Wogonin ameliorates hyperglycemia and dyslipidemia via PPARα activation in db/db mice

Eun Jung Bak, Jinmoon Kim, Yun Hui Choi, Ji Hye Kim, Dong Eun Lee, Gye Hyeong Woo, Jeong Heon Cha, Yun Jung Yoo

Research output: Contribution to journalArticlepeer-review

34 Citations (Scopus)

Abstract

Background & aims: Wogonin is a flavonoid extracted from the root of Scutellaria baicalensis Gerogi. We evaluated the therapeutic effects of wogonin using db/db mice. Methods: Mice received wogonin or vehicle by oral gavage for 2 weeks. Blood glucose, insulin, and cholesterol levels were measured, and liver morphology was observed with histopathological analysis. The mRNA expression levels of PPARα, PPARγ, and adiponectin in the liver and white adipose tissue (WAT) were determined by real-time PCR. Immunoblotting for AMPK and PPARγ, and adipocyte differentiation were investigated invitro using 3T3-L1 cells. A luciferase assay was used to measure PPARα and PPARγ binding activity. Results: The wogonin group showed decreased weight gain without a change in food intake and improved glucose tolerance. Serum insulin and cholesterol levels in the wogonin group were significantly decreased compared to those in the control group. The wogonin group also showed less accumulation of lipid droplets and glycogen in the liver. PPARα and PPARγ expression levels in the liver and WAT and adiponectin expression level in WAT in the wogonin group were higher than those in the control group. In 3T3-L1 cells, wogonin was shown to stimulate AMPK activation in a dose-dependent manner. The presence of wogonin did not affect adipocyte differentiation or PPARγ protein level during adipogenesis. Notably, wogonin enhanced PPARα but not PPARγ transactivation. Conclusions: These indicate that wogonin may have beneficial effects on glucose and lipid metabolism related to enhanced PPARα and adiponectin expression via AMPK activation. Importantly, wogonin did not cause deleterious effects, such as weight gain and fatty liver. Wogonin might be a useful therapeutic agent to treat type 2 diabetes.

Original languageEnglish
Pages (from-to)156-163
Number of pages8
JournalClinical Nutrition
Volume33
Issue number1
DOIs
Publication statusPublished - 2014 Feb

Bibliographical note

Funding Information:
This research was supported by Basic Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science, and Technology (R13-2003-013-04002-0).

All Science Journal Classification (ASJC) codes

  • Nutrition and Dietetics
  • Critical Care and Intensive Care Medicine

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