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Title: | Purple Rice Bran Improves Hepatic Insulin Signaling via Activation of Akt and Stabilization of IGF in Diabetic Rats |
Authors: | Ei Ei Hlaing Supicha Rungcharoenarrichit Narissara Lailerd Sittiruk Roytrakul Pichapat Piamrojanaphat |
Authors: | Ei Ei Hlaing Supicha Rungcharoenarrichit Narissara Lailerd Sittiruk Roytrakul Pichapat Piamrojanaphat |
Keywords: | Agricultural and Biological Sciences;Biochemistry, Genetics and Molecular Biology |
Issue Date: | 16-Jan-2019 |
Abstract: | © 2019 Elsevier Inc. All rights reserved. Hepatic insulin resistance is common in diabetic patients. Purple rice was proved to have antidiabetic activity. The underlying molecular mechanisms of antidiabetic activity of purple rice still need to be explored. Therefore, this study analyzed the proteomic profiling of the liver tissue of type 2 diabetes rats with or without purple rice bran supplement. From the hepatic protein profiling, around 2669 peptides were identified. Protein-chemical interaction and protein-protein interaction was done by using STITCH and STRING, respectively. Interestingly, polypeptide N-acetylgalactosaminyltransferase 5 (Galnt5), insulin-like growth factor-binding protein 4 precursor (Igfbp4), kinesin light chain 3 (Klc 3), KH-type splicing regulatory protein isoform CRA_b (Khsrp), aurora kinase A-interacting protein (Aurkip 1), and calmodulin-regulated spectrin-associated protein 3 (Camsap3) which expressed only in the liver of diabetic rats with purple rice bran supplement showed interaction with the other proteins involving insulin signaling. The levels of gene expression in glucose 6 phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK) were suppressed while in protein kinase B (Akt) was activated in diabetic rats supplemented with purple rice bran. In addition, glucose transporter 2 (Glut 2) proteins and phosphorylated Akt (p-Akt) protein expression were increased with purple rice bran supplement. By combination of these data, purple rice bran could promote hepatic glucose uptake and increase insulin sensitivity while hepatic gluconeogenesis was inhibited. |
URI: | https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85081529810&origin=inward http://cmuir.cmu.ac.th/jspui/handle/6653943832/67534 |
Appears in Collections: | CMUL: Journal Articles |
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