ESPE Abstracts (2015) 84 P-2-368

Effect of Visfatin on Gene Expression of Insulin Signaling Molecules in SW872 Adipocytes

Li Ruizhen


Children’s Hospital of Wuhan City, Wuhan, Hubei, China


Background: To evaluate potential function of visfatin in SW872 adipocytes under the conditions which produce insulin resistance by free fatty acids (FFAs). Then to explore the mechanism of visfatin on the level of signal molecules.

Objective and hypotheses: To evaluate the effects of visfatin on the mRNA expressions of the insulin signal molecules including insulin receptor substrate 1 (IRS1), IRS2, and phosphatidylinositol 3 kinase (PI3K) on the states of insulin resistant in SW872 adipocytes. We hypotheses that visfatin may promote the glucose transport and play a physiological role in the insulin resistance in SW872 adipocytes by modulating the signalling molecules of IRS1, IRS2, and PI3K.

Method: Preadipocytes of the line SW872 were cultured and induced to differentiate to be mature SW872 adipocytes. Then the cells were treated with oleate at concentration of 1.0 mmol/l for 24 h to induce insulin resistance. And the cells were cultured with visfatin at concentration of 100 nmol/l for 1 h, then the mRNA was extracted. RT-PCR method was used to detect the mRNA levels of IRS1, IRS2, and PI3K.

Results: The mRNA expression levels of IRS1, IRS2, and PI3K in SW872 adipocytes were significantly increased stimulated by 100 nmol/l visfatin. Compared with control group, the mRNA levels of IRS1, IRS2, and PI3K were increased respectively by 36.54% (P<0.01), 12.81% (P<0.05), and 55.69% (P<0.01). In the insulin resistant states, after the stimulating of visfatin, the mRNA expression levels of IRS1, IRS2, and PI3K were increased by 26.98% (P<0.05), 35.59% (P<0.05), and 27.61% (P<0.01). In the insulin resistant states, compared with the control group (0 ng/ml visfatin group), the mRNA expression levels of IRS1, IRS2, and PI3K were decreased by 16.52% (P<0.05), 37.60% (P<0.05), and 31.68% (P<0.01); moreover their mRNA levels were decreased by 18.22% (P<0.01), 22.16% (P<0.05), and 33.47% (P<0.01) after the stimulating of visfatin.

Conclusion: Taken together these data suggest that visfatin may promote the glucose transport and play a physiological role in the insulin resistance in SW872 adipocytes by modulating the signalling molecules of IRS1, IRS2, and PI3K.

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