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Biomedical subjects

Yongsoon Park

Publications and source records attributed to Yongsoon Park.

8 recordsLinked to original sources

Central obesity as a risk factor for prostatic hyperplasia.

OBJECTIVE: Obesity-related metabolic diseases may influence prostatic hyperplasia. This study examined the impact of obesity on prostate volume in men without overt obesity-related metabolic diseases. RESEARCH METHODS AND PROCEDURES: We recruited 146 men over the age of 40 years who did not have overt obesity-related diseases, such as diabetes, impaired fasting glucose, hypertension, or dyslipidemia. Transrectal ultrasonography was performed on all subjects. The subjects were divided into three groups according to their BMI: normal (18.5 to 22.9 kg/m2), overweight (23 to 24.9 kg/m2), and obese (> or = 25 kg/m2), and two groups according to their waist circumference: normal waist (< or = 90 cm) and central obesity (> 90 cm). The classification of the subgroups was based on the Asia-Pacific criteria of obesity. We compared the prostate volume among subgroups and assessed factors related to prostatic hyperplasia. RESULTS: Mean prostate volume was 18.8 +/- 5.0, 21.8 +/- 7.2, and 21.8 +/- 5.6 mL in the normal, overweight, and obese groups, respectively, and was 20.0 +/- 5.9 and 23.7 +/- 5.3 mL in the normal waist and central obesity group, respectively. Prostate volume was significantly greater in the obese group than in the normal group (P = 0.03) and in the central obesity group compared with the normal waist group (P = 0.002). Prostate volume was positively correlated with BMI and waist circumference after adjustment for age. After adjusting for confounding factors, central obesity was an independent factor affecting prostatic hyperplasia, which was defined as a prostate volume > 20 mL (odds ratio = 3.37, p = 0.037). Relative to men with both low BMI (18.5 to 22.9 kg/m2) and normal waist circumference, those with high BMI (> or = 25 kg/m2) and central obesity were at significantly increased risk of prostatic hyperplasia (odds ratio = 4.88, p = 0.008). However, those with high BMI (> or = 25 kg/m2) and normal waist circumference were not at significantly increased risk. DISCUSSION: Prostate volume was greater in the obese and central obesity groups than in the normal group after patients with overt obesity-related metabolic diseases were excluded. Although both BMI and waist circumference were positively correlated with prostate volume, central obesity was the only independent factor affecting prostate hyperplasia. We suggest that central obesity is an important risk factor for prostatic hyperplasia.

Abdominal Fat↗

Obesity is the only independent factor associated with ultrasound-diagnosed non-alcoholic fatty liver disease: a cross-sectional case-control study.

OBJECTIVE: There is increasing interest in ultrasound-diagnosed non-alcoholic fatty liver disease (NAFLD) in the ambulatory care setting. The aim of this study was to determine the clinical and metabolic features of ultrasound-diagnosed NAFLD. MATERIAL AND METHODS: Fifty ultrasound-diagnosed NAFLD patients who had not consumed alcohol for at least the previous 3 months were matched with 100 controls by age and gender distribution. Clinical, biochemical, and nutritional variables were compared between the ultrasound-diagnosed NAFLD patients and the controls. Conditional logistic regression analyses were used to identify independent factors associated with ultrasound-diagnosed NAFLD. RESULTS: The ultrasound-diagnosed NAFLD patients had higher values on the anthropometric measurements than those of the controls. Aspartate aminotransferase (ASAT), alanine aminotransferase (ALAT), uric acid, and gamma-glutamyl transpeptidase levels were higher in the ultrasound-diagnosed NAFLD patients than those in the controls (p<0.001). The ASAT/ALAT ratio of the ultrasound-diagnosed NAFLD patients was lower than that of the controls (p<0.001). Total cholesterol, triglycerides, high-density lipoprotein (HDL)-cholesterol, non-HDL-cholesterol, atherogenic index, fasting glucose, systolic blood pressure (BP), diastolic BP, and pulse pressure were higher in the ultrasound-diagnosed NAFLD patients than in the control subjects, while lipoprotein(a) was lower. There were no significant differences in low-density lipoprotein (LDL)-cholesterol levels or nutritional intake between patients and controls. Abnormal ASAT or ALAT, hypertriglyceridemia, lower HDL-cholesterol levels, silent myocardial ischemic pattern on electrocardiogram (ECG), impaired fasting glucose, and obesity were common among the ultrasound-diagnosed NAFLD patients. The only independent factor associated with ultrasound-diagnosed NAFLD was obesity (p<0.001). CONCLUSIONS: Our data suggest that NAFLD diagnosed by ultrasound is associated with hypertriglyceridemia, impaired fasting glucose, silent myocardial ischemic pattern of ECG, obesity, and abnormal liver tests in adults. Among these factors, obesity was the only independent factor associated with ultrasound-diagnosed NAFLD.

Alanine Transaminase↗

Triacylglycerol-rich lipoprotein margination: a potential surrogate for whole-body lipoprotein lipase activity and effects of eicosapentaenoic and docosahexaenoic acids.

BACKGROUND: Margination occurs when blood borne particles attach to the vessel wall. Triacylglycerol-rich lipoprotein (TRL) particles marginate when they bind to endothelial lipoprotein lipase (LpL). OBJECTIVE: This study was undertaken to determine whether TRL margination reflects in vivo LpL activity and whether n-3 fatty acids affect fasting and fed TRL margination. DESIGN: Healthy subjects (n = 33) began with a 4-wk, placebo (olive oil; 4 g/d) run-in period and were then randomly assigned to 4 wk of treatment with 4 g/d of ethyl esters of either safflower oil (SAF; control), eicosapentaenoic acid (EPA), or docosahexaenoic acid (DHA). Margination volume (MV) was calculated by subtracting true from apparent plasma volume. RESULTS: MVs were 3 times as great during the fasting state as during the fed state (P < 0.0001). In both the fasting and the fed states, MV was significantly correlated with plasma triacylglycerol and TRL half-lives. In the fed state, MV was also correlated with preheparin LpL, whereas in the fasting state it was not. There was no significant correlation between preheparin LpL and postheparin LpL in the fasting state. Relative to SAF, EPA and DHA supplementation resulted in higher MVs by 64% and 53% (both P < 0.001), respectively, in the fasting state, without significantly reducing fasting triacylglycerol concentrations. In the fed state, DHA doubled the MV (P < 0.05), whereas EPA had no significant effect. CONCLUSIONS: The correlations between MV and TRL half-lives and preheparin LpL suggest that MV could be a reflection of whole-body LpL binding capacity. The increases in MVs with EPA and DHA supplementation suggest that these fatty acids may increase the amount of endothelial-bound LpL or its affinity for TRL.

Administration, Oral↗

Cardiovascular disease and long-chain omega-3 fatty acids.

PURPOSE OF REVIEW: Of all known dietary factors, long-chain omega-3 fatty acids may be the most protective against death from coronary heart disease. New evidence has confirmed and refined the cardioprotective role of these fatty acids. RECENT FINDINGS: Omega-3 fatty acid supplementation reduces the risk of sudden cardiac death and death from any cause within 4 months in post-myocardial infarction patients. Evidence continues to accrue for benefits in the primary prevention of coronary heart disease and stroke, and an anti-arrhythmogenic mechanism is emerging as the most likely explanation. SUMMARY: Current evidence suggests that individuals with coronary artery disease may reduce their risk of sudden cardiac death by increasing their intake of long-chain omega-3 fatty acids by approximately 1 g per day.

Cardiovascular Diseases↗

Clinical usefulness of the two-site Semmes-Weinstein monofilament test for detecting diabetic peripheral neuropathy.

The present study was done to validate the two-site Semmes-Weinstein (SW) monofilament test in identifying patients at risk of lower-extremity complications in clinical setting. The SW monofilament test and nerve conduction study were conducted on type 2 diabetic patients (n=37) at Pusan National University Hospital in Korea. As the duration of diabetes mellitus was longer, neuropathy identified by nerve conduction study and complications of diabetes were more severe (p<0.01). The number of sites unable to perceive SW monofilament (p<0.001) was larger in patients with lower-extremity neuropathy symptoms than those without symptoms. Sensitivity and specificity at two sites (the third and fifth metatarsal head sites) were 93% and 100%, respectively. In conclusion, the two-site SW monofilament test was a sensitive, specific, simple, and inexpensive screening tool for identifying diabetic peripheral neuropathy in clinical setting.

Aged↗

Omega-3 fatty acid supplementation accelerates chylomicron triglyceride clearance.

Omega-3 fatty acids (FAs) reduce postprandial triacylglycerol (TG) concentrations. This study was undertaken to determine whether this effect was due to reduced production or increased clearance of chylomicrons. Healthy subjects (n = 33) began with a 4-week, olive oil placebo (4 g/d) run-in period. After a 4-week wash-out period, subjects were randomized to supplementation with 4 g/d of ethyl esters of either safflower oil (SAF), eicosapentaenoic acid (EPA), or docosahexaenoic acid (DHA) for 4 weeks. Results for EPA and DHA were similar, and therefore the data were combined into one omega-3 FA group. Omega-3 FA supplementation reduced the postprandial TG and apolipoprotein B (apo B)-48 and apoB-100 concentrations by 16% (P = 0.08), 28% (P < 0.001), and 24% (P < 0.01), respectively. Chylomicron TG half-lives in the fed state were reduced after omega-3 FA treatment (6.0 +/- 0.5 vs. 5.1 +/- 0.4 min; P < 0.05), but not after SAF (6.9 +/- 0.7 vs. 7.1 +/- 0.7 min). Omega-3 FA supplementation decreased chylomicron particle sizes (mean diameter; 293 +/- 44 vs. 175 +/- 25 nm; P < 0.01) and increased preheparin lipoprotein lipase (LPL; 0.6 +/- 0.1 vs. 0.9 +/- 0.1 micromol/h/ml; P < 0.05) activity during the fed state, but had no effect on postheparin LPL or hepatic lipase activities. The results suggest that omega-3 FA supplementation accelerates chylomicron TG clearance by increasing LPL activity, and that EPA and DHA are equally effective.

Administration, Oral↗

EPA, but not DHA, decreases mean platelet volume in normal subjects.

The first indication of platelet activation is an increase in mean platelet volume (MPV). n-3 FA are known to inhibit platelet function and to reduce the risk for coronary heart disease. The purpose of this study was to determine the effects of EPA and DHA on MPV. Healthy subjects received olive oil placebo for 4 wk and then were randomly assigned to receive 4 g of ethyl esters of either safflower oil (n = 11), EPA (n = 10), or DHA (n = 12) for 4 wk. At the end of placebo run-in and treatment periods, MPV (fL; mean +/- SEM) and platelet count (PLT-CT; 10(3)/microL blood) were measured in the basal state and after ex vivo stimulation with collagen (10 microg/mL), cold (4 degrees C), and heat (37 degrees C). Unlike DHA, EPA lowered MPV as compared with safflower oil (7.2 +/- 0.1 vs. 7.5 +/- 0.1 fL; P < 0.05) and raised PLT-CT (211 +/- 18 vs.192 +/- 18 10(3)/microL; P < 0.05) in the fasting state. Collagen and cold significantly increased MPV whereas heat lowered MPV regardless of treatment. All stimuli decreased PLT-CT. EPA significantly increased platelet EPA (0.2 +/- 0.1 vs. 3.3 +/- 0.4%) and docosapentaenoic acid (DPA; 2.2 +/- 0.3 vs. 2.9 +/- 0.3%) concentrations, but not DHA. DHA treatment significantly increased DHA (1.4 +/- 0.2 vs. 4.1 +/- 0.5%) and DPA (2.0 +/- 0.4 vs. 3.0 +/- 0.4%) concentrations, but not EPA. In conclusion, EPA, but not DHA, reduces platelet activation, an early step in platelet aggregation.

Administration, Oral↗

Mean platelet volume as an indicator of platelet activation: methodological issues.

BACKGROUND: Mean platelet volume (MPV) is increased in patients at high risk for athero-thrombotic diseases. Thus, an elevated MPV may be a risk marker for platelet activation. METHODS: Healthy subjects with normal triglyceride (TG) levels (90+/-6 mg/dl; n = 40) or mild hypertriglyceridemia (161+/-79 mg/dl; n = 32) were studied. MPV was measured in fasting blood samples before and after stimulation with collagen (10 micro g/ml), and exposure to 4 or 37 degrees C. Samples from the normotriglyceridemic subjects were tested again 4 h after consuming a high-fat drink. RESULTS: Collagen and exposure to 4 degrees C increased MPV, whereas incubation at 37 degrees C lowered MPV regardless of TG level. There was no significant difference in unstimulated MPV between the fasting and the fed states in the normotriglyceridemic subjects (both 7.2+/-0.1 fl; mean+/-SEM), nor between the latter group and hypertriglyceridemic subjects (7.0+/-0.1 fl). There was a significant negative relation between MPV and fasting TG level. CONCLUSIONS: This study suggests that MPV response to low-dose collagen may be a useful indicator of platelet propensity to activation. Further studies are warranted to correlate MPV with classical platelet aggregation tests and with the use of platelet-active drugs.

Adult↗