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Objective The study the effect on cardiac remodeling induced by low level adiponectin(APN)and insulin resistance(IR).Methods 16 wild-type C57 mice were randomly divided into control and IR groups.16 APN gene knockout mice were randomly divided into APNKO and APNKO+IR groups.The IR and APNKO+IR groups were a high-fat feed to induce insulin resistance.After 12 weeks,cholesterol(TC),triglycerides(TG),fasting plasma glucose(FPG), fasting insulin(FINS) were measured.HOMA-IR,HWI and LVWI were calculated.The left ventricular myocardial were examined by microscopy to observe the degree of myocardial fibrosis,and the protein expression of matrix metalloproteinase-9(MMP-9) and APN in myocardial were detected with western blot.ResultsLow level APN and IR increased heart weight, left ventricular weight, HWI, LVWI(P<0.05).There were interaction between IR and low level APN on the TC,TG, FPG, FINS, and the index related myocardial fibrosis(P<0.05), and they were positive effect.There was also interaction effect between IR and low level APN on myocardial APN expression, but it was the negative effects (P<0.05).Conclusions Both low level adiponectin and insulin resistance could lead to cardiac remodeling synergistically.
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Objective: To explore the impact of insulin resistance (IR) and adiponectin (APN) lacking on myocardial remodeling in experimental mice. Methods:16 normal C57 mice were divided into 2 groups: Control group and IR group; in addition, 16 APN gene knockout(APNKO) mice were divided into another 2 groups: APNKO group and APNKO+IR group.n=8 in each group. The mice in Control group and APNKO group were fed with normal diet, in IR group and APNKO+IR group were fed with high fat diet to create the IR model. All animals were treated for 12 weeks. Blood levels of total cholesterol(TC), triglycerides(TG),fasting plasma glucose(FPG) and fasting insulin(FINS) were examined; heart weight and left ventricular weight were measured; left ventricular myocardial morphological changes and the degree of ifbrosis were assessed by HE staining and Masson staining; protein expressions of myocardial matrix metalloproteinase-9 (MMP-9) and APN were detected by immunehistochemistry and Western blot analysis. Results: Compared with Control group, IR group, APNKO group and APNKO+IR group showed elevated blood levels of TC, TG, FPG and FINS; increased heart weight and left ventricular weight, allP<0.05; IR group, APNKO group and APNKO+IR group presented more myocardial hypertrophy, decreased protein expression of APN and increased protein expression of MMP-9, allP<0.05.Conclusion: IR and APN lacking could incur myocardial remodeling in experimental mice and they had synergistically facilitated effect.
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Objective To investigate the association of serum adiponectin and tumor necrosis factor alpha (TNF-α) with endothelial damages in metabolic syndrome (MS) patients. Methods One-hundred and five patients diagnosed as MS were recruited as cases and 37 subjects without characteristics of MS were recruited as controls. The cases were divided into two groups according to the level of serum von Willebrand factor (vWF) :normal endo-thelial functional MS group (57 patients) and abnormal endothelial functional MS group (48 patients). Serum adi-ponectin concentration was measured by enzyme-linked immanosorbont assay (ELISA). Serum TNF-α concentration was measured by radioimmunoassay (RIA). Results The concentration of serum adiponectin in normal subjects (10.5 mg/L [SD:3.2]) was significantly higher than both that of normal endothelial functional MS group (7.9 mg/L [SD :2.2]) and abnormal endothelial functional MS group (6.5 μg/L [SD :2.5]) (P < 0.05). The concen-tration of serum TNF-α in normal subjects(0.17 μg/L [SD :0.04]) were significantly lower than that of normal en-dothelial functional MS group (0.19 μg/L [SD:0.05]) and abnormal endothelial functional MS group (0.23 ng/mi [SD: 0.06]) (P< 0.05). The level of serum adiponectin were negatively correlated with TNF-α(r=- 0.555, P < 0.01). Logistic regression analysis results showed that high level of TNF-α was a risk factor of endo-thelial damages (OR = 20.649, P = 0.035), whereas high level of serum adiponectin protected against endothelial damages (OR = 0.340,P=0.006). Conclusions Low level of serum adiponectin and high level of serum TNF-α may correlate with endothelial damages in MS patients.
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Objective To detect the mechanism of serum uric acid (UA) in different types of coronary heart disease (CHD).Methods 88 patients were divided into three groups：the control group，stable angina (SA) group and acute coronary syndrom (ACS) group.The levels of UA，alpha-granule membrane protein 140 (GMP-140)，von Willebrand factor(vWF)，plasminogen activator inhabitor typed (PAI-1)，Thromboxane B_2 (TXB_2) and C-reacting protein(CRP) were measured.Results ①UA and CRP in ACS group were higher than that in SA group and control group [(392.1±68.57) μmol/L and (42.2±39.4) mg/L vs (370.50±58.80) μmol/L and (18.9±17.1) mg/L vs (286.00±65.31) μmol/L and (2.5±0.7) mg/L，P＜0.05)].For UA，there was no difference between ACS and SA group(P＞0.05)；CRP was higher in ACS group than in SA group (P＜0.05).②vWF and TXB_2 were higher in ACS[(1.65±0.48)%，(19.73±18.66)ng/L]and SA group[(1.35±0.49)%，(11.18±10.71) ng/L]than in control group[(1.07±0.26)%，(6.46±5.41) ng/L，P＜0.05]，and those were higher in ACS group than in SA group (P＜0.05).③GMP-140 and PAI-1 were higher in ACS [(13.04±0.99) μg/L and (65.65±14.76) μg/L]and SA group[(12.55±0.74) μg/L and (62.69±12.24) μg/L]than in control group [(12.32±0.29) μg/L，(50.78±13.88) μg/L，P＜0.05].There were no differences between ACS and SA group (P＞0.05).④Comparing hyperuricemia group and non-hyperuricemia group in CHD patients：the CRP(71.3±18.9) mg/L，vWF(1.08±0.52) %，GMP-140(13.57±1.11) μg/L，TXB_2 (57.26±47.84)ng/L，PAI-1 (72.12±9.23) μg/L in ACS group possessing hyperuricemia were higher than non-hyperuricemia group [CRP (20.7±17.9) mg/L，vWF (0.84±0.54) %，GMP-140 (13.23±1.07) μg/L，TXB_2 (26.70 + 23.83) ng/L，PAI-1 (61.30±12.07) μg/L](t=7.394，0.008，0.227，7.605，0.421，P＜0.05)；CRP(31.1±18.9)mg/L and TXB2 (21.54±3.90) ng/L in SA group possessing hyperuricemia group were higher than non-hyperuricemia group[(10.9±10.1)mg/L and (5.02±4.93) ng/L，t=0.494，8.669，P＜0.05].Logistic stepwise regression analysis indicated that the related factors with ACS were UA(OR=1.046)，CRP(OR=7.615)，PAI-1(OR=1.301)，PT(OR=0.300)and TG(OR=2.243) (P＜0.05).Conclusions UA is an important risk factor in CHD patients.UA can induce different types of CHD by damaging blood vessel endothelium function，activating platelet，changing coagulation and causing inflammatory.
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Objective To study the distribution of As and other trace elements in drinking water,grain and soil of arsenism disease area in Tumotezuoqi of Inner-Mongloia and to provide theoretical bases for the prevention and treatment of endemic arsenism and improving water quality.Methods The concentrations of As and other trace elements in well-water,wheat,corn,sorghum and soil were determined using neutron activation analysis.Results The result showed that the arsenic contents in drinking water of Tumotezuoqi were from139to899?g /L,which were much higher than that of the allowance limit(