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The citrus fruit flavonoid naringenin suppresses hepatic glucose production from Fao hepatoma cells
Author(s) -
Purushotham Aparna,
Tian Min,
Belury Martha. A.
Publication year - 2009
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.200700514
Subject(s) - naringenin , flavonoid , chemistry , food science , traditional medicine , biochemistry , medicine , antioxidant
Hepatic gluconeogenesis is the major source of fasting hyperglycemia. Here, we investigated the role of the citrus fruit flavonoid naringenin, in the attenuation of hepatic glucose production from hepatoma (Fao) cells. We show that naringenin, but not its glucoside naringin, suppresses hepatic glucose production. Furthermore, unlike insulin‐mediated suppression of hepatic glucose production, incubation of hepatocytes with the phosphatidylinositol 3‐kinase (PI3‐kinase) inhibitor Ly294002 had no effect on the ability of naringenin to suppress hepatic glucose production. Further, naringenin did not increase phosphorylation of Akt at Ser473 or, Thr308, indicating this down‐stream target of PI3‐kinase is also not a player in naringenin‐mediated suppression of hepatic glucose production. Importantly, like the dimethylbiguanide, metformin, naringenin significantly decreased cellular ATP levels without increasing cell cytotoxicity. Together, these results suggest that the aglycone, naringenin, has a role in the attenuation of hyperglycemia and may exert this effect in a manner similar to the drug, metformin.