Background: The association between the triglyceride-glucose (TyG) index and mortality in cardiovascular disease (CVD) patients with diabetes or pre-diabetes remains unclear. This study aimed to investigate the relationship between baseline TyG index and all-cause and cardiovascular (CV) mortality in CVD patients with diabetes or pre-diabetes among American adults. . Methods: This study enrolled 1072 CVD patients with diabetes or pre-diabetes from the National Health and Nutrition Examination Survey (2001–2018). Mortality outcomes were determined by linking to National Death Index (NDI) records up to December 31, 2019. Multivariate Cox proportional hazards models were constructed to analyze explore the associations between baseline TyG index and mortality. Non-linear correlations were explored using restricted cubic splines, and a two-piecewise Cox proportional hazards model for both sides of the inflection point was constructed. Results: During 7541 person-years of follow-up, a total of 461 all-cause deaths and 154 CVD-related deaths were recorded. The restricted cubic splines revealed a U-shaped association between the baseline TyG index with all-cause and CVD mortality in CVD patients with diabetes or pre-diabetes. Specifically, baseline TyG index lower than the threshold values (TyG index < 9.05 in all-cause mortality and < 8.84 in CVD mortality) was negatively associated with mortality (HR 0.47, 95% CI = 0.27–0.81 for all-cause mortality and HR 0.25, 95% CI = 0.07–0.89 for CVD mortality). In contrast, baseline TyG index higher than the threshold values (TyG index > 9.05 in all-cause mortality and > 8.84 in CVD mortality) was positively associated with mortality (HR 1.42, 95% CI = 1.02–1.99 for all-cause mortality and HR 1.77, 95% CI = 1.08–2.91 for CVD mortality). Conclusions: A U-shaped association was observed between the baseline TyG index with CVD and all-cause mortality in CVD patients with diabetes or pre-diabetes in a American population. The thresholds of 8.84 and 9.05 for CVD and all-cause mortality, respectively.

The study aimed to evaluate the effectiveness and safety of long-term use of closed-loop insulin system (CLS) in non-pregnant patients with type 1 diabetes mellitus (T1DM) using systematic review and meta-analysis. A literature search was performed using MEDLINE, EMBASE, and the Cochrane Library. Randomized controlled trials (RCTs) on long-term use (not less than 8 weeks) of CLS in patients with T1DM were selected. Meta-analysis was performed with RevMan V.5.3.5 to compare CLS with controls (continuous subcutaneous insulin infusion with blinded continuous glucose monitoring or unblinded sensor-augmented pump therapy or multiple daily injections or predictive low-glucose suspend system) in adults and children with type 1 diabetes. Research quality evaluation was conducted using the Cochrane risk of bias tool. Eleven RCTs (817 patients) that satisfied the eligibility criteria were included in the meta-analysis. Compared with controls, the CLS group had a favorable effect on the proportion of time with sensor glucose level in 3.9–10 mmol/L (10.32%, 8.70% to 11.95%), above 10 mmol/L (−8.89%, −10.57% to −7.22%), or below 3.9 mmol/L (−1.09%, −1.54% to −0.64%) over 24 hours. The CLS group also had lower glycated hemoglobin levels (−0.30%, −0.41% to −0.19%), and glucose variability, coefficient of variation of glucose, and SD were lower by 1.41 (−2.38 to −0.44, p=0.004) and 6.37 mg/dL (−9.19 mg/dL to −3.55 mg/dL, p<0.00001). There were no significant differences between the CLS and the control group in terms of daily insulin dose, quality of life assessment, and satisfaction with diabetes treatment. CLS is a better solution than control treatment in optimizing blood glucose management in patients with T1DM. CLS could become a common means of treating T1DM in clinical practice.

Background: Coronary heart disease (CHD) is not only a macrovascular complication of type 2 diabetes mellitus (T2DM). Cardiovascular disease (CVD) is one of the leading causes of mortality among individuals with T2DM. Reducing the risk of adverse cardiovascular events (MACE) is crucial for the management of patients with CHD. This study aimed to investigate the effect of glycemic control on CHD severity and 3-point MACE (3p-MACE) risk in patients with T2DM and CHD. Methods: 681 patients with both T2DM and CHD throughout October 2017 and October 2021 who were hospitalized in the second affiliated hospital of Nanchang university were included. A total of 300 patients were eventually enrolled in this retrospective cohort research. The severity of CHD in these patients was assessed, and the primary outcome during follow-up was recorded, with the primary result being the 3-point major adverse cardiovascular event (3p-MACE). The correlation between baseline glycated hemoglobin A1c (b-HbA1c) and the severity of CHD was evaluated by logistic regression analysis. The effect of b-HbA1c and follow-up HbA1c (f-HbA1c) levels on the risk of 3p-MACE were investigated by cox regression analysis. Results: b-HbA1c was positively correlated with the severity of CHD (r = 0.207, p = 0.001), and patients with b-HbA1c > 9% were more likely to have severe CHD. The HRs for b-HbA1c and f-HbA1c on the risk of 3p-MACE were 1.24 (95% CI 0.94–1.64, p = 0.123) and 1.32 (95% CI 1.02–1.72, p = 0.036), respectively. Patients with f-HbA1c ≥8.6% had a higher risk of 3p-MACE than f-HbA1c < 8.6% (HR = 1.79, 95% CI 1.16–2.79, p = 0.009). Conclusion: In patients with both T2DM and CHD, b-HbA1c was an independent predictive factor of severe CHD. f-HbA1c was an independent predictive factor of 3p-MACE. Having the f-HbA1c below 8.6% significantly reduced the risk of 3p-MACE.

Activation of hepatic stellate cells (HSCs) is a key inducer of liver fibrogenesis in nonalcoholic fatty liver disease (NAFLD). Exosomes play an important role between hepatocytes and HSCs. This study aims to explore the role of exosomes derived from palmitic acid (PA)-treated hepatocytes in regulating HSCs (LX-2 cell) proliferation and activation and the underlying mechanisms. Exosomes were isolated from PA-treated human normal hepatocytes and incubated with LX-2 cells. Cell Counting Kit-8 (CCK-8) was performed to determine LX-2 cell proliferation, and the expression of fibrosis markers α-smooth muscle actin (α-SMA) and collagen type 1 α1 (CoL1A1) were examined to evaluateLX-2 cell activation. PA induced hepatocytes to release more exosomes enriched in miR-107. Mechanically, on the one hand, exosomes from PA-treated hepatocytes shuttled miR-107 to LX-2 cells, where miR-107 activated Wnt signaling by targeting DKK1 and thereby induced LX-2 cell activation; on the other hand, PA-treated hepatocytes derived exosomes also delivered miR-107 to CD4 + T lymphocytes, where miR-107 elevated IL-9 expression by targeting Foxp1, which bound to the IL-9 promoter in CD4 + T cells and suppressed Th9 cell differentiation and reduced IL-9 expression, and thus promoted LX-2 cell activation by activating Raf/MEK/ERK signaling pathway.