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Cited 30 time in webofscience Cited 31 time in scopus
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Pterocarpan-Enriched Soy Leaf Extract Ameliorates Insulin Sensitivity and Pancreatic beta-Cell Proliferation in Type 2 Diabetic Miceopen access

Authors
Kim, Un-HeeYoon, Jeong-HyunLi, HuaKang, Ji-HyunJi, Hyeon-SeonPark, Ki HunShin, Dong-HaPark, Ho-YongJeong, Tae-Sook
Issue Date
Nov-2014
Publisher
MDPI
Keywords
Glycine max; insulin sensitivity; pancreas; pterocarpans; type 2 diabetes
Citation
MOLECULES, v.19, no.11, pp 18493 - 18510
Pages
18
Indexed
SCIE
SCOPUS
Journal Title
MOLECULES
Volume
19
Number
11
Start Page
18493
End Page
18510
URI
https://scholarworks.gnu.ac.kr/handle/sw.gnu/18677
DOI
10.3390/molecules191118493
ISSN
1420-3049
1420-3049
Abstract
In Korea, soy (Glycine max (L.) Merr.) leaves are eaten as a seasonal vegetable or pickled in soy sauce. Ethyl acetate extracts of soy leaves (EASL) are enriched in pterocarpans and have potent alpha-glucosidase inhibitory activity. This study investigated the molecular mechanisms underlying the anti-diabetic effect of EASL in C57BL/6J mice with high-fat diet (HFD)-induced type 2 diabetes. Mice were randomly divided into normal diet (ND), HFD (60 kcal% fat diet), EASL (HFD with 0.56% (wt/wt) EASL), and Pinitol (HFD with 0.15% (wt/wt) pinitol) groups. Weight gain and abdominal fat accumulation were significantly suppressed by EASL. Levels of plasma glucose, HbA1c, and insulin in the EASL group were significantly lower than those of the HFD group, and the pancreatic islet of the EASL group had greater size than those of the HFD group. EASL group up-regulated neurogenin 3 (Ngn3), paired box 4 (Pax4), and v-maf musculoaponeurotic fibrosarcoma oncogene homolog A (MafA), which are markers of pancreatic cell development, as well as insulin receptor substrate 1 (IRS1), IRS2, and glucose transporter 4 (GLUT4), which are related to insulin sensitivity. Furthermore, EASL suppressed genes involved in hepatic gluconeogenesis and steatosis. These results suggest that EASL improves plasma glucose and insulin levels in mice with HDF-induced type 2 diabetes by regulating beta-cell proliferation and insulin sensitivity.
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