Seoul National University · 医学
Professor Soo Lim's research lab focuses on the pathophysiological mechanisms linking body fat distribution, particularly visceral and ectopic fat depots, to cardiometabolic diseases such as insulin resistance, type 2 diabetes, and nonalcoholic fatty liver disease (NAFLD). The lab investigates the role of adipose tissue heterogeneity, mitochondrial dysfunction, and environmental toxins—especially persistent organic pollutants (POPs)—in driving metabolic syndrome and its complications. Using advanced body composition assessment tools like BIA and DXA, the lab evaluates the accuracy of clinical measurements in aging and obese populations to improve risk prediction and early intervention strategies.
Figures are computed from collected data and may differ slightly.
The average of overweight individual can have differential fat depots in target organs or specific compartments of the body. This ectopic fat distribution may be more of a predictive factor for cardiovascular risk than obesity. Abdominal visceral obesity, a representative ectopic fat, is robustly associated with insulin resistance and cardiovascular risk. Fat depots in the liver and muscle tissue cause adverse cardiometabolic risk by affecting glucose and lipid metabolism. Pericardial fat and pe
Our findings are consistent with the hypothesized role of android fat as a pathogenic fat depot in the MS. Measurement of android fat may provide a more complete understanding of metabolic risk associated with variations in fat distribution.
We evaluate the accuracy of whole body muscle mass (WBMM) and appendicular skeletal muscle mass (ASMM) assessed by bioelectrical impedance analysis (BIA) using an InBody770 machine (InBody, Seoul, Korea) referenced to dual-energy X-ray absorptiometry (DXA) in 507 people (mean age 63.7 ± 10.8 years, body mass index (BMI) 25.2 ± 3.5 kg/m2). Mean WBMMs measured by BIA and DXA were 49.3 ± 6.6 kg and 46.8 ± 6.5 kg in men and 36.1 ± 4.7 kg and 34.0 ± 4.8 kg in women, respectively. The respective effec
Nonalcoholic fatty liver disease (NAFLD) is a chronic condition characterized by fat accumulation combined with low-grade inflammation in the liver. A large body of clinical and experimental data shows that increased flux of free fatty acids from increased visceral adipose tissue and de novo lipogenesis can lead to NAFLD and insulin resistance. Thus, individuals with obesity, insulin resistance, and dyslipidaemia are at the greatest risk of developing NAFLD. Conversely, NAFLD is a phenotype of c
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