Serum Uric Acid as a Predictor for the Development of Nonalcoholic Fatty Liver Disease in Apparently Healthy Subjects: A 5-Year Retrospective Cohort Study

BACKGROUND/AIMS: This study evaluated the relationship between hyperuricemia and nonalcoholic fatty liver disease (NAFLD) by comparing the incidence rates of NAFLD in relation to serum uric acid levels in apparently healthy subjects during a 5-year period. METHODS: Among 15,638 healthy Korean subjects who participated in a health-screening program in 2003 and 2008, respectively, 4954 subjects without other risk factors were enrolled in this study. We compared the incidence rates of NAFLD in 2008 with respect to baseline uric acid levels. RESULTS: In 2003, serum uric acid levels were categorized into the following quartiles: 0.6-3.9, 3.9-4.8, 4.8-5.9, and 5.9-12.6 mg/dL. The incidence of NAFLD in 2008 increased with the level of baseline uric acid (5.6%, 9.8%, 16.2%, and 20.9%, respectively; p<0.05). Multiple logistic regression analysis demonstrated that hyperuricemia was associated with the development of NAFLD. When compared to the subjects in quartile 1, the odds ratio (OR) for the incidence of NAFLD for quartiles 2, 3, and 4 were 1.53 (95% confidence interval [CI], 1.09-2.16; p=0.014], 1.69 (95% CI, 1.17-2.44; p=0.005), and 1.84 (95% CI, 1.25-2.71; p=0.002), respectively. CONCLUSIONS: High serum uric acid levels appear to be associated with an increased risk of the development of NAFLD.

Alpha-vitamin E derivative, RRR-alpha-tocopheryloxybutyric acid inhibits the proliferation of prostate cancer cells / 亚洲男科学杂志(英文版)

<p><b>AIM</b>To investigate the activity of RRR-alpha-tocopheryloxybutyric acid (TOB), an ether analog of RRR-alpha-tocopheryl succinate (VES), in prostate cancer cells.</p><p><b>METHODS</b>VES and TOB were used to treat prostate cancer LNCaP, PC3, and 22Rv1 cells and primary-cultured prostate fibroblasts. The proliferation rates were determined by MTT assay, the cell viabilities were determined by trypan blue exclusion assay, and the cell deaths were evaluated by using Cell Death Detection ELISA kit. The protein expression levels were determined by Western blot analysis.</p><p><b>RESULTS</b>The MTT growth assay demonstrated that TOB could effectively suppress the proliferation of prostate cancer cells, but not normal prostate fibroblasts. Mechanism dissections revealed that TOB reduced cell viability and induced apoptosis in prostate cancer cells similar to VES. In addition, both TOB and VES suppressed prostate-specific antigen (PSA) at the transcriptional level leading to reduced PSA protein expression. Furthermore, vitamin D receptor (VDR) expression increased after the addition of TOB.</p><p><b>CONCLUSION</b>Our data suggests that the VES derivative, TOB, is effective in inhibiting prostate cancer cell proliferation, suggesting that TOB could be used for both chemopreventive and chemotherapeutic purposes in the future.</p>

Reversal of arterial stiffness by treatment with the angiotensin receptor antagonist irbesartan in essential hypertension / 대한내과학회지

BACKGROUND: Alterations of mechanical properties in the vasculature may contribute to complications of hypertension. Since angiotensin II plays a pivotal role in these vascular abnormalities, we tested the hypothesis that the AT1 angiotensin receptor antagonist irbesartan, in contrast to the beta-blocker atenolol, would correct artery stiffness in essential hypertensive patients. METHODS: Thirty untreated essential hypertensive patients (48 +/- 7 years, range 35-65; 72% male) were randomly assigned in a single-blind fashion to irbesartan or atenolol treatment for 6 months. Fifty one age/sex-matched normotensive subjects were also studied. Systemic arterial stiffness (augmentation index; AI) was measured by the pressure transfer function using radial pulse tonometry. RESULTS: Both treatments reduced blood pressure (BP) to a comparable degree (irbesartan: 160 +/- 19/105 +/- 13 to 133 +/- 16/92 +/- 10 mmHg, p<0.01; atenolol: 166 +/- 17/113 +/- 9 to 132 +/- 15/90 +/- 8 mmHg, p<0.01). Other hemodynamic parameters of peripheral and central arteries showed similar degree of reduction, except significant reduction of central pulse pressure with irbesartan treatment (42 +/- 20 to 29 +/- 8 mmHg, p=0.01 vs 41 +/- 14 to 34 +/- 12 mmHg of atenolol treatment). After 6-month treatment, systemic arterial stiffness (AI) was significantly reduced from 28 +/- 11 to 21 +/- 11% (p=0.01) after irbesartan but atenolol treatment showed no change (from 29 +/- 8 to 29 +/- 13%). Reversal of arterial stiffness correlated mostly with reduction of central pulse pressure (r=0.63, p<0.01). CONCLUSION: The AT1 angiotensin antagonist irbesartan corrected the altered arterial stiffness from patients with essential hypertension by reduction of central pulse pressure, whereas the beta-blocker atenolol had no effect.