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KMID : 1161420150180010076
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Journal of Medicinal Food
2015 Volume.18 No. 1 p.76 ~ p.82
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p-Synephrine Suppresses Glucose Production but Not Lipid Accumulation in H4IIE Liver Cells
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Cui Zhigang
Lee Young-Il
Lee Young-Ki
Park Deok-Bae
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Abstract
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p-Synephrine, the primary protoalkaloid in the extract of bitter orange and other citrus species, has gained interest due to its lipolytic activity in adipose tissues. We previously found that p-synephrine stimulates glucose consumption via AMP-activated protein kinase (AMPK) in L6 skeletal muscle cells. This study investigated the effect of p-synephrine on glucose production and lipid accumulation in H4IIE rat liver cells. Glucose production was increased in H4llE cells that were incubated in glucose-free medium but decreased dose dependently (1?100 μM) with p-synephrine treatment. Protein levels of glucose-6-phosphatase (G6Pase) and phosphoenol pyruvate carboxykinase (PEPCK) were also decreased by treatment (4?h) with p-synephrine. Antagonists against α- and β-adrenergic receptors (phentolamine and propranolol) and other inhibitors against signaling molecules did not interrupt p-synephrine-induced suppression in glucose production. However, H7 (an inhibitor of serine/threonine kinases PKA, PKC, and PKG) significantly blocked p-synephrine-induced suppression of glucose production and further increased basal glucose production. Unlike the suppressive effect on glucose production, p-synephrine failed to affect palmitic acid-induced cytoplasmic lipid accumulation. Protein levels of fatty acid synthase (FAS) and phosphorylation levels of AMPK and ACC were not changed by p-synephrine. Altogether, p-synephrine can suppress glucose production but does not affect lipid accumulation in H4IIE liver cells.
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KEYWORD
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glucose production, H4IIE liver cells, lipid accumulation, p-synephrine
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