saline (control) for 14 weeks. Glycemic control, hepatocarcinogenesis, and liver histology were compared between the groups. Fasting blood glucose levels were significantly lower in the liraglutide group than in the control group (210.0 ± 17.3 mg/dL vs. 601.8 ± 123.6 mg/dL), and fasting insulin levels were significantly increased by liraglutide (0.18 ± 0.06 ng/mL vs. 0.09 ± 0.03 ng/mL). Liraglutide completely suppressed hepatocarcinogenesis, whereas HCC was observed in all control mice (average tumor count, 5.5 ± 3.87; average tumor size, 8.1 ± 5.0 mm). Liraglutide significantly ameliorated steatosis, inflammation, and hepatocyte ballooning of non-tumorous lesions in the liver compared with the control findings, and insulin-positive β-cells were observed in the pancreas in liraglutide-treated mice but not in control mice. In conclusion, liraglutide ameliorated NASH and suppressed hepatocarcinogenesis in diabetic mice. GLP-1 receptor agonists can be used to improve the hepatic outcome of diabetes.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>32785012</pmid><doi>10.3390/ijms21165722</doi><orcidid>https://orcid.org/0000-0001-8542-1434</orcidid><orcidid>https://orcid.org/0000-0001-8753-6016</orcidid><orcidid>https://orcid.org/0000-0002-6263-1436</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | International journal of molecular sciences, 2020-08, Vol.21 (16), p.5722 |
| issn | 1422-0067 1661-6596 1422-0067 |
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| source | MDPI - Multidisciplinary Digital Publishing Institute; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Agonists Animals Beta cells Blood glucose Blood Glucose - analysis Carcinogenesis - drug effects Carcinoma, Hepatocellular - prevention & control Diabetes mellitus Diabetes Mellitus, Experimental - chemically induced Diabetes Mellitus, Experimental - complications Diabetes Mellitus, Experimental - drug therapy Diet, High-Fat - adverse effects Disease Models, Animal Fasting GLP-1 receptor agonists Glucagon Glucagon-like peptide 1 Glucagon-Like Peptide-1 Receptor - agonists Hepatocellular carcinoma High fat diet Histology Hypoglycemic Agents - administration & dosage Insulin Insulin - blood Insulin resistance Kinases Liraglutide - administration & dosage Liver Liver cancer Liver Neoplasms - prevention & control Male Mice Mice, Inbred C57BL Non-alcoholic Fatty Liver Disease - complications Non-alcoholic Fatty Liver Disease - drug therapy Non-alcoholic Fatty Liver Disease - etiology Obesity Pancreas Steatosis Streptozocin Streptozocin - adverse effects Treatment Outcome Tumors |
| title | Glucagon-Like Peptide-1 Receptor Agonist Prevented the Progression of Hepatocellular Carcinoma in a Mouse Model of Nonalcoholic Steatohepatitis |
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