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Young Sung Suh  (Suh YS) 2 Articles
Proinflammatory Cytokines and Insulin Resistance in Nonobsese Women with High Body Fat and Low Fat Free Mass.
Young Sung Suh, In Kyu Lee, Dae Hyun Kim
Korean Diabetes J. 2007;31(2):136-143.   Published online March 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.2.136
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  • 2 Crossref
AbstractAbstract PDF
BACKGROUND
Adipose tissue produces and releases a variety of proinflammatory cytokines. The aim of this study was to investigate whether proinflammatory cytokines are increased and insulin resistance is presented in nonobese women with high body fat and low fat free mass. METHODS: Sixty nonobese adult premenopausal women (body mass index, BMI < 25 kg/m2) were included in this study. Body composition was determined by dual energy absoprtiometry (DXA). Fasting glucose, lipid profiles, tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), C reactive protein (CRP) and basal insulin were measured. RESULTS: The subjects with high body fat (> or = 30%) had higher CRP levels (P = 0.024), IL-6 levels (P = 0.008), insulin levels (P = 0.003), and homeostasis model assessment-IR (HOMA-IR) (P = 0.020) than those of the subjects with low body fat. In a subset of 32 subjects with high body fat (> or = 30%), the number of subjects with high fat free mass index (FFMI) (> or = 13.5 kg/m2) had higher atherogenic index than that of subjects with low FFMI (FFMI < 13.5 kg/m2) (P < 0.05). IL-6 was correlated with % body fat, fat mass index (FMI), and fat mass (P < 0.05). HOMA-IR was correlated with % body fat and FMI (P < 0.05). To investigate predictors of cytokines and HOMA-IR, multiple regression analysis was used. % body fat was a predictor for IL-6 and, while age and % body fat were predictors of HOMA-IR in study subjects. Conclusions: This study suggests that insulin resistance may be present in nonobese women with high body fat and low fat free mass.

Citations

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  • The Effect of Low Intensity Exercise on Expression of Inflammatory Response and Apoptosis in Rats with Obesity Induced by a High-Fat Diet
    Dong-Hun Choi, Joon-Yong Cho
    Exercise Science.2018; 27(1): 40.     CrossRef
  • Experiences of Health Related Lifestyles in High Body Fat but Non-obese Female College Students in Korea
    Jeongsoo Kim
    Osong Public Health and Research Perspectives.2014; 5(1): 68.     CrossRef
Polymorphism of Melanocortin-4 Receptor and Obesity.
Hye Soon Kim, In Kyu Lee, Young Sung Suh
Korean Diabetes J. 2003;27(2):123-131.   Published online April 1, 2003
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AbstractAbstract PDF
BACKGROUND
The application of genetics to obesity has made remarkable progress in recent years. The melanocortin-4 receptor (MC4R) regulates food intake, and possibly that of energy expenditure. The MC4R gene is the most prevalent obesity gene found to date in humans. The prevalence of single nucleotide substitution, replacing valine with isoleucine, at codon 103 was studied, and the role of the MC4R gene polymorphism on the body weight, fat distribution and lipid profile were determined. METHODS: Anthropometry and biochemical studies were performed on 226 subjects (82 male and 144 female subjects). The MC4R genotype was determined by a polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) method. The body fat distributions were measured by computerized tomography. RESULTS: The frequencies of the homozygotes, Val103Val and Val103/Ile, were 88.9 and 11.1%, respectively. The frequencies of the heterozygotes were similar (11.8 vs. 10.6%) in the control and obese groups. However, the heterozygotes had lower waist-to-hip ratios (WHR) (p=0.033) and visceral fat masses (p=0.038) compared to the homozygotes. In the obese group, the heterozygotes had lower body mass indices (BMI) and visceral fat masses (p=0.043 and p=0.044, respectively). The heterozygote males had lower BMI and fasting plasma glucose levels (p=0.046 and p<0.001, respectively) than the homozygote males. The heterozygote females tended to have lower WHR (p=0.081) than the homozygote females. CONCLUSION: These results suggest that mutations in the MC4R gene are likely to be a cause of human obesity, and possibly of metabolic syndrome.

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