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Bong Soo Cha

Publications and source records attributed to Bong Soo Cha.

39 records · Page 3Linked to original sources

Visceral fat thickness measured by ultrasonography can estimate not only visceral obesity but also risks of cardiovascular and metabolic diseases.

BACKGROUND: Visceral obesity is closely associated with cardiovascular disease and the metabolic syndrome. Estimating the amount of visceral fat is important and requires a straightforward, reliable, and practical method. OBJECTIVE: We investigated whether visceral fat thickness (VFT) measured by ultrasonography can adequately assess visceral fat accumulation and predict cardiovascular or metabolic diseases. DESIGN: Diabetic patients (240 men and 106 women) underwent ultrasonography to estimate visceral fat accumulation. RESULTS: The visceral adipose tissue area had the best correlation with VFT (r = 0.799, P < 0.001). VFT correlated with HDL-cholesterol, triacylglycerol, and high-sensitivity C-reactive protein concentrations, the homeostasis model assessment for insulin resistance, and the intima-media thickness at the common carotid artery (r = -0.30, 0.39, 0.34, 0.31, and 0.33, respectively; P < 0.05) in men and with triacylglycerol and high-sensitivity C-reactive protein concentrations and the homeostasis model assessment for insulin resistance (r = 0.33, 0.44, and 0.30, respectively; P < 0.05) in women. Men in the middle and high VFT tertiles had a higher odds ratio (OR) of coronary artery disease [ORs: 4.48 (95% CI: 1.29, 5.51) and 2.04 (1.06, 3.94), respectively; P = 0.016], hypertriacylglycerolemia [ORs: 2.87 (1.41, 5.86) and 1.91 (1.24, 2.95), respectively; P = 0.003], and the metabolic syndrome [ORs: 3.38 (1.61, 7.10) and 1.95 (1.16, 3.27), respectively; P = 0.003] than did those in the low tertile, after adjustment for age, waist circumference, and body mass index. CONCLUSION: VFT might be a reliable index for assessing the amount of visceral fat and for identifying diabetic patients, particularly men, who are at high risk of cardiovascular disease.

Abdomen↗

Delayed treatment with lithospermate B attenuates experimental diabetic renal injury.

Extracellular matrix (ECM) accumulation in the glomerular mesangium is a characteristic feature of diabetic nephropathy. While transforming growth factor-beta1 (TGF-beta1) is the final mediator of ECM accumulation, reactive oxygen species (ROS) and protein kinase C (PKC) are the upstream signaling molecules that mediate hyperglycemia-induced ECM expansion. Magnesium lithospermate B (LAB) is an active component isolated from Salvia miltiorrhizae with known renoprotective properties due to its antioxidative effects. Thus, the present study examined the effects of LAB on renal injury in streptozotocin-induced diabetic rats (STZR) and on the activation of mesangial cells cultured under high glucose conditions. Ten micrtograms of LAB/kg per day was started 8 wk after streptozotocin injection and continued for a period of 8 wk. It significantly suppressed renal malondialdehyde (MDA), microalbuminuria, glomerular hypertrophy, mesangial expansion, and the upregulation of renal TGF-beta1, fibronectin, and collagen in STZR without significantly affecting plasma glucose. Both 30 mM of glucose and 100 uM of H(2)O(2) significantly increased TGF-beta1 and fibronectin protein secretion by mesangial cells. LAB at 10 micro g/ml inhibited high glucose- and H(2)O(2)-induced TGF-beta1 and fibronectin secretion. LAB also inhibited glucose-induced intracellular ROS generation and PKC activation in mesangial cells, but it did not directly inhibit PKC activity at dosages that inhibited ROS generation. The in vitro data of this study show that LAB inhibits ROS generation leading to PKC activation and TGF-beta1 and fibronectin upregulation in mesangial cells cultured under high glucose conditions. Moreover, delayed treatment with LAB was found to significantly suppress the progression of renal injury in STZR. LAB may become a new therapeutic agent for the treatment of diabetic nephropathy.

Albuminuria↗

Left-ventricular diastolic dysfunction may be prevented by chronic treatment with PPAR-alpha or -gamma agonists in a type 2 diabetic animal model.

OBJECTIVES: The aim of this study was to determine whether the peroxisome proliferator-activated receptor (PPAR) ligands could prevent left-ventricular diastolic dysfunction (LVDD) in rats with advanced diabetes. In addition, this study examined whether the activity of malonyl-CoA decarboxylase (MCD), which is an enzyme related to the degradation of malonyl-CoA that is known to regulate the fatty acid metabolism, is changed by the diabetic state itself or by treatment with the PPAR ligands. METHODS: Male Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a model of type 2 diabetes, aged 28 weeks, were divided into 3 groups: the untreated, pioglitazone-treated (10 mg/kg/d), and fenofibrate-treated (150 mg/kg/d) groups. The rats were treated for 10 weeks. Male Long-Evans Tokushima Otsuka (LETO) rats were used as nondiabetic control. Doppler echocardiography and measurements of the MCD activity at the myocardium were performed. RESULTS: At the age of 38 weeks, the OLETF rats treated with either pioglitazone or fenofibrate showed an improvement in the plasma glucose levels after glucose loading as well as an improvement in the fasting plasma insulin, triglyceride, and FFA levels compared to the untreated OLETF rats. The untreated OLETF rats showed a prolonged deceleration time of the E-wave (DTE) (74.3 +/- 3.7 vs LETO, 56.3 +/- 3.8 ms, P < 0.05) and a reduced ratio of the peak early diastolic velocity wave to the late diastolic wave (E/A ratio) (1.25 +/- 0.06 vs LETO 1.54 +/- 0.08, P < 0.05). Pioglitazone treatment in the OLETF rats improved the DTE (51.6 +/- 1.7 ms, P < 0.05), and the fenofibrate treatment also improved the DTE (61.4 +/- 4.3 ms, P < 0.05) and E/A ratio (1.57 +/- 0.05, P < 0.05) compared to the untreated OLETF rats. The parameters related to the systolic function did not change among the groups at both pre- and post-treatments. The MCD activity of the myocardium was remarkably lower in the OLETF rats compared to the LETO rats (3.26 +/- 0.38 vs 7.76 +/- 0.84 nmol/min/mg protein, P < 0.05). The pioglitazone and fenofibrate treatments resulted in an increase in the MCD activity compared to that in the untreated rats (7.20 +/- 0.74 and 8.33 +/- 0.83 nmol/min/mg protein, P < 0.05, respectively). CONCLUSIONS: The PPAR-alpha or -gamma agonists prevented LVDD in the advanced diabetic rat hearts, possibly through an improvement in the fatty acid metabolism in the myocardium or a correction of the hyperglycemia and/or hyperlipidemia.

Animals↗