| Objective To observe the influence of pioglitazone and glipizide on the platelet activation in patients with type 2 diabetes and mechanism.Methods A two-group parallel study was conducted in 80 patients with T2DM (HbA1c>7%) undergoing treatment with metformin. Patients were randomly assigned to receive add-on therapy with glipizide (Group G) or pioglitazone (Group P). Setting up healthy non-diabetic non-obese as control group (Group N). At the beginning of the study, FPG, HbA1c, TG, HDL, LDL, adiponectin, vWF, hs-CRP, MDA, HOMA-IR, markers of platelet function (platelet CD62P binding, P-selectin expression and ADP-induced platelet aggregation) were measured. In week 12, the markers of platelet function were mearsured, and compared with the results inspected in week 0 separately, as well as to make comparison between group P and group G.Results1. At the baseline, FPG, HbAlc, TG, LDL, BMI, HOMA-IR, vWF, MDA, hsCRP in DM group (group G and group P) were higher than those in Group N (P<0.01). HDL, adiponectin were lower than those in Group N (P<0.01). Markers of platelet function (platelet CD62P binding, P-selectin expression and ADP-induced platelet aggregation) in DM group were higher than those in Group N (P<0.01).2. At the baseline, there were no significant differences in baseline characteristics (FPG, HbAlc, TG, HDL, LDL, BMI, HOMA-IR, vWF, MDA, hsCRP, adiponectin) between Group P and Group G (P>0.05).3. At the baseline, there were no significant differences in markers of platelet function (platelet CD62P binding, P-selectin expression and ADP-induced platelet aggregation) between Group P and Group G (P>0.05).4. After 12 weeks, compared with the baseline, platelet CD62P binding, P-selectin expression and ADP-induced platelet aggregation in Group G were lower (P<0.01) BMI was higher(P<0.01), FBG, HbA1c, HOMA-IR, LDL, TG were lower (P<0.01), no significant changes were observed in SBP, DBP, HDL, adiponectin, hsCRP, MDA, vWF (P>0.05).5. Correlation analysis showed that ADP-induced platelet aggregation in Group G was positively correlated with FBG (r=0.569, P<0.01), HbAlc (r=0.534, P<0.01) and HOMA-IR (r=0.531, P<0.01)6. After 12 weeks, compared with the baseline, platelet CD62P binding, P-selectin expression and ADP-induced platelet aggregation in Group P were lower (P<0.01) HDL, adiponectin were higher (P<0.01), FBG, HbA1C, HOMA-IR, LDL, TG, DBP, hsCRP, MDA, vWF were lower (P<0.01), no significant changes were observed in SBP, BMI (P>0.05).7. Correlation analysis showed that ADP-induced platelet aggregation in Group P was positively correlated with FBG (r=0.449, P<0.01), HbAlc (r=0.432, P<0.01), HOMA-IR (r=0.725, P<0.01),DBP (r=0.301, P<0.05),TG (r=0.527, P<0.01), vWF (r=0.682, P<0.01),hsCRP (r=0.642, P<0.01),MDA (r=0.693, P<0.01), and was negatively correlated with adiponectin (r=-0.402, P<0.01)8. After 12 weeks, FPG, HbA1C, and adiponectin in Group P were higher than those in Group G (P<0.01), HOMA-IR, vWF, MDA, hsCRP were lower than in Group G (P<0.01), no significant differences were observed in BMI, SBP, DBP, HDL-C (P>0.05).9. After 12 weeks, platelet CD62P binding, P-selectin expression and ADP-induced platelet aggregation in Group G were higher than those in Group P ((P<0.01).Conclusion The platelet activation in patients with T2DM was enhanced. Glipizide and pioglitazone can reduce the platelet activation in patients with T2DM while lowering blood glucose. Add-on therapy with pioglitazone may be more effective than glipizide for inhibiting platelet activation. Pioglitazone may have the effect of inhibiting platelet activation independent of lowering blood glucose. It may be concerned with improving insulin resistance, reducing oxidative stress, anti-inflammation, improving endothelial function.Objective To observe the effects of pioglitazone and glipizide on platelet aggregation in vitro.Methods The study was conducted in 60 healthy non-obese people in our hospital medical center. Each blood specimen was divided into 7 copies. The first was in the natural condition (Group N), the second was incubated with 2 umol/L pioglitazone for 30 minutes (Group P2), the third was incubated with 10 umol/L pioglitazone for 30 minutes (Group P10), the fourth was incubated with 2 umol/L glipizide for 30 minutes (Group G2), the fifth was incubated with 10umol/L glipizide for 30 minutes (Group G10), the sixth was incubated with 20umol/L nitroglycerin for 3 minutes (Group N20), the seventh was incubated with 40umol/L nitroglycerin for 3 minutes (Group N40), The platelet aggregation induced by ADP was compared.Results1. Nitroglycerin inhibited the platelet aggregation induced by ADP of healthy people in vitro with concentration dependence. (P< 0.01).2. There was no significant difference of the platelet aggregation induced by ADP between Group P2 and Group N (P>0.05). There was no significant difference of the platelet aggregation induced by ADP between Group P10 and Group N (P>0.05). There was no significant difference of the platelet aggregation induced by ADP between Group P2 and Group P10 (P>0.05)3. There was no significant difference of the platelet aggregation induced by ADP between Group G2 and Group N (P>0.05). There was no significant difference of the platelet aggregation induced by ADP between Group G10 and Group N (P>0.05). There was no significant difference of the platelet aggregation induced by ADP between Group G2 and Group G10 (P>0.05)Conclusion The pioglitazone and glipizide did not show a direct inhibitory effect on platelet aggregation in vitro. |
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