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  • American Diabetes Association  (9)
  • 1
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    413-P: Renal Tubular Damage Marker, Urinary N-acetyl-b-d-glucosaminidase, as a Predictive Marker of Hepatic Fibrosis in Type 2 Diabetes
    American Diabetes Association ; 2021
    In:  Diabetes Vol. 70, No. Supplement_1 ( 2021-06-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 70, No. Supplement_1 ( 2021-06-01)
    Abstract: Background: Nonalcoholic steatohepatitis is closely associated with the progression of diabetic kidney disease (DKD) in type 2 diabetes (T2D). We investigated whether urinary N-acetyl-β-D- glucosaminidase(u-NAG), an early renal tubular damage biomarker in DKD, could be related to the degree of hepatic fibrosis in patients with T2D. Methods: A total of 300 patients with T2D were enrolled in the study. Hepatic steatosis and fibrosis were determined using transient elastography. The levels of urinary biomarkers, including u-NAG, albumin, protein, and creatinine, and glucometabolic parameters were measured. Results: Based on the median value of u-NAG to creatinine (u-NCR), subjects were divided into normal and high u-NCR groups. The high u-NCR group showed a significantly longer duration of diabetes, worsened hyperglycemia, and a more enhanced hepatic fibrosis index. A higher u-NCR was associated with a greater odds ratio for the risk of higher hepatic fibrosis stage (F2 OR 1.99; 95% CI [1.04-3.82]; F3 and F4 OR 2.40, 95% CI [1.52-3.80] ). In addition, u-NCR was an independent predictive marker for more advanced hepatic fibrosis even after adjusting for several confounding factors (β = 1.58, P & lt;0.01). Conclusions: The elevation of u-NAG was independently associated with a higher degree of hepatic fibrosis in patients with T2D. Considering the common metabolic milieu of renal and hepatic fibrosis in T2D, the potential use of u-NAG as an effective urinary biomarker reflecting hepatic fibrosis in T2D needs to be validated in the future. Disclosure H. Kim: None. Y. Kim: None. M. Lee: None. Y. Lee: None. E. Kang: None. B. Cha: None. B. Lee: None.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db21-413-P
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2021
    detail.hit.zdb_id: 1501252-9
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  • 2
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    SGLT2 Inhibitors Suppress NLRP3 Inflammasome Activity via Changes in Ketones and Insulin in Type 2 Diabetes and Cardiovascular Diseases
    American Diabetes Association ; 2018
    In:  Diabetes Vol. 67, No. Supplement_1 ( 2018-07-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 67, No. Supplement_1 ( 2018-07-01)
    Abstract: SGLT2 inhibitors significantly reduce cardiovascular events in humans with T2D; however, the underlying mechanism remains unclear. Activation of NLRP3 inflammasome and subsequent IL-1β release induces atherosclerosis and heart failure. Recently, it was revealed that ketone bodies, i.e., β-hydroxybutyrate (BHB) suppresses activation of NLRP3 inflammasome in macrophages. As SGLT2 inhibitors cause increases in serum BHB by pharmacologic profile, we assessed the effect of SGLT2 inhibitor on NLRP3 inflammasome activity. In a randomized, active-controlled study, a total of 61 patients with T2D and high cardiovascular risk (mean age and HbA1C were 64.4 years and 7.32%, respectively) received SGLT2 inhibitor or sulfonylurea for 30 days. NLRP3 inflammasome activation was analyzed in macrophages and the serum levels of glucose, BHB, and insulin from baseline to the end of treatment were tested. While SGLT2 inhibitor’s glucose-lowering capacity was similar to sulfonylurea, it significantly decreased IL-1β secretion compared to baseline (2,394 ± 236 to 1,748 ± 295 pg/mL, p & lt;0.001), whereas sulfonylurea had no effect on IL-1β secretion (2,273 ± 279 to 2,755 ± 331 pg/mL, p = 0.05) (time × group interaction p & lt;0.001). SGLT2 inhibitor caused a significant increase in fasting serum BHB and decrease in serum insulin, while sulfonylurea had no significant effects on these measurements. We performed ex vivo experiments using human macrophages to investigate whether BHB and insulin could affect NLRP3 inflammasome activity. BHB dose-dependently inhibited IL-1β secretion from macrophages. However, co-treatment with insulin attenuated the inhibitory effect of BHB on NLRP3 inflammasome activation. In conclusion, SGLT2 inhibitors attenuate NLRP3 inflammasome activation, in part, via increased serum BHB and decreased serum insulin and glucose, which might help to explain the cardioprotective effects of SGLT2 inhibitor (clinicaltrials.gov NCT02964572). Disclosure Y. Lee: None. S. Kim: None. J. Bae: None. B. Lee: None. E. Kang: None. C. Ahn: None. B. Cha: None.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db18-164-OR
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2018
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  • 3
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    1531-P: Spontaneous Ketonuria Is Associated with Reduced Incidence of Diabetes
    American Diabetes Association ; 2019
    In:  Diabetes Vol. 68, No. Supplement_1 ( 2019-06-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 68, No. Supplement_1 ( 2019-06-01)
    Abstract: Objective: Ketones may be regarded as a thrifty fuel for peripheral tissues, but their clinical prognostic significance still remains unclear. We investigated the association between spontaneous fasting ketonuria and incident diabetes in conjunction with changes in metabolic parameters in a large population-based, observational study. Research Design and Methods: We analyzed a total of 8,703 individuals free of diabetes at baseline in the Korean Genome and Epidemiology Study, a community-based, 12-year prospective study. Subjects with (n=195) or without fasting ketonuria were 1:4 matched by propensity score. Incident diabetes was defined as: fasting plasma glucose ≥126 mg/dL, 2-hour glucose ≥200 mg/dL on biennial 75g oral glucose tolerance test, or current antidiabetic medication. Using Cox regression models, hazard ratios for developing diabetes associated with the presence of ketonuria at baseline were analyzed. Results: Over 12 years, of the 925 subjects in the propensity score matched cohort, 190 (20.5%) developed diabetes. The incidence rate of diabetes was significantly lower in subjects with spontaneous ketonuria compared to those without ketonuria (adjusted hazard ratio 0.64 [95% confidence interval=0.42-0.99]. This result was replicated in the whole cohort (HR 0.67 [95% CI: 0.46-0.98] after multivariate adjustment). During follow-up, subjects with ketonuria at baseline maintained lower 1-hour and 2-hour glucose levels, and a higher insulinogenic index during follow-up despite comparable baseline values. Conclusions: The presence of spontaneous fasting ketonuria was significantly associated with a reduced incidence rate of diabetes, independently of metabolic parameters. Our findings suggest spontaneous fasting ketonuria is a stable phenotype and a novel signature in the modulation of glucose metabolism. Disclosure S.J. Cho: None. I. Lee: None. S. Lee: None. E. Kang: None. E. Ferrannini: None. Y. Lee: None. G. Kim: None. B. Cha: None.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db19-1531-P
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2019
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  • 4
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    Comparison of Xenogeneic Encapsulated Islet Transplantation in Nonhuman Primates With and Without Immunosuppression
    American Diabetes Association ; 2018
    In:  Diabetes Vol. 67, No. Supplement_1 ( 2018-07-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 67, No. Supplement_1 ( 2018-07-01)
    Abstract: Previously, we have shown the long-term efficacy and biocompatibility of chitosan-coated alginate capsule in allogeneic islet transplantation with canine models of diabetes. In this study, we compared the efficacy and immune response of chitosan-coated alginate capsule in xenogeneic islet transplantation with non-human primates (NHPs). Porcine islets were encapsulated alginate crosslinked with BaCl2, followed by suspension in chitosan solution. Encapsulated porcine islets were transplanted intraperitoneally in NHPs with and without immunosuppressants. Anti-αGal IgM and IgG was measured from the day of transplantation. After transplantation of encapsulated porcine islets, hyperglycemia and exogenous insulin requirements were decreased in the NHP recipients. Porcine C-peptide was detected in plasma after transplantation, but decreased with time. Anti-αGal IgM and IgG began to increase a week after transplantation in NHP without immunosuppressants, while they showed little increase in NHP with immunosuppressants. Exogenous insulin began to be administered to the NHP recipients from 3 to 5 days after transplantation regardless of immunosuppressants. However, daily insulin requirement increased earlier in NHP without immunosuppressants than those with immunosuppressants. Retrieved encapsulated porcine islets from showed fibrosis more than 70% in NHP without immunosuppressants, whereas only 5% of retrieved capsules showed fibrosis in NPH with immunosuppressants. In addition, in NPH with immunosuppressants, dithizone positive islets were observed over a month after transplantation. The use of immunosuppressants in xenogeneic encapsulated islet transplantation in NHP may help reduce fibrosis and improve islet function by modulating immune reaction. Disclosure E. Lee: None. H. Park: None. J. Kim: None. Y. Yang: None. J. Lim: None. H. Kim: None. S. Lee: None. J. Cho: None. B. Cha: None. K. Yoon: None.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db18-28-OR
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2018
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  • 5
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    Circulating Netrin-1 as a Novel Biomarker for Impaired Fasting Glucose and Newly Diagnosed Type 2 Diabetes Mellitus
    American Diabetes Association ; 2018
    In:  Diabetes Vol. 67, No. Supplement_1 ( 2018-07-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 67, No. Supplement_1 ( 2018-07-01)
    Abstract: Aims/Hypothesis: Netrin-1 has been introduced as a neuronal guidance cue, acting as a chemoattractant and chemorepulsive force during axonal migration. In recent studies, netrin-1 was shown to play various roles including tissue regeneration and modulation of inflammatory action. Inflammation is one of the major contributing factors in the development of insulin resistance and type 2 diabetes (T2DM). However, little is known about the possible relationship between serum netrin-1 and the risk of T2DM. Therefore, we investigated the association between levels of netrin-1 and glycometabolic parameters. Methods: Serum samples were collected from a total of 218 individuals (41 normal controls, 85 subjects with impaired fasting glucose (IFG) and 92 subjects with newly diagnosed T2DM). Clinical and biochemical parameters were assessed after receiving consent. Netrin-1 levels were determined by commercial enzyme-linked immunosorbent assay. Spearman correlation analyses and multivariable-adjusted linear regression analyses were conducted to examine the relationship between serum netrin-1 levels and glycometabolic parameters. Results: Serum netrin-1 level in subjects with IFG or T2DM was significantly higher than in normal control subjects (mean netrin-1 level; normal, IFG and T2DM; 275.9, 436.6 and 441.0 pg/mL, respectively; p for trend & lt;0.001). Serum netrin-1 levels had a significant positive correlation with fasting glucose, HbA1c, HOMA-IR, AST and ALT. Meanwhile, statistically inverse correlation was found between netrin-1 and HDL cholesterol and eGFR levels. In addition, Serum netrin-1 was independently associated with the presence of IFG or T2DM after adjusting covariates and potential confounders. In terms of the AUC, serum netrin-1 levels presented an AUC of 0.784 for the prediction of IFG or T2DM. Conclusions/Interpretation: Our results suggest that netrin-1 may be a new biomarker for early detection for IFG or T2DM (Clinical trial no. NCT02650830). Disclosure H. Jung: None. J. Bae: None. E. Han: None. G. Kim: None. J. Lee: None. S. Kim: None. B. Lee: None. E. Kang: None. C. Ahn: None. B. Cha: None. Y. Lee: None.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db18-1535-P
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2018
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  • 6
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    1650-P: Metabolically Healthy Obese Status and Incident Dementia Events among 5.7 Million Elderly People
    American Diabetes Association ; 2019
    In:  Diabetes Vol. 68, No. Supplement_1 ( 2019-06-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 68, No. Supplement_1 ( 2019-06-01)
    Abstract: Background: Obese individuals with normal metabolic profiles, so-called “metabolically healthy obese (MHO)” status has shown better clinical outcomes via previous studies. However, studies dealing with the association between MHO and dementia, which is deeply associated with metabolic disorders, were still insufficient. We designed this study to assess the association between MHO and the risk of incident dementia. Methods: The present study is a retrospective cohort study, including 5,669,488 patients aged 60 years old or over without any history of dementia, by using the National Health Insurance System of South Korea. Subjects were divided into 4 groups based on their metabolic health and obesity status. Metabolic health was determined based on the criteria of metabolic syndrome by Adult Treatment Panel-III. Obesity was judged based on the baseline body mass index. The incidence of dementia was checked and compared longitudinally between 4 groups. Results: When we put the metabolically healthy non-obese group to the reference value (hazard ratio (HR) = 1), MHO group showed the lowest incidence of dementia (HR 0.87, 95% confidence interval (CI) 0.86-0.88). This trend was more prominent when we followed up the risk of Alzheimer’s disease as a subgroup analysis (HR 0.85, 95% CI 0.83-0.86). Non-obese subjects with metabolic syndrome showed significantly increased risk for overall dementia (HR 1.20, 95% CI 1.19-1.21), especially for vascular dementia (HR 1.41, 95% CI 1.38-1.45). Conclusion: MHO status was associated with lower risk for dementia, especially for Alzheimer’s disease. Disclosure J. Bae: None. J. Lee: None. Y. Cho: None. M. Lee: None. S. Lee: None. I. Lee: None. E. Kang: None. S.J. Cho: None. K. Han: None. B. Cha: None. Y. Lee: None.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db19-1650-P
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2019
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  • 7
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    385-P: Effects of Ertugliflozin on Podocyte in High-Fat Diet–Induced Diabetic Kidney Disease Model, In Vivo and In Vitro
    American Diabetes Association ; 2022
    In:  Diabetes Vol. 71, No. Supplement_1 ( 2022-06-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 71, No. Supplement_1 ( 2022-06-01)
    Abstract: Early stage of diabetic kidney disease (DKD) involves loss of podocytes, consequently causing albuminuria. SGLT2 inhibitors demonstrated renoprotective effects in DKD, but the mechanism for protection in early DKD is unclear. Here, we investigated the effects of ertugliflozin in high-fat diet (HFD) -induced DKD model, in vivo and in vitro. 5-week-old male C57BL/6J mice were supplemented with HFD for 24 weeks to develop HFD-induced DKD. Ertugliflozin was administrated orally by pre-mixing with HFD for 16 weeks. We evaluated body weight, random blood glucose levels, albuminuria and glucose and insulin tolerance test were performed at 12 weeks after ertugliflozin administration. The renal cortex was collected for histologic examination and SGLT2 expression on podocytes were measured. Albuminuria was significantly decreased in ertugliflozin group compared with HFD group at 12 weeks of ertugliflozin administration (p=0.011) . Body weight, random and fasting blood glucose was not significantly different between HFD group. Glucose and insulin tolerance test showed significant improvement in ertugliflozin group compared with HFD group at 12 weeks (p=0.0004) . In immunohistochemistry studies, glomerular volume and mesangial expansion were attenuated in the ertugliflozin group by 27.6% and 27.8% respectively, compared to HFD group (p=0.002 and p=0.005, respectively) . Glomerular basement membrane thickness was decreased by 45.4% in ertugliflozin group compared to HFD group (p=0.0004) . Significant increase of SGLT2 mRNA expression by 1.6-4.8 fold after 24 hour-albumin expose was observed and SGLT2 protein was increased 1.1-1.3 fold compared to control. Ertugliflozin attenuated diabetic kidney disease in HFD-induced DKD by mitigating glomerular integrity, preserving podocyte morphology, with decreased albuminuria. Upregulation of SGLT2 in podocyte in albuminuric DKD could be suggested as possible target for renoprotective action of SGLT2 inhibitor. Disclosure H.Kim: None. B.Cha: None. H.Lee: None. B.Lim: None. H.Choi: None. E.Kang: None. Y.Kim: None. R.Kim: None. S.Lee: None. Y.Yang: None. H.Park: None. N.Jeon: None. M.Lee: None. Y.Lee: None. Funding Severance Hospital Research fund for Clinical excellence (SHRC) (C-2021-0007)
    Type of Medium: Online Resource
    ISSN: 0012-1797
    URL: Article
    DOI: 10.2337/db22-385-P
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2022
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  • 8
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    Exogenous Delta-Like 1 Homolog (DLK1)-Fc Treatment Attenuates Muscle Atrophy in Both Dexamethasone and High-Fat Diet–Induced Obesity Mice Models
    American Diabetes Association ; 2018
    In:  Diabetes Vol. 67, No. Supplement_1 ( 2018-07-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 67, No. Supplement_1 ( 2018-07-01)
    Abstract: Skeletal muscle degeneration is accelerated in elderly patients with diabetes and the imbalance between muscle growth and wasting can lead to metabolic dysfunction. DLK1 is a member of the EGF-like family and essential for skeletal muscle development and regeneration. To identify whether exogenous DLK1 treatment can prevent muscle wasting, we assessed muscle mass as well as muscle differentiation and atrophy markers in two different models: dexamethasone and high fat diet (HFD)-induced obesity mice models (n=7-8 per each group). In the dexamethasone model, mice were divided into (1) control, (2) dexamethasone treatment (1mg/Kg, 2 weeks), and (3) DLK1 (0.8mg/Kg, 2 weeks) and dexamethasone treatment groups. In the HFD model, mice were divided into (1) control, (2) HFD (60% calories from fat, 8 weeks), and (3) HFD with DLK1 treatment (0.8mg/Kg, 8 weeks) groups. The expressions of genes related to muscle differentiation and atrophy were determined using RT-PCR. We observed that dexamethasone reduced muscle mass and markedly increased atrophy makers including atrogin-1 and murf-1. DLK1 treatment attenuated these degenerative changes. Furthermore, the level of myostatin, which inhibits muscle cell growth, was reduced in DLK1 treatment group compared to dexamethasone group. Additionally, compared to HFD group, DLK1 inhibited muscle atrophy by increasing the differentiation marker: myoD, and decreasing the atrophy markers: mysotatin, atrogin-1, and murf-1. Taken together, these results suggest that DLK1 attenuates both dexamethasone and HFD-induced muscle atrophy in mice by suppressing the downstream signaling of myostatin/atrogin-1/murf-1 pathway. The increased expression of myoD indicates that DLK1 treatment can also improve the quality of muscle formation. Our study implies that DLK1 could be a promising candidate in the treatment of aging or diabetes-related sarcopenia, characterized by muscle atrophy and dysfunction. Disclosure J. Lee: None. M. Lee: None. H. Jung: None. J. Lee: None. Y. Cho: None. J. Bae: None. Y. Lee: None. B. Lee: None. E. Kang: None. B. Cha: None.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db18-1911-P
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2018
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  • 9
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    1368-P: Relative Risk of Nonalcoholic Fatty Liver Disease between Women and Men according to Glycemic Status
    American Diabetes Association ; 2023
    In:  Diabetes Vol. 72, No. Supplement_1 ( 2023-06-20)
    Details
    In: Diabetes, American Diabetes Association, Vol. 72, No. Supplement_1 ( 2023-06-20)
    Abstract: Background: Nonalcoholic fatty liver disease (NAFLD) is closely associated with type 2 diabetes (T2D). However, there is no current study for NAFLD risk stratification by sex and glycemic status. We investigated whether different glycemic status may interfere with metabolic effects affecting NAFLD according to sex. Methods: A total of 552 patients with normal glucose tolerance (NGT), prediabetes, and diabetes, were evaluated for odds ratio (OR) and hazard ratio (HR) for NAFLD (above steatosis stage 1) in cross-sectional and longitudinal study, respectively. Univariate analyses and subgroup analyses were performed to determine the risk factors for developing NAFLD according to sex and glycemic status. Hepatic steatosis and fibrosis were determined using transient elastography and body composition was analyzed by Inbody. Results: In cross-sectional study, men with prediabetes and diabetes exhibited greater relative differences in metabolic syndrome, triglyceride and HDL cholesterol than women with prediabetes and diabetes when compared with their NGT counterparts. There was no difference in OR for NAFLD observed comparing women and men with prediabetes or diabetes. After 2.6 years of follow up, we found that women with prediabetes showed significantly increased HR (HR 1.81; 95% CI 1.01-3.26; p = 0.049) of NAFLD than men with prediabetes (HR 0.83; 95% CI 0.54-1.30; p =0.42), even after adjusting several confounders. Visceral fat area was significantly higher in women with prediabetes and diabetes compared to men throughout the study. Insulin resistance (HOMA-IR≥2.5) was prediabetes-specific risk factor, contributing for prevalent NAFLD (OR 6.56; 95% CI 1.15-37.31; p=0.034) without interaction between sex and insulin resistance (p=0.99). Conclusions: Women with prediabetes showed higher risk for developing NAFLD compared to men due to greater burden of metabolic dysregulation between adipose tissue and insulin resistance. Disclosure H.Kim: None. S.Lee: None. M.Lee: None. Y.Lee: None. E.Kang: None. B.Cha: None.
    Type of Medium: Online Resource
    ISSN: 0012-1797
    URL: Article
    DOI: 10.2337/db23-1368-P
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2023
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