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タイトル: | Oral Administration of Apple Procyanidins Ameliorates Insulin Resistance via Suppression of Pro-inflammatory Cytokines Expression in Liver of Diabetic ob/ob Mice |
著者: | Ogura, Kasane Ogura, Masahito https://orcid.org/0000-0002-7107-2752 (unconfirmed) Shoji, Toshihiko Sato, Yuichi Tahara, Yumiko Yamano, Gen Sato, Hiroki Sugizaki, Kazu Fujita, Naotaka Tatsuoka, Hisato https://orcid.org/0000-0002-0669-6825 (unconfirmed) Usui, Ryota https://orcid.org/0000-0002-4641-0158 (unconfirmed) Mukai, Eri Fujimoto, Shimpei Inagaki, Nobuya Nagashima, Kazuaki |
著者名の別形: | 長嶋, 一昭 稲垣, 暢也 |
キーワード: | apple procyanidins insulin resistance inflammation ob/ob mouse |
発行日: | 23-Nov-2016 |
出版者: | American Chemical Society (ACS) |
誌名: | Journal of Agricultural and Food Chemistry |
巻: | 64 |
号: | 46 |
開始ページ: | 8857 |
終了ページ: | 8865 |
抄録: | Genetic factors are important determinants of the onset and progression of diabetes mellitus. Numerous susceptibility genes for type 2 diabetes, including potassium voltage-gated channel, KQT-like subfamily Q, member1 (KCNQ1), have been identified in humans by genome-wide analyses and other studies. Experiments with genetically modified mice have also implicated various genes in the pathogenesis of diabetes. However, the possible effects of the parent of origin for diabetes susceptibility alleles on disease onset have remained unclear. Here, we show that a mutation at the Kcnq1 locus reduces pancreatic β-cell mass in mice by epigenetic modulation only when it is inherited from the father. The noncoding RNA KCNQ1 overlapping transcript1 (Kcnq1ot1) is expressed from the Kcnq1 locus and regulates the expression of neighboring genes on the paternal allele. We found that disruption of Kcnq1 results in reduced Kcnq1ot1 expression as well as the increased expression of cyclin-dependent kinase inhibitor 1C (Cdkn1c), an imprinted gene that encodes a cell cycle inhibitor, only when the mutation is on the paternal allele. Furthermore, histone modification at the Cdkn1c promoter region in pancreatic islets was found to contribute to this phenomenon. Our observations suggest that the Kcnq1 genomic region directly regulates pancreatic β-cell mass and that genomic imprinting may be a determinant of the onset of diabetes mellitus. |
著作権等: | This document is the Accepted Manuscript version of a Published Work that appeared in final form in Journal of Agricultural and Food Chemistry, copyright © American Chemical Society after peer review and technical editing by the publisher. To access the final edited and published work see http://dx.doi.org/10.1021/acs.jafc.6b03424. The full-text file will be made open to the public on 23 Nov. 2017 in accordance with publisher's 'Terms and Conditions for Self-Archiving'. この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。 This is not the published version. Please cite only the published version. |
URI: | http://hdl.handle.net/2433/217455 |
DOI(出版社版): | 10.1021/acs.jafc.6b03424 |
PubMed ID: | 27792335 |
出現コレクション: | 学術雑誌掲載論文等 |
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