Trends of serum 25(OH) vitamin D and association with cardiovascular disease and all-cause mortality: from NHANES survey cycles 2001-2018.

Background: The focus of this survey is on survey data for adults aged 20 and above, covering nine survey cycles from 2001 to 2018. Additionally, the present study explored the correlation between vitamin D concentrations and both cardiovascular disease (CVD) and all-cause mortality. Objective: The objectives of this study were to evaluate the trend of changes in the serum 25(OH)D concentration changes in US adults during the survey period, the prevalence of vitamin D deficiency, and the current status of vitamin D dietary intake and supplementation. Methods: In-home health interviews were performed using meticulously designed questionnaires that gathered information on demographic details, socioeconomic conditions, dietary patterns, and overall health status. Health assessments were conducted in specially designed mobile centers. Results: Survey data from 2001 to 2018 revealed a rise in serum 25(OH)D levels, from a weighted mean (95% CI) of 65.6 (63.8-67.4) nmol/L during 2001-2002 to 73.5 (70.4-76.5) nmol/L during 2017-2018, among US adults, while overall vitamin D deficiency rates remained stable (p = 0.152). Notably, in adults aged 20-39, 25(OH)D levels decreased (p = 0.002 for trend), and 25(OH)D deficiency increased (p = 0.003 for trend), especially among those with low incomes (deficiency >30%). Upon multivariable adjustment, an L-shaped relationship was found between serum 25(OH)D concentrations and both CVD and all-cause mortality (p < 0.001 for nonlinearity), as corroborated by sensitivity analyses. Conclusion: From 2001 to 2018, US adults experienced a significant increase in their serum 25(OH) D concentration. However, subgroups of individuals, including young adults and individuals with lower socioeconomic status, exhibited a heightened risk of 25(OH)D deficiency. Furthermore, an L-shaped relationship was found between 25(OH)D concentration and both all-cause and CVD mortality among US adults.

Therapeutic outcome of dapagliflozin in patients with type 2 diabetes and non-alcoholic fatty liver disease: a meta-analysis of randomized controlled trials.

Introduction: The efficacy of dapagliflozin remains controversial for patients with type 2 diabetes and non-alcoholic fatty liver disease. We conduct this meta-analysis to explore the influence of dapagliflozin versus placebo on the treatment efficacy of type 2 diabetes complicated with non-alcoholic fatty liver disease. Methods: We have searched PubMed, EMbase, Web of science, EBSCO, and Cochrane library databases through November 2021 for randomized controlled trials (RCTs) assessing the efficacy of dapagliflozin versus placebo for type 2 diabetes complicated with non-alcoholic fatty liver disease. This meta-analysis is performed using the random-effect model. Results: Four RCTs are included in the meta-analysis. Overall, compared with patients with type 2 diabetes and non-alcoholic fatty liver disease, dapagliflozin treatment is associated with significantly reduced alanine aminotransferase (ALT, standard mean difference [SMD]=-1.27; 95% confidence interval [CI]span style="font-family: 'Times New Roman'">=-1.60 to -0.95; P<0.00001), aspartate-aminotransferase (AST, SMD=-1.37; 95% CI=-2.08 to -0.65; P=0.0002), fasting glucose (SMD=-0.78; 95% CI=-1.28 to -0.27; P=0.003) and HbA1c (SMD=-0.77; 95% CI=-1.21 to -0.34; P=0.0005), but demonstrated no obvious influence on homeostatic Model Assessment of Insulin Resistance (HOMA-IR, SMD=-0.36; 95% CI=-0.86 to 0.14; P=0.16). Conclusions: Dapagliflozin benefits to improve hepatic function and glucose control in patients with type 2 diabetes and non-alcoholic fatty liver disease, as evidenced by the reduction in ALT, AST, fasting glucose and HbA1c.

H2S mitigates severe acute pancreatitis through the PI3K/AKT-NF-κB pathway in vivo.

AIM: To study the effect of hydrogen sulfide (H2S) on severe acute pancreatitis (SAP) in a rat model. METHODS: Sprague-Dawley (SD) rats were administered an intraperitoneal injection of saline containing 20% L-Arg (250 mg/100 g) hourly for over 2 h to induce SAP. The rats were treated with DL-propargylglycine (PAG, 50 mg/kg) or different dosages of NaHS (5 mg/kg, 10 mg/kg, 20 mg/kg or 100 mg/kg). PAG or NaHS was administered 1 h before induction of pancreatitis. Rats were sacrificed 24 h after the last L-Arg injection. Blood and pancreas tissues were collected. RESULTS: The H2S and cystathionine-γ-lyase mRNA levels in SAP rats were significantly lower than those in the control group, and treatment with PAG further reduced the H2S level. Nevertheless, H2S was significantly increased after NaHS administration compared with the SAP group, and the degree of upregulation was associated with the NaHS dosage. NaHS reduced the levels of plasma amylase, interleukin-6 and myeloperoxidase in pancreatic tissue. NaHS suppressed the degradation of IκBα and the activity of nuclear factor-κB, as well as the phosphorylation of PI3K/AKT. CONCLUSION: H2S plays an anti-inflammatory role in SAP in vivo.