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  • Title: [Expression and regulation of retinol binding protein 4 mRNA in human adipose tissue in obese and type 2 diabetics].
    Author: Liu XH, Wei L, Wang LY, Zhu CY, Bao YQ, Jia WP.
    Journal: Zhonghua Yi Xue Za Zhi; 2010 May 11; 90(18):1251-4. PubMed ID: 20646597.
    Abstract:
    OBJECTIVE: To study the RBP4 mRNA expression between subcutaneous and visceral adipose tissue in obese and type 2 diabetic patients and to investigate the factors that influence RBP4 mRNA expression in Human visceral adipose tissue. METHODS: 9 individuals with normal weight normal glucose regulation subjects, 9 obesity subjects and 9 type 2 diabetes subjects were enrolled. All of the subjects were prepared to undergone an operation because of nondiabetes disease. Subcutaneous and visceral adipose tissue were taken out as soon as cultured. RT-PCR and Real-time PCR were used to assay the relative expression of RBP4 mRNA. RESULTS: RBP4 mRNA level in visceral adipose tissue of obesity group was (2.10 +/- 1.84), and that of type 2 diabetes group was (1.54 +/- 0.46), both were significantly higher than that in normal weight normal glucose group (0.75 +/- 0.28, P < 0.01, P < 0.05). RBP4 mRNA level in subcutaneous adipose tissue of the three groups were (1.05 +/- 0.15 vs 0.99 +/- 0.14 vs 1.13 +/- 0.07), no difference among them(P > 0.05). Insulin, dexamethasone, pioglitazone, free fatty acids can significantly increase RBP4 mRNA expression, compared with the control group, respectively, have an increase of 2.13 times, 0.84 times, 2.04 times, 4.88 times; however, tumor necrosis factor-alpha can significantly lower RBP4 mRNA level, compared with the control group decreased by 38%. CONCLUSION: RBP4 mRNA expression in visceral adipose tissue were significantly higher in obesity and type 2 diabetes subjects. In vitro system, RBP4 gene expression in visceral adipose tissue of normal weight normal glucose subjects was regulated by insulin, dexamethasone, pioglitazone, palmitic acid and TNF-alpha, such factors were also participated in the pathophysiological process of insulin resistance and type 2 diabetes.
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