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Background: Baicalin, isolated from Scutellaria baicalensis, has been reported to have anti-inflammatory effect by inhibiting expression of cell adhesion molecules and migration of leukocytes in vascular cells. However, there is a limited evidence on its anti-inflammatory effect in hyperglycemia-associated milieu in other cells. Hyperglycemia and its associated factors are known to induce diabetic nephropathy by exacerbating inflammation, especially, in proximal convoluted tubule. Herein, we investigated whether baicalin exerts anti-inflammatory and anti-fibrosis effects on human renal proximal tubular cells in hyperglycemia induced conditions. Method: HK-2 cell was maintained in normal glycemic (5.78mM glucose) or in hyperglycemic (30mM glucose) condition with or without advanced glycation end-products (AGE) and tumor necrosis factor alpha (TNFα). In each condition, baicalin was treated at 10uM. Cell viability was determined by MTT assay. Gene and protein expression of multiple inflammatory and fibrosis markers including toll-like receptor 2 (TLR2), TLR4, fibronectin, collagen IV α1 (ColIVα1), collagen IV α2 (ColIVα2), transforming growth factor β (TGFβ), intercellular adhesion molecule 1 (ICAM1), and vascular adhesion molecule 1 (VCAM1) were evaluated by PCR and WB, respectively. Results: Baicalin had no effect on cell viability. Baicalin significantly decreased gene expression of ColIVα2 in response to TNFα stimulation in normal glycemic condition (p=0.038). In hyperglycemic condition, baicalin decreased gene expressions of ICAM1 (p=0.049) and VCAM1 (p=0.049) significantly in AGE treated cells; and it significantly decreased gene expressions of TGFβ (p=0.038) and ICAM1 (p=0.017) in TNFα treated cells. Baicalin also decreased protein expression of ICAM1 in response to AGE (p=0.048) and TNFα (p=0.040) stimulation in hyperglycemic condition. Conclusion: Baicalin attenuated fibrosis process by hyperglycemia associated factors in HK-2 cell. Disclosure J. Nam: None. J. Kim: None. K. Park: None. S. Lee: None. J. Nam: None. J. Park: None. S. Park: None. Y. Kim: None. C. Ahn: None.

Objective: FSTL1, an extracellular glycoprotein, is a novel myokine that is secreted by skeletal muscle. However, its functions in metabolism remain unclear, Adipose tissue is one of the important organs for maintaining energy homeostasis. FSTL1 is known to induce inflammatory response and inhibit insulin-mediated Akt signaling pathway, we aimed to investigate whether FSTL1 play metabolic roles in human adipose tissue. We hypothesized that FSTL1 increases lipolysis through its putative receptor DIP2A (Disco interacting protein 2 homolog A). Methods: Human primary adipocytes were treated with recombinant FSTL1 in dose and time dependent manner. To determine its lipolytic activity, pHSL ser563,565,660, perilipin, AMPK, PKA were determined by western blot and the rate of free fatty acid was assessed. Expression of DIP2A was determined by PCR and western blot. DIP2A was knocked-down to examine whether it mediates metabolic effects of FSTL1. Results: FSTL1 did not affect catecholamine-induced lipolysis via PKA. FSTL1, however, increased lipolysis through AMPK activation and, subsequently, HSL ser565 phosphorylation in dose dependent manner. It was found that DIP2A expression did not change during differentiation of human primary adipocyte, suggesting that it is not involved in adipocyte maturation. Conclusion: FSTL1 increased basal lipolysis through AMPK activation. AMPK is well known sensor of the intracellular energy state and serves to regulate various signals. Its activation provides ATP by FA oxidation. Therefore, FSTL1 may play an important in the regulation of energy homeostasis. FSTL1 also has effect through DIP2A. These findings suggest that DIP2A plays important roles in FSTL1 mediated lipolysis. Disclosure C. Ahn: None. A. Choi: None. J. Kim: None. K. Park: None. S. Lee: None. J. Nam: None. S. Park: None. M. Kim: None. Y. Kim: None. J. Nam: None. S. Kang: None. J. Park: None.

Introduction: NK cells are cytotoxic lymphocytes critical to innate immunity. The purpose of this study is to find out the difference in NK cell activity between type 2 diabetes patients and controls, and to investigate the association between NK cell activity and glucose control. Methods: 49 subjects were enrolled in this study, with 23 type 2 diabetes patients and 26 normal glucose tolerant controls. Anthropometric and biochemical parameters were assessed. Homeostatic model assessment (HOMA) was calculated for insulin resistance. NK cell activity was measured using a newly developed NK Vueⓡ Kit (ATgen, Seoul), which is a method of detecting and comparing interferon-gamma level from NK cells. Results: NK cell activity was lower in type 2 diabetes patients compared to control subjects. There was a significant inverse linear relationship between NK cell activity and fasting plasma glucose after adjusting for age and gender (r = -0.346, P = 0.045). Postprandial glucose and HbA1c showed a similar tendency with NK cell activity (r = -0.313 and -0.241, and P = 0.072 and 0.17, respectively). Regression analysis showed HbA1c, fasting glucose and postprandial glucose to be independent predictors of NK cell activity (beta = -0.303, -0.360, -0.356, and P = 0.034, 0.011, 0.033). There was no relationship between NK cell activity and HOMA-IR. Conclusions: NK cell activity was lower in type 2 diabetes compared to controls, and it was significantly related to degree of hyperglycemia. A further, larger population study is warranted to confirm the possible correlation. Disclosure J. Kim: None. K. Park: None. S. Lee: None. M. Kim: None. J. Nam: None. S. Kang: None. J. Park: None. C. Ahn: None. Y. Kim: None.

Background: Recently, the triglyceride glucose (TyG) index has been considered a surrogate marker of insulin resistance. Insulin resistance is a well known pathogenic factor in nonalcoholic fatty liver disease (NAFLD). However, few studies have investigated the relationship between the TyG index and liver fibrosis in subjects with NAFLD. Thus, we investigated the relationship between the TyG index and liver fibrosis in Korean adults. Methods: In total, 5158 participants who underwent ultrasonography in a health promotion center were enrolled. Anthropometric profiles and multiple metabolic risk factors were measured. The TyG index was calculated as ln [fasting triglycerides (mg/dL) × fasting glucose (mg/dL)/2], and the insulin resistance index of homeostasis model assessment (HOMA-IR) was estimated. NAFLD was diagnosed by ultrasonography, and degree of liver fibrosis was assessed by NAFLD fibrosis score (NFS). Significant liver fibrosis was defined as NFS ≥ -1.5. Results: All subjects were stratified into four groups based on their TyG indices. Significant differences were observed in metabolic parameters among the groups, and the prevalence of NAFLD and liver fibrosis by NFS significantly increased with increasing TyG index. When classifying the severity of NAFLD into three groups, there was a significant correlation between the severity of NAFLD and the TyG index. In the logistic regression analysis after adjustment for multiple risk factors, the odds ratio for the prevalence of liver fibrosis, when comparing the highest and lowest quartiles of the TyG index was 1.92 (95% CI: 1.46-2.53; P for trend < 0.01); the odds ratio for the prevalence of liver fibrosis, when comparing the highest and lowest quartiles of HOMA-IR was 2.92 (95% CI: 1.12-2.40; P for trend Conclusion: There is a significant association between the TyG index and liver fibrosis of NAFLD, but HOMA-IR was superior to TyG index for predicting liver fibrosis in NAFLD patients. Disclosure M. Kim: None. J. Kim: None. K. Park: None. S. Lee: None. J. Nam: None. S. Kang: None. J. Park: None. C. Ahn: None. Y. Kim: None.