Biomedical subjects

Yun Jin Kim

Publications and source records attributed to Yun Jin Kim.

3 recordsLinked to original sources

PubMed2006

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↗

PubMed2006

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↗

PubMed2004

Changes in plasma ghrelin concentration immediately after gastrectomy in patients with early gastric cancer.

Although the majority of circulating ghrelin originates from the stomach, no prospective study of the proportion of ghrelin derived from the stomach has been reported. Patients with early gastric cancer who underwent gastric resection were divided into three groups according to the extent and site of gastric resection: subtotal gastrectomy group (n = 24), proximal gastrectomy group (n = 4), and total gastrectomy group (n = 12). Patients with advanced gastric cancer who underwent gastrojejunostomy without gastrectomy served as the bypass group (n = 5). Blood samples were collected from all patients preoperatively, at 1 h after gastric resection or gastrojejunostomy, and on postoperative d 1, 3, and 7. The plasma ghrelin level was determined in all samples and expressed as a percentage of the preoperative level. In the bypass group, no significant drop in the ghrelin level was observed at 1 h after gastrojejunostomy, and the ghrelin level remained stable through postoperative d 7. In the subtotal gastrectomy group, the ghrelin concentration reached a nadir of 38.8 +/- 12.9% of preoperative levels at 1 h after gastric resection and then gradually increased to 88.1 +/- 13.2% by postoperative d 7. In the proximal gastrectomy group, the nadir ghrelin level was 24.5 +/- 15.4% at 1 h after gastric resection and was followed by a gradual recovery. However, the recovery rate was slower than that in the subtotal gastrectomy group, with the ghrelin level reaching only 47.6 +/- 18.8% by postoperative d 7 (P < 0.05). In the total gastrectomy group, the nadir ghrelin level was 28.6 +/- 11.1% at 1 h after gastric resection and remained at 30.0 +/- 13.2% until postoperative d 7. These results suggest that compensatory ghrelin production can occur in the remnant stomach after the surgical removal of part of the stomach and that the proximal fundus is more important than the distal antrum and body in terms of the capacity for ghrelin production. The principal site of ghrelin production is clearly the stomach, which contributes 70% of the circulating ghrelin concentration.

Adult↗