Estrogens induce visfatin expression in 3T3-L1 cells.
Visfatin is a 56 kDa protein that is overexpressed in pregnant women. Like insulin, 2 nM visfatin induced GLUT 4 translocation from the cytosolic fraction to the membrane in 3T3-L1 cells. We have previously reported that visfatin induces glucose uptake into 3T3-L1 cells. These two actions define visfatin as an insulinomimetic. Three estrogens are elevated in pregnancy. Estradiol, the predominant estrogen, estriol, produced by the fetal liver and the pro-estrogen progesterone are all higher during pregnancy than in nonparous women. 3T3-L1 cells were treated with 150 ng/ml estriol, 16 ng/ml estradiol or 190 ng/ml progesterone to reflect the circulating concentrations of these steroids during pregnancy. Estriol treatment produced a 2.5-fold increase in visfatin gene expression. Estradiol and progesterone had small but insignificant effects on visfatin gene expression. In a second experiment, cells were treated with a combination of all three steroids together at the same concentrations listed above. The combination treatment produced a 13-fold increase in visfatin gene expression. These data suggest that the estriol, estradiol and progesterone exert a synergistic effect on visfatin gene expression. Taken together these data suggest that visfatin may play a physiological role during pregnancy. Since visfatin potently and efficaciously induced GLUT 4 translocation in a cell culture model, any hypothetical role for visfatin in pregnancy should include the possibility that it may play a role in maternal/fetal glucose metabolism or distribution. Two possibilities present: either maternal visfatin is overexpressed as a protective response in the pregnant female to compensate for the insulin resistance that often accompanies pregnancy or the excess visfatin is a compensatory response to ensure adequate glucose delivery to the growing fetus.
Zhou
Jingyu
J
Department of Physiology, Brody School of Medicine at East Carolina University, Greenville, NC 27858, USA.
Seidel
Edward R
ER
D041721:3T3-L1 Cells; D000818:Animals; D002462:Cell Membrane / Q000378:metabolism; D016207:Cytokines / Q000235:genetics* / Q000494:pharmacology; D003593:Cytoplasm / Q000378:metabolism; D004958:Estradiol / Q000494:pharmacology; D004964:Estriol / Q000494:pharmacology; D004967:Estrogens / Q000494:pharmacology*; D005260:Female; D015870:Gene Expression / Q000187:drug effects / Q000235:genetics*; D005786:Gene Expression Regulation / Q000502:physiology; D051275:Glucose Transporter Type 4 / Q000378:metabolism; D007328:Insulin / Q000494:pharmacology; D051379:Mice; D054409:Nicotinamide Phosphoribosyltransferase / Q000235:genetics* / Q000494:pharmacology; D011247:Pregnancy; D011374:Progesterone / Q000494:pharmacology
D016207:Cytokines; D004967:Estrogens; D051275:Glucose Transporter Type 4; D007328:Insulin; C495693:Slc2a4 protein, mouse; D011374:Progesterone; D004958:Estradiol; D054409:Nicotinamide Phosphoribosyltransferase; C495867:nicotinamide phosphoribosyltransferase, mouse; D004964:Estriol