Relationship between uric acid and arterial stiffness in the elderly with metabolic syndrome components / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>High uric acid (UA) levels and metabolic syndrome (MS) are risk factors for atherosclerotic diseases. Brachial-ankle pulse wave velocity (baPWV) is a valid and reproducible measurement by which to assess arterial stiffness and a surrogate marker of atherosclerosis. However, little is known about the relationship between them, especially in elderly Chinese with MS components who are at high risk for atherosclerotic diseases.</p><p><b>METHODS</b>One thousand and twenty Chinese subjects (159 women) older than 60 years of age (mean age (70.6 ± 5.7) years) with at least one MS component underwent routine laboratory tests, and baPWV measurements were analyzed.</p><p><b>RESULTS</b>Participants were divided into four groups by MS components. The mean age did not significantly differ among the MS component groups. We found that not only the diagnostic factors (blood pressure, body mass index (BMI), lipids, glucose) of MS but also baPWV, UA, insulin, homeostasis model of assessment for insulin resistence index (HOMAIR) levels increased, and high density lipoprotein (HDL)-C decreased with an increased number of MS components (test for trend P < 0.05). The association between UA and baPWV was observed after adjustment for gender, age, blood pressure, BMI, serum creatinine and high density lipoprotein, and insulin resistance (r = 0.186, P < 0.0001). There were increases in the odds ratios for the association between the number of components of MS, UA and baPWV, even after adjustment for traditional risk factors. However, after adjustment for insulin or HOMA-IR, there were no significant differences in the multivariate odds ratios among the number of MS components for UA.</p><p><b>CONCLUSIONS</b>The UA level is positively associated with baPWV and MS, but the association between UA and MS is dependent on insulin resistance. Furthermore, baPWV is independently associated with MS in our study population.</p>

Sleep apnea hypopnea syndrome and liver injury / 中华医学杂志(英文版)

<p><b>OBJECTIVE</b>A general review was made of studies involving: (1) the relationship between sleep apnea hypopnea syndrome/sleep apnea style intermittent hypoxia and liver injury and (2) the mechanism that causes the liver injury.</p><p><b>DATA SOURCES</b>The data used in this review were mainly from Medline and PubMed published in English from 1993 to February 2009. The search term was "sleep apnea hypopnea syndrome".</p><p><b>STUDY SELECTION</b>(1) Clinical and laboratory evidence that sleep apnea hypopnea syndrome and sleep apnea style intermittent hypoxia leads to liver injury; (2) the mechanism that causes the liver injury.</p><p><b>RESULTS</b>The effect of sleep apnea hypopnea syndrome and sleep apnea style intermittent hypoxia on the liver function is characterized by serum aminotransferase elevation. The liver histological injury includes hepatic steatosis, hepatocyte ballooning, lobular inflammation, lobular necrosis, and liver fibrosis. Sleep apnea hypopnea syndrome and sleep apnea style intermittent hypoxia can cause insulin resistance and oxidative stress.</p><p><b>CONCLUSIONS</b>Sleep apnea hypopnea syndrome and sleep apnea style intermittent hypoxia can lead to chronic liver injury, which, in most cases, is shown as nonalcoholic fatty liver disease. Insulin resistance and oxidative stress caused by sleep apnea hypopnea syndrome and sleep apnea style intermittent hypoxia play an important role in the mechanism of chronic liver disease development.</p>

Effects of high-fat plus ethanol diet on myocardial ultrastructure in rats / 中华预防医学杂志

<p><b>OBJECTIVE</b>To study the effects of high-fat plus ethanol diet on myocardial ultrastructure in rats.</p><p><b>METHODS</b>40 male SD rats in seventy-eight-week old were randomly divided into four groups: group A was control group, fed with common feedstuff; group B was high-fat diet group, freely foraging high-fat feedstuff; group C was ethanol group, the rats were intragastrically administered 60% ethanol solution twice a day by 1 ml/kg; group D was high-fat diet and ethanol group, the rats freely foraged high-fat feedstuff, and ethanol solution was intragastrically administered as before. After 12 weeks, blood samples were taken through jugular vein, the concentration of blood cholesterol (TG), triglycerides (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL), apolipoprotein A1 (Apo-A1), apolipoprotein B (Apo-B), and alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBIL) were determined. The cardiac index was also determined for all groups and the cardiac morphous were observed by high resolution Doppler ultrasound, and myocardial ultrastructure was observed by transmission electron microscope.</p><p><b>RESULTS</b>After experiment, TG levels of groups A, B, C, D were (1.07 +/- 0.21), (2.34 +/- 0.72), (1.33 +/- 0.42) and (1.75 +/- 0.65) mmol/L, respectively (F = 8.323, P = 0.000); TC levels were (1.74 +/- 0.38), (5.66 +/- 1.74), (1.70 +/- 0.44) and (5.65 +/- 2.95) mmol/L, respectively (F = 13.670, P = 0.000); HDL levels were (0.65 +/- 0.11), (2.99 +/- 0.54), (0.52 +/- 0.13) and (2.06 +/- 0.26) mmol/L, respectively (F = 112.225, P = 0.000); LDL levels were (0.74 +/- 0.22), (1.87 +/- 0.90), (0.60 +/- 0.26) and (1.54 +/- 0.78) mmol/L, respectively (F = 7.318, P = 0.001); Apo-A1 levels were (0.25 +/- 0.10), (0.31 +/- 0.14), (0.21 +/- 0.05) and (0.36 +/- 0.11) g/L, respectively (F = 3.015, P = 0.047); Apo-B levels were (0.18 +/- 0.03), (0.11 +/- 0.04), (0.16 +/- 0.03) and (0.39 +/- 0.13) g/L, respectively (F = 15.621, P = 0.000); ALT levels were (111.25 +/- 20.18), (447.13 +/- 89.25), (173.13 +/- 44.01) and (198.25 +/- 39.81) U/L, respectively (F = 58.708, P = 0.000); AST levels were (105.50 +/- 9.99), (483.00 +/- 16.80), (120.75 +/- 5.09) and (276.88 +/- 10.48) U/L, respectively (F = 1906.624, P = 0.000);TBIL levels were (1.35 +/- 0.12), (1.66 +/- 0.18), (1.89 +/- 0.15) and (2.68 +/- 0.35)U/L, respectively (F = 55.006, P = 0.000); cardiac indexes were (3.02 +/- 0.22)%, (3.21 +/- 0.16)%, (3.26 +/- 0.26)% and (3.43 +/- 0.27)%, respectively (F = 16.150, P = 0.000). There were changes of cardiac morphous in group C and D, but not in group A and B; the myocardial ultrastructure was normal in Group A, but light to heavy changes were found in group B, C and D.</p><p><b>CONCLUSION</b>High-fat diet and excessive intake of ethanol significantly induce abnormal lipid metabolism. High-fat diet induces the changes of myocardial ultrastructure before cardiac morphous and electrocardiogram, and intake of ethanol changes cardiac muscle in microstructure and macroscopy. High-fat diet plus ethanol may worsen this injury farther.</p>