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The plasma atherogenic index (AIP) has been suggested as a useful independent predictor of cardiovascular diseases (CVDs) in high CV risk patients. We investigated the association between AIP and arterial stiffness measured by brachial–ankle pulse wave velocity (baPWV) in healthy adults. A total of 3468 healthy subjects without any metabolic or CV diseases were enrolled. Anthropometric and CV risk factors were measured. The AIP was defined as the base 10 logarithm of the ratio of the concentration of triglycerides to high-density lipoprotein-cholesterol. Subjects were classified into AIP quartiles. There were gradual deteriorations in metabolic parameters and increase in baPWV across the increasing AIP quartiles. In a fully adjusted analysis, compared with Q1 (lowest quartile) group, the odds ratio (95% confidence interval) for increased baPWV was higher in Q2 1.51, Q3 1.64, and Q4 (highest quartile) 2.77 among men, and Q2 1.09, Q3 1.55, and Q4 1.83 among women (all P trend

Type 2 diabetes is the fastest growing metabolic disease in the world. Recently, muscle is considered an endocrine organ which secretes various peptides that play an important role in insulin resistance and metabolic syndrome. We assessed 4 different myokines, irisin, interleukin-13 (IL-13), follistatin-related protein-1 (FSTL-1), and fractalkine, in normal, prediabetes, and diabetes patients. A total of 126 participants who visited Gangnam Severance Hospital were enrolled and divided into normal, prediabetes, and diabetes groups based on oral glucose tolerance test and hemoglobin a1c. A cross-sectional study was conducted to measure and compare serum levels of irisin, IL-13, FSTL-1, and fractalkine among the groups. Irisin level showed a tendency to increase in prediabetes group compared to normal group (P

Additional file 1: Supplementary Table 1. Odds ratios for CAC progression according to AIP tertiles

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.

Title: Elevated TyG index predicts progression of coronary artery calcification Objective: To investigate the TyG index association with coronary artery calcification(CAC) progression in adult Koreans. Research design and methods: Various cardiovascular risk factors and anthropometric profiles were assessed in 1175 subjects, who previously had CAC evaluation, at least twice, by multi-detector CT in a health care center. TyG index was determined using ln[fasting triglycerides (mg/dL) × fasting glucose (mg/dL)/2]. A difference of ≥ 2.5 units between the square roots of the baseline and follow-up coronary artery calcium scores (CACS) was considered as CAC progression. Results: CAC progression was seen in 282 subjects (24%) during 4.2 years follow-up. Based on TyG index, patients were stratified into three groups. Follow-up CACS and incidence of CAC progression markedly elevated with rising TyG index tertile. Logistic regression analysis adjusted for different risk factors, revealed the odds ratio for CAC progression to be 1.88 (95% CI: 1.21-2.92; P

Background The elderly population is growing rapidly worldwide and sarcopenia, which is considered as a new geriatric syndrome has become an important issue. In particular, diabetes is known to be an important risk factor for sarcopenia. In this study, we investigated the effects of Korean Red Ginseng (KRG) on biomarkers of sarcopenia in middle and old age diabetes patients. Patients and methods This study was a randomized, double-blind, placebo-controlled trial. Participants were randomly allocated to either the placebo or KRG group and took corresponding tablets for 24 weeks. The primary outcomes were changes in sarcopenia biomarkers at week 24. Secondary outcomes were changes in inflammatory and antioxidant markers and lean body mass at week 24. Results Fifty-nine patients completed the study. Follistatin and sex hormone binding globulin (SHBG) were significantly improved in KRG group. In the subgroup analysis, female postmenopausal patients over the age of 55 showed a significant improvement in serum SHBG, follistatin, and growth differentiation factor 15 (GDF-15) and an attenuated reduction in Troponin T (TNT) after the administration of KRG. Conclusion Twenty-four week administration of KRG in diabetes patients resulted in a significant improvement in follistatin and SHBG levels, especially in old postmenopausal women. A further, larger population study with a longer follow-up period is warranted to verify and understand the effects of KRG on sarcopenia.

OBJECTIVE To investigate the triglyceride-glucose (TyG) index association with coronary artery calcification (CAC) progression in adult Koreans. RESEARCH DESIGN AND METHODS Various cardiovascular risk factors and anthropometric profiles were assessed in 1,175 subjects who previously had a CAC evaluation at least twice by multidetector computed tomography in a health care center. The TyG index was determined using ln(fasting triglycerides [mg/dL] × fasting glucose [mg/dL]/2). The CAC progression was defined as either incident CAC in a CAC-free population at baseline or an increase of ≥2.5 units between the square roots of the baseline and follow-up coronary artery calcium scores (CACSs) of subjects with detectable CAC at baseline. RESULTS CAC progression was seen in 312 subjects (27%) during 4.2 years follow-up. On the basis of the TyG index, subjects were stratified into three groups. Follow-up CACS and incidence of CAC progression were markedly elevated with rising TyG index tertile. Logistic regression analysis adjusted for various risk factors revealed an odds ratio for CAC progression of 1.82 (95% CI 1.20–2.77; P ≤ 0.01) when the highest and lowest TyG index tertiles were compared. CONCLUSIONS The TyG index is an independent predictor of CAC progression.

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.

Background Recently, the triglyceride glucose (TyG) index has been considered a surrogate marker of insulin resistance which is a well-known pathogenic factor in nonalcoholic fatty liver disease (NAFLD). However, few studies have investigated the relationship between the TyG index and NAFLD. Thus, we investigated the relationship between the TyG index and NAFLD and the effectiveness of the TyG index compared with the homeostasis model assessment of insulin resistance (HOMA-IR) in identifying NAFLD in Korean adults. Methods Participants of 4,986 who underwent ultrasonography in a health promotion center were enrolled. The TyG index was calculated as ln [fasting triglycerides (mg/dL)×fasting glucose (mg/dL)/2], and HOMA-IR was estimated. NAFLD was diagnosed by ultrasonography. Results Significant differences were observed in metabolic parameters among the quartiles of the TyG index. The prevalence of NAFLD significantly increased with increment in the TyG index. After adjusting for multiple risk factors, a logistic regression analysis was performed. When the highest and lowest quartiles of the TyG index and HOMA-IR were compared, the odds ratios for the prevalence of NAFLD were 2.94 and 1.93 (95% confidence interval, 2.32 to 3.72 and 1.43 to 2.61; both P for trend

Dementia is one of the most important neurological disorders in the elderly population. The significance of vascular risk factors for dementia remains controversial. This study aimed to determine the effects of vascular risk factors, such as blood pressure, diabetes and smoking in the mid-life or the late-life on dementia risk. The data in this prospective cohort study came from 3252 dementia events occurring over 14 years among 848,505 Koreans aged 40-95 years insured by the National Health Insurance Corporation who had a biennial medical evaluation during 1992-1995. Data on clinical dementia during the period 1993-2006 were examined in relation to vascular risk factors. The age adjusted incidence per 100,000 was 31.9 for men and 45.0 for women, respectively. In multivariate Cox proportional hazard models, diabetes increased the risk of either dementia in Alzheimer's disease or vascular dementia in men and women, controlling for age, hypertension, total cholesterol, alcohol drinking, and smoking. Hypertension also increased vascular dementia in both men [Hazard ratio (HR)=2.6, 95% confidence interval (CI)=1.7-3.8] and women (HR=2.3, 95%CI=1.6-3.3). The association of hypertension or diabetes on risk of vascular dementia, however, among the group aged older than 65 was attenuated but remained as significant in men. There was no interaction between hypertension and diabetes on the risk of dementia. This study demonstrates that diabetes and hypertension increased the risk of vascular dementia. Treatment for these risk factors may reduce the risk of vascular dementia.