RESUMEN
ObjectiveTo investigate the effects of mefformin on the levels of serum retinol-binding protein 4 (RBP-4),high sensitive C reactive protein (hs-CRP) and tumor necrosis factorα (TNF-α) in patients with impaired glucose tolerance(IGT) and metabolic syndrome(MS). MethodsSixty patients with IGT and MS were divided into mefformin treatment group (30 cases) and life-style intervention group (30 cases) by random digits table. Body mass index (BMI),the levels of HbAic, HOMA-IR, blood fat, RBP-4,hs-CRP, TNF- α were measured both before and 16 weeks after treatment in the two groups and compared.ResultsThe levels of HbA1c, HOMA-IR, RBP-4, hs-CRP and TNF- α were significantly lower in mefformin treatment group than those in life-style intervention group [(5.09 + 0.26 )％ vs. (5.69 ± 0.49 )％, 2.95 ± 0.63vs. 3.49 ± 0.78, ( 18.69 ± 6.50) mg/L vs.(26.20 ± 6.97) mg/L, (2.37 ± 0.53) mg/L vs.(2.99 ± 0.57) mg/L,(9.49 ± 2.37) μ g/L vs. ( 14.33 ± 2.62) μ g/L] (P ＜ 0.01 ). The results of multiple linear regression showed that correlations were found between the changes of RBP-4 and BMI,HOMA-IR,hs-CRP,TNF-α(β =0.284,0.506,0.274,0.230,P ＜0.01 ),and HOMA-IR was the most important limiting factor. Conclusions Mefformin can improve insulin sensitivity of the patients with IGT and MS, and depress the levels of RBP-4,hs-CRP and TNF- α. Meanwhile mefformin has anti-inflammatory effect.
RESUMEN
The purpose of this study was to clarify the characteristics of the pacemaker cells in the left ventricular outflow tract (aortic vestibule) and compare them with those of the cells in the sinoatrial node (SAN). By using conventional intracellular microelectrode technique to record their action potentials, some ionic channel blockers were used to observe their electrophysiological effects on the two types of pacemaker cells in the rabbit, especially on the ionic movement during phase 0 and phase 4. The results obtained are as follows. (1) Perfusion with 1 micromol/L verapamil (VER) resulted in a significant reduction in the amplitude of action potential (APA), maximal rate of depolarization (V(max)), absolute value of the maximal diastolic potential (MDP), velocity of diastolic depolarization (VDD) and rate of pacemaker firing (RPF), and also a prolongation of the 90% of the duration of action potential (APD(90)) in the pacemaker cells of the SAN and aortic vestibule (P<0.05). (2) Perfusion with 180 micromol/L nickel chloride (NiCl2) resulted in a decrease in VDD in the two types of the pacemaker cells (P<0.01). APA, V(max) and RPF fell notably, and the APD(90) prolonged in the sinoatrial node cells (P<0.05). (3) 2 mmol/L 4-aminopyridine (4-AP) led to a increase in VDD in both types of pacemaker cells (P<0.01). At the same time the absolute values of MDP, APA and V(max) decreased significantly, and APD(90) prolonged notably (P<0.05). During the perfusion, RPF in SAN increased markedly, while RPF in aortic vestibule exhibited no significant change. (4) 2 mmol/L cesium chloride (CsCl) led to a decrease in VDD and RPF in the two types of the pacemaker cells (P<0.05).These results suggested: (1) the ion currents in phase 0 and phase 4 of depolarization and repolarization of slow-response activity in aortic vestibule are similar to those in dominant pacemaker cells of sinoatrial node; (2) for the pacemaker cells in the left ventricular outflow tract, Ca(2+) current is the main depolarizing ion current of the phase 0, K(+) current is the main factor responsible for the repolarization. Attenuation of K(+) current is responsible for the phase 4 spontaneous depolarization. In addition, it seems that I(Ca-T), I(Ca-L) and I(f ) play some role in the pacemaker currents.