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Articles by J. S. Nam
Total Records ( 2 ) for J. S. Nam
  H. C. Kim , Y. J. Cho , C. W. Ahn , K. S. Park , J. C. Kim , J. S. Nam , Y. S. Im , J. E. Lee , S. C. Lee and H. K. Lee
  Aims: Low serum nerve growth factor (NGF) levels have been reported in patients with diabetic peripheral neuropathy (DPN), but the role of NGF in the development of neuropathy is unclear. Thus, we investigated the associations of serum NGF level and NGF receptor activity with the presence and severity of DPN.
Methods: One hundred and thirty-six patients with Type 2 diabetes were included in this cross-sectional study. Serum NGF levels were measured by ELISA. Expressions of NGF receptors (TrkA and p75NTR) were measured by immunohistochemical staining. The presence and severity of DPN were assessed by neuropathy disability score (NDS) and by corneal nerve fibre length (cNFL) and nerve branch density (cNBD) using in vivo confocal microscopy.
Results: Patients with DPN had higher serum NGF levels (56–451 pg/ml) than patients without DPN (4–54 pg/ml). However, in DPN patients, serum NGF was negatively associated with neuropathy severity (mild 222 ± 64 pg/ml; moderate 114 ± 17 pg/ml; severe 89 ± 20 pg/ml). This negative association was consistent in all severity indices (NDS, P < 0.001; cNFL, P < 0.001; cNBD P = 0.010) even after adjustment for age, sex, diabetes duration, insulin use, fasting glucose and glycated haemoglobin. Although NGF receptor activities had significantly (P < 0.05) negative associations with the presence and severity of neuropathy, these associations were not significant when adjusted for other factors.
Conclusions: Serum NGF level was positively associated with the presence of DPN but negatively associated with neuropathy severity in DPN patients. The change in serum NGF might be a consequence of, rather than a contributor to, the early development of DPN.
  J. S. Nam , J. Y. Nam , J. S. Yoo , M. Cho , J. S. Park , C. W. Ahn , B. S. Cha , E. J. Lee , S. K. Lim , K. R. Kim and H. C. Lee
  Aim We examined the effect of rosiglitazone on insulin sensitivity, abdominal fat and mid-thigh intramuscular fat distribution, and plasma concentrations of adipocytokines in patients with Type 2 diabetes.
Methods Rosiglitazone was administered at a daily dose of 4 mg to 42 Type 2 diabetes patients [age 32–70 years, body mass index (BMI) 17.5–32.6 kg/m2, 15 women, 27 men] for 12 weeks. Various anthropometric and metabolic profiles, plasma adiponectin, leptin, and resistin levels were measured, and insulin resistance was calculated from the short insulin tolerance test. Body fat composition was assessed by computed tomography.
Results Twelve weeks' rosiglitazone treatment resulted in improved insulin resistance despite increases in body weight and BMI. There was a significant decrease in abdominal visceral adipose tissue area (145 ± 65.6 vs. 129 ± 73.1 cm2, P = 0.049). Mid-thigh low-density muscle area (TLDMA) increased from 23 ± 9.6 to 26 ± 8.2 cm2 (P = 0.009). There were significant changes in plasma adipocytokines, but they were not significantly correlated with changes in insulin resistance.
Conclusions Rosiglitazone treatment resulted in an improvement of insulin responsiveness in Type 2 diabetic subjects, which was associated with the redistribution of visceral and subcutaneous adipose tissue, an increase in TLDMA, and changes in serum adipocytokine levels. Further studies are needed to elucidate the insulin sensitizing mechanism of rosiglitazone on peripheral skeletal muscles.
 
 
 
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