Prostaglandin F2alpha enhances glucose consumption through neither adipocyte differentiation nor GLUT1 expression in 3T3-L1 cells

被引：15

作者：

Kamon, J ^{[1
]}

Naitoh, T ^{[1
]}

Kitahara, M ^{[1
]}

Tsuruzoe, N ^{[1
]}

机构：

[1] Nissan Chem Ind, Shiraoka Res Stn Biol Sci, Minamisaitama, Saitama 3490294, Japan

来源：

CELLULAR SIGNALLING | 2001年 / 13卷 / 02期

关键词：

PGF(2)alpha; glucose uptake; glucose transporter; adipocyte differentiation; thiazolidinedione; 3T3-L1; cell;

D O I：

10.1016/S0898-6568(00)00137-6

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Arachidonic acid (AA) at 0.2 mM enhances glucose uptake through increased levels of glucose transporter (GLUT) 1 protein in 3T3-L1 adipocytes. Since AA is a precursor of prostaglandins (PGs), we investigated the effect of PGs on glucose consumption in 3T3-L1 cells. Among several PGs, only prostaglandin F(2)alpha (PGF(2)alpha) enhanced glucose consumption in 3T3-L1 cells treated with dexamethasone (DEX), 3-isobutyl-1-methyl-xanthine (IBMX), and insulin. To study the mechanism of PGF(2)alpha-enhanced glucose consumption, we investigated the effect of PGF(2)alpha on glycerol-3-phosphate dehydrogenase (GPDH) activity, triglycerides (TGs) content, and the expression of GLUT1 protein. PGF(2)alpha suppressed GPDH activity and did not increase the expression of GLUT1 protein in 3T3-L1 cells treated with DEX, IBMX, and insulin. These results suggest that PLA-stimulated glucose uptake is not through the effect of PGF(2)alpha. Our results indicate that PGF(2)alpha is a unique regulator of adipocyte differentiation (suppression) and glucose consumption (enhancement) in 3T3-L1 cells. (C) 2001 Elsevier Science Inc. All rights reserved.

引用

页码：105 / 109

页数：5

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