Cited 19 times in
β-Cell-protective effect of 2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid as a glutamate dehydrogenase activator in db/db mice
DC Field | Value | Language |
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dc.contributor.author | 이현철 | - |
dc.contributor.author | 한승진 | - |
dc.date.accessioned | 2014-12-19T17:06:04Z | - |
dc.date.available | 2014-12-19T17:06:04Z | - |
dc.date.issued | 2012 | - |
dc.identifier.issn | 0022-0795 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/90778 | - |
dc.description.abstract | 2-Aminobicyclo-(2,2,1)-heptane-2-carboxylic acid (BCH) is an activator of glutamate dehydrogenase (GDH), which is a mitochondrial enzyme with an important role in insulin secretion. We investigated the effect of BCH on the high-glucose (HG)-induced reduction in glucose-stimulated insulin secretion (GSIS), the HG/palmitate (PA)-induced reduction in insulin gene expression, and HG/PA-induced β-cell death. We also studied whether long-term treatment with BCH lowers blood glucose and improves β-cell integrity in db/db mice. We evaluated GSIS, insulin gene expression, and DNA fragmentation in INS-1 cells exposed to HG or HG/PA in the presence or absence of BCH. An in vivo study was performed in which 7-week-old diabetic db/db mice were treated with BCH (0.7 g/kg, n = 10) and placebo (n = 10) every other day for 6 weeks. After treatment, an intraperitoneal glucose tolerance test and immunohistological examinations were performed. Treatment with BCH blocked HG-induced GSIS inhibition and the HG/PA-induced reduction in insulin gene expression in INS-1 cells. In addition, BCH significantly reduced HG/PA-induced INS-1 cell death and phospho-JNK level. BCH treatment improved glucose tolerance and insulin secretion in db/db mice. BCH treatment also increased the ratio of insulin-positive β-cells to total islet area (P < 0.05) and reduced the percentage of β-cells expressing cleaved caspase 3 (P < 0.05). In conclusion, the GDH activator BCH improved glycemic control in db/db mice. This anti-diabetic effect may be associated with improved insulin secretion, preserved islet architecture, and reduced β-cell apoptosis. | - |
dc.description.statementOfResponsibility | open | - |
dc.format | application/pdf | - |
dc.relation.isPartOf | JOURNAL OF ENDOCRINOLOGY | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Amino Acids, Cyclic/pharmacology* | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Apoptosis/drug effects | - |
dc.subject.MESH | Blood Glucose/analysis | - |
dc.subject.MESH | Cell Line, Tumor | - |
dc.subject.MESH | Diabetes Mellitus/drug therapy | - |
dc.subject.MESH | Diabetes Mellitus/physiopathology* | - |
dc.subject.MESH | Drug Synergism | - |
dc.subject.MESH | Enzyme Activation/drug effects | - |
dc.subject.MESH | Gene Expression/drug effects | - |
dc.subject.MESH | Glucose/pharmacology | - |
dc.subject.MESH | Glutamate Dehydrogenase/physiology* | - |
dc.subject.MESH | Insulin/blood | - |
dc.subject.MESH | Insulin/genetics | - |
dc.subject.MESH | Insulin/secretion | - |
dc.subject.MESH | Insulin-Secreting Cells/drug effects* | - |
dc.subject.MESH | Insulin-Secreting Cells/physiology* | - |
dc.subject.MESH | Insulinoma | - |
dc.subject.MESH | Mice | - |
dc.subject.MESH | Pancreatic Neoplasms | - |
dc.subject.MESH | Rats | - |
dc.title | β-Cell-protective effect of 2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid as a glutamate dehydrogenase activator in db/db mice | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Internal Medicine (내과학) | - |
dc.contributor.googleauthor | Seung Jin Han | - |
dc.contributor.googleauthor | Sung-E Choi | - |
dc.contributor.googleauthor | Sang-A Yi | - |
dc.contributor.googleauthor | Soo-Jin Lee | - |
dc.contributor.googleauthor | Hae Jin Kim | - |
dc.contributor.googleauthor | Dae Jung Kim | - |
dc.contributor.googleauthor | Hyun Chul Lee | - |
dc.contributor.googleauthor | Kwan Woo Lee | - |
dc.contributor.googleauthor | Yup Kang | - |
dc.identifier.doi | 10.1530/JOE-11-0340 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A03301 | - |
dc.contributor.localId | A04302 | - |
dc.relation.journalcode | J01392 | - |
dc.identifier.eissn | 1479-6805 | - |
dc.identifier.pmid | 22131441 | - |
dc.contributor.alternativeName | Lee, Hyun Chul | - |
dc.contributor.alternativeName | Han, Seung Jin | - |
dc.contributor.affiliatedAuthor | Lee, Hyun Chul | - |
dc.contributor.affiliatedAuthor | Han, Seung Jin | - |
dc.citation.volume | 212 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 307 | - |
dc.citation.endPage | 315 | - |
dc.identifier.bibliographicCitation | JOURNAL OF ENDOCRINOLOGY, Vol.212(3) : 307-315, 2012 | - |
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