ABSTRACT
Objective:To detect the serum levels of CTRP3 and 25(OH) D in the individuals with different glucose metablism states,and to discuss the influence factors and analyze their relationships with insulin resistance(IR).Methods:Forty-four patients newly diagnosed T2DM(T2DM group),42 patients with impaired glucose regulation(IGT group),and 54 cases of normal controls(normal control group) were selected.The serum CTRP3, FPG,HbA1c,FIns,TG,TC,HDL-C, LDL-C,FIns of the subjects in various groups were determined, respectively;the BMI,HOMA-IR,HOMA-β were calculated.Pearson correlation analysis was used to analyze the correlation between two factors and multivariate stepwise regression analysis was used to analyze the influencing factors of HOMA-IR and HOMA-β.Results:Compared with normal control group, the serum levels of HDL-C, 25(OH)D and HOMA-β of the patients in IGT group were significantly decreased (P<0.05); the levels of serum FPG, HbA1c, TG, TC, FIns and BMI, HOMA-IR of the patients in T2DM group were significantly increased (P<0.05), while the levels of serum CTRP3, HDL-C, 25(OH)D and HOMA-β were significantly decreased(P<0.05). Compared with IGT group, the levels of serum FPG, HbA1c, TG, FIns, and HOMA-IR of the patients in T2DM group were significantly increased (P<0.05), and the level of serum HDL-C and HOMA-β were significantly decreased (P<0.05).The serum CTRP3 level was negatively correlated with the levels of HbA1c, FIns and HOMA-IR (r=-0.391,P<0.05;r=-0.198,P<0.05;r=-0.481,P<0.05); the 25(OH)D level was negatively correlated with the TG, FPG levels and HOMA-IR (r=-0.209,P<0.05 r=-0.406, P<0.05;r=-0.306,P<0.05), and positively correlated with HOMA-β (r=0.329, P<0.05) in the different glucose tolerance individuals. HbA1c and CTRP3 were the independent influencing factors of HOMA-IR, and 25(OH)D, FPG and HbA1c were the independent influencing factors of HOMA-β.Conclusion:The serum CTRP3 and 25(OH)D levels are negatively correlated with IR,and they have the inhibitory effects in the occurrence and development of diabetes mellitns.
ABSTRACT
AIM:To investigate the effects of C1q/TNF related protein 3 (CTRP3) on the insulin sensitivity of insulin resistant 3T3-L1 adipocytes.METHODS: The insulin resistance model of 3T3-L1 adipocytes was induced by palmic acid cultivation.The adipocytes were treated with different concentrations of recombinant CTRP3 protein (10, 50, 250,1 250 μg/L) for 12 h, and for different times (2, 6, 12, 24 h) at the concentration of 250μg/L.The glucose con-sumption was detected by the glucose oxidase method.The glucose transport ratio was measured by 2-deoxidation-[3H]-glucose intake method.The contents of TNF-αand IL-6 in the supernatant were detected by ELISA.The mRNA expression of TNF-α, IL-6 and glucose transporter-4 (GLUT-4) was measured by real-time PCR.The protein expression of GLUT-4 was detected by Western blotting.RESULTS:Compared with normal control ( NC) group, the glucose consumption and glucose intake ratio of insulin resistance ( IR) group was decreased by 50.6%and 57.9%, respectively.Compared with IR group, with the increase in CTRP3 (10, 50, 250,1 250 μg/L) in intervention groups, the glucose consumptions were in-creased by 22.1%, 42.9%, 76.6% and 80.5%, respectively, and the glucose intake ratios were increased by 39.0%, 68.0%, 108.0%and 111.0%, respectively.With the increased duration (2, 6, 12 and 24 h) of CTRP3 treatment at the concentration of 250 μg/L, the glucose intake ratio was increased by 23.0%, 79.0%, 109.0%and 114.0%, respectively. The contents of TNF-αand IL-6 in the supernatant were decreased by 17.4%and 17.1%respectively as treated with CTRP3 at the concentration of 250 μg/L for 12 h, and the mRNA expression of TNF-αand IL-6 was decreased by 26.0% and 18.9%respectively, while the mRNA and protein expression of GLUT-4 was increased by 61.5%and 55.6%respectively. CONCLUSION:CTRP3 may increase the insulin sensitivity of insulin resistant 3T3-L1 adipocytes by down-regulating the expression of inflammatory factors, improving the insulin signal transduction and increasing the expression of GLUT-4.