Hexane Extract of Orthosiphon stamineus Induces Insulin Expression and Prevents Glucotoxicity in INS-1 Cells.
- Author:
Hae Jung LEE
1
;
Yoon Jung CHOI
;
So Young PARK
;
Jong Yeon KIM
;
Kyu Chang WON
;
Jong Keun SON
;
Yong Woon KIM
Author Information
- Publication Type:Original Article
- Keywords: Glucose-stimulated insulin secretion, Insulin mRNA; Glucotoxicity; Orthosiphon stamineus
- MeSH: Glucose; Hyperglycemia; Insulin*; Orthosiphon*; Phosphatidylinositol 3-Kinase; Phosphatidylinositol 3-Kinases; Phosphorylation; RNA, Messenger
- From:Diabetes & Metabolism Journal 2015;39(1):51-58
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND: Hyperglycemia, a characteristic feature of diabetes, induces glucotoxicity in pancreatic beta-cells, resulting in further impairment of insulin secretion and worsening glycemic control. Thus, preservation of insulin secretory capacity is essential for the management of type 2 diabetes. In this study, we evaluated the ability of an Orthosiphon stamineus (OS) extract to prevent glucotoxicity in insulin-producing cells. METHODS: We measured insulin mRNA expression and glucose-stimulated insulin secretion (GSIS) in OS-treated INS-1 cells after exposure to a high glucose (HG; 30 mM) concentration. RESULTS: The hexane extract of OS elevated mRNA expression of insulin as well as pancreatic and duodenal homeobox-1 of INS-1 cells in a dose-dependent manner. The hexane OS extract also increased the levels of phosphorylated phosphatidylinositol 3-kinase (PI3K) in a concentration-dependent manner. Additionally, Akt phosphorylation was elevated by treatment with 100 and 200 micromol of the hexane OS extract. Three days of HG exposure suppressed insulin mRNA expression and GSIS; these expressions were restored by treatment with the hexane OS extract. HG elevated peroxide levels in the INS-1 cells. These levels were unaffected by OS treatment under both normal and hyperglycemic conditions. CONCLUSION: Our results suggested that the hexane extract of OS elevates insulin mRNA expression and prevents glucotoxicity induced by a 3-day treatment with HG. This was associated with the activation of PI-3K and Akt.
