Table_1_Elevated triglyceride-glucose-body mass index associated with lower probability of future regression to normoglycemia in Chinese adults with prediabetes: a 5-year cohort study.docx

ObjectiveDespite the clear association of TyG-BMI with prediabetes and the progression of diabetes, no study to date has examined the relationship between TyG-BMI and the reversal of prediabetes to normoglycemia.Methods25,279 participants with prediabetes who had physical examinations between 2010 and 2016 were enrolled in this retrospective cohort study. The relationship between baseline TyG-BMI and regression to normoglycemia from prediabetes was examined using the Cox proportional hazards regression model in this study. Additionally, the nonlinear association between TyG-BMI and the likelihood of regression to normoglycemia was investigated using the Cox proportional hazards regression with cubic spline function. Competing risk multivariate Cox regression analysis was conducted, with progression to diabetes as a competing risk for prediabetes reversal to normoglycemia. Furthermore, subgroup analyses and a series of sensitivity analyses were performed.ResultsAfter adjusting for covariates, the results showed that TyG-BMI was negatively associated with the probability of returning to normoglycemia (per 10 units, HR=0.970, 95% CI: 0.965, 0.976). They were also nonlinearly related, with an inflection point for TyG-BMI of 196.46. The effect size (HR) for TyG-BMI to the right of the inflection point (TyG-BMI ≥ 196.46) and the probability of return of normoglycemia was 0.962 (95% CI: 0.954, 0.970, per 10 units). In addition, the competing risks model found a negative correlation between TyG-BMI and return to normoglycemia (SHR=0.97, 95% CI: 0.96-0.98). Sensitivity analyses demonstrated the robustness of our results.ConclusionThis study demonstrated a negative and nonlinear relationship between TyG-BMI and return to normoglycemia in Chinese adults with prediabetes. Through active intervention, the combined reduction of BMI and TG levels to bring TyG-BMI down to 196.46 could significantly increase the probability of returning to normoglycemia.</p

Additional file 1 of Link between triglyceride-glucose-body mass index and future stroke risk in middle-aged and elderly chinese: a nationwide prospective cohort study

Additional file 1: Table S1. Collinearity screening. Table S2. Factors influencing the risk of stroke were analyzed by univariate Cox proportional hazards regression. Table S3. Association of TG, FPG, TyG and BMI with stroke risk in different models. Table S4. Multivariate logistic regression analysis of the association between different TyG-BMI change groups (change from 2011 to 2015) and stroke risk. Table S5. The Baseline Characteristics of participants on both sides of the inflection point. Figure S1. showed the distribution of TyG-BMI across survey years after categorizing participants using the K-means algorithm. It was observed that participants in Class 1 exhibited overall low TyG-BMI levels (2011: 182.77 ± 22.56; 2015: 185.26 ± 24.08), whereas overall high TyG-BMI levels were exhibited by participants in Class 2 (2011: 245.52 ± 27.03; 2015: 250.24 ± 31.61)

Additional file 1 of Relationship between glycated hemoglobin levels and three-month outcomes in acute ischemic stroke patients with or without diabetes: a prospective Korean cohort study

Supplementary Materials 1

Renal SDF-1 protein levels following LC treatment.

<p>Kidney homogenates from mice subjected to I/R injury and treated with LV or LC were analysed for SDF-1 protein using ELISA. LC treatment resulted in an increase of SDF-1 levels compared with the concentration found in homogenates from LV-treated animals that reached statistical significance (n  =  4-6 per group, **<i>P</i> <0.01). Animals were sacrificed 24 h following ischaemia.</p

Kidney tissue injury over time following 30min of bilateral renal ischenmia-reperfusion injury.

<p>C57BL/6 mice were subjected to sham or bilateral ischemia by clamping the renal pedicles for 30 min and then removing the clamps and confirming reperfusion. Mice were sacrificed at various times and kidney samples were collected. (A and B) BUN and serum creatinine were measured to determine renal function.The data shown were the means±SD. n = 6 per group. *<i>P</i> <0.05, vs sham; **<i>P</i> <0.01, vs sham(C) Photomicrograps of H & E-stained kidney sections (200×). All fields were chosen form cortex and outer medulla. Tubular damage is marked with arrows.</p

Regional location of SDF-1 in I/R kidney. (A) Immunohistochemistry staining of SDF-1 in the kidney also showed that IR-induced expression of SDF-1 was further distributed into the surrounding corticomedullary and outer medullary region compared to sham-operated mice.

<p>The kidney sections from sham-operated mice were used as control. (upper panels original magnification 200×; bottom panels 400×). (B) Quantification of SDF-1 positive area. Values are means ± SD. **<i>P</i> <0.01, vs sham.</p

Tubular injury is attenuated in LC-treated mice (A) Histology of mice shows increased tubular injury in the LV+I/R group compared with LC+I/R. (200×).

<p>Tubular damage is marked with arrows.(B) Semiquantitative analysis of tubular damage in LC-treated and LV-treated kidney at 24h after reperfusion. Values are means ± SD; n = 6 per group. *<i>P</i> <0.05, vs I/R+LV. (C) Serum creatinine values are shown 24hours after I/R±macrophage infusion. **<i>P</i> <0.01, vs I/R+LV.</p

Proinflammatory macrophages accumulation following I/R.

<p>Photographs depicting macrophage in LV and LC treated mice exposed to sham operation or I/R. (arrows, 400×).</p

SDF-1 protein levels after ischemia-reperfusion (I/R) injury.

<p>(A)Levels of SDF-1 were determined by ELISA using whole-kidney homogenates obtained from sham-operated animals or animals sacrificed at Day 1, 3 or 7 following ischaemia. The amount of SDF-1 at Day 1 was significantly higher compared with that found in sham-operated mice, and with still significantly elevated levels at day 3. Values are means ± SD; n = 6 per group. **<i>P</i> <0.01, vs sham; *<i>P</i> <0.05, vs sham. (B) SDF-1 mRNA levels after ischemia-reperfusion (I/R) injury. Real-time polymerase chain reaction (PCR) quantification of SDF-1 mRNA showed a significant increase at day 1 after ischemia. Values are means ± SD; n = 6 per group. *<i>P</i> <0.05, vs sham.</p

IKKε Knockout Prevents High Fat Diet Induced Arterial Atherosclerosis and NF-κB Signaling in Mice

<div><p>Aims</p><p>Atherosclerosis is a public health concern affecting many worldwide, but its pathogenesis remains unclear. In this study we investigated the role of IKKε during the formation of atherosclerosis and its molecular mechanism in the mouse aortic vessel wall.</p><p>Methods and Results</p><p>C57BL/6 wild-type or IKKε knockout mice bred into the ApoE knockout genetic background were divided into 4 groups: (1) wild-type (WT), (2) ApoE knockout (AK), (3) IKKε knockout (IK), (4) or both ApoE and IKKε knockout (DK). Each group of mice were fed with a high fat diet (HFD) for 12 weeks from 8 weeks of age. Immunohistochemistry and Western blotting analysis demonstrated obvious increases in the expression of IKKε in the AK group compared with the WT group, especially in the intima. Serum lipid levels were significantly higher in the AK and DK groups than in the other two groups. Staining with hematoxylin-eosin and Oil Red, as well as scanning electron microscopy revealed less severe atherosclerotic lesions in the DK group than in the AK group. Immunofluorescence and Western blot analysis demonstrated obvious increases in the expression of NF-κB pathway components and downstream factors in the AK group, especially in the intima, while these increases were blocked in the DK group.</p><p>Conclusion</p><p>The knockout of IKKε prevented significant atherosclerosis lesions in the mouse aorta from in both wild-type and ApoE knockout mice fed a HFD, suggesting that IKKε may play a vital role in HFD-induced atherosclerosis and would be an important target for the treatment of atherosclerosis.</p></div