The potential relationship between vitamin D (VitD) status and metabolic control in patients with type 2 diabetes mellitus (T2DM) warrants further study. We aimed to evaluate the relationship between the serum 25-hydroxyvitamin D [25(OH)D] level and various parameters in patients with T2DM. We analyzed retrospectively data from 276 Korean patients with T2DM whose serum 25(OH)D level was measured in our hospital. Nondiabetic healthy subjects who visited the hospital for health screening were selected as the control group (Non-DM, n=160). Compared with control subjects, patients with T2DM had a lower serum 25(OH)D level (15.4±0.5 vs. 12.9±0.4 ng/ml, p<0.01). Eleven percent of T2DM patients were VitD "insufficient" (20-29 ng/ml) and 87% of the patients were VitD "deficient" (<20 ng/ml). The serum 25(OH)D level was significantly related to serum fibrinogen, triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), ferritin, the urine albumin creatinine ratio, and hemoglobin A1C (HbA1C). In a multivariate logistic regression analysis, high levels of HbA1C, TG, and LDL-C were independently associated with VitD deficiency in T2DM patients. The results of the present study show that the majority of Koreans with T2DM are VitD deficient, and the serum 25(OH)D level in patients with T2DM is related to lipid and glucose parameters. Further studies are required of the relationship of VitD with fibrinogen and other related parameters.

BackgroundDipeptidyl peptidase 4 (DPP-4, also known as CD26) binds with adenosine deaminase (ADA) to activate T lymphocytes. Here, we investigated whether ADA activity is specifically affected by treatment with DPP-4 inhibitor (DPP4I) compared with other anti-diabetic agents.MethodsFasting ADA activity, in addition to various metabolic and biochemical parameters, were measured in 262 type 2 diabetes mellitus (T2DM) patients taking various anti-diabetic agents and in 46 non-diabetic control subjects.ResultsADA activity was increased in T2DM patients compared with that in non-diabetic control subjects (mean±standard error, 23.1±0.6 U/L vs. 18.6±0.8 U/L; P<0.05). ADA activity was correlated with fasting plasma glucose (r=0.258, P<0.05), HbA1c (r=0.208, P<0.05), aspartate aminotransferase (r=0.325, P<0.05), and alanine aminotransferase (r=0.248, P<0.05). Compared with the well-controlled T2DM patients (HbA1c<7%), the poorly controlled group (HbA1c>9%) showed significantly increased ADA activity (21.1±0.8 U/L vs. 25.4±1.6 U/L; P<0.05). The effect of DPP4I on ADA activity in T2DM patients did not differ from those of other oral anti-diabetic agents or insulin. T2DM patients on metformin monotherapy showed a lower ADA activity (20.9±1.0 U/L vs. 28.1±2.8 U/L; P<0.05) compared with that of those on sulfonylurea monotherapy.ConclusionOur results show that ADA activity is increased in T2DM patients compared to that in non-diabetic patients, is positively correlated with blood glucose level, and that DPP4I has no additional specific effect on ADA activity, except for a glycemic control- or HbA1c-dependent effect.

Aims This observational study aimed to investigate the association between beta-blocker therapy and clinical outcomes in patients with acute myocardial infarction (AMI), especially with mid-range or preserved left ventricular systolic function. Methods and results Among 13 624 patients enrolled in the Korea Acute Myocardial Infarction Registry-National Institute of Health (KAMIR-NIH), 12 200 in-hospital survivors were selected. Patients with beta-blockers showed significantly lower 1-year major adverse cardiac events (MACE), which was a composite of cardiac death, MI, revascularization, and readmission due to heart failure [9.7 vs. 14.3/100 patient-year; hazard ratio (HR) 0.84, 95% confidence interval (CI) 0.72–0.97; P = 0.022). However, this association had a significant interaction with left ventricular ejection fraction (LVEF). Beta-blocker therapy at discharge was associated with lower 1-year MACE in patients with LVEF ≤40% (HR 0.63, 95% CI 0.48–0.81; P &lt; 0.001), and 40% &lt;LVEF &lt; 50% (HR 0.69, 95% CI 0.51–0.94; P = 0.020), but not in patients with LVEF ≥50% (HR 1.16, 95% CI 0.91–1.48; P = 0.234). Conclusions Beta-blocker therapy at discharge was associated with better 1-year clinical outcomes in patients with reduced or mid-range LVEF after AMI, but not in patients with preserved LVEF. These data suggested that the long-term beta-blocker therapy may be guided by LVEF.

Background: New-onset diabetes after transplantation (NODAT) is a serious complication following liver transplantation (LT). The present study aimed to investigate the incidence of and risk factors for NODAT using the Korean Organ Transplantation Registry (KOTRY) database.Methods: Patients with history of pediatric transplantation (age ≤18 years), re-transplantation, multi-organ transplantation, or pre-existing diabetes mellitus were excluded. A total of 1,919 non-diabetic adult patients who underwent a primary LT between May 2014 and December 2017 were included. Risk factors were identified using Cox regression analysis. Results: NODAT occurred in 19.7% (n=377) of adult liver transplant recipients. Multivariate analysis showed steroid use, increased age, and high body mass index (BMI) in recipients, and implantation of a leftside liver graft was closely associated with NODAT in adult LT. In living donor liver transplant (LDLT) patients (n=1,473), open donor hepatectomy in the living donors, steroid use, small for size liver graft (graft to recipient weight ratio ≤0.8), increased age, and high BMI in the recipient were predictive factors for NODAT. The use of antimetabolite and basiliximab induction reduced the incidence of NODAT in adult LT and in adult LDLT. Conclusions: Basiliximab induction, early steroid withdrawal, and antimetabolite therapy may prevent NODAT after adult LT. High BMI or advanced age in liver recipients, open donor hepatectomy in living donors, and small size liver graft can predict the occurrence of NODAT after adult LT or LDLT.

No abstract

No abstract

No abstract

The microbiota–gut–brain axis (MGBA) is a bidirectional signaling pathway mediating the interaction of the microbiota, the intestine, and the central nervous system. While the MGBA plays a pivotal role in normal development and physiology of the nervous and gastrointestinal system of the host, its dysfunction has been strongly implicated in neurological disorders, where intestinal dysbiosis and derived metabolites cause barrier permeability defects and elicit local inflammation of the gastrointestinal tract, concomitant with increased pro-inflammatory cytokines, mobilization and infiltration of immune cells into the brain, and the dysregulated activation of the vagus nerve, culminating in neuroinflammation and neuronal dysfunction of the brain and behavioral abnormalities. In this topical review, we summarize recent findings in human and animal models regarding the roles of the MGBA in physiological and neuropathological conditions, and discuss the molecular, genetic, and neurobehavioral characteristics of zebrafish as an animal model to study the MGBA. The exploitation of zebrafish as an amenable genetic model combined with in vivo imaging capabilities and gnotobiotic approaches at the whole organism level may reveal novel mechanistic insights into microbiota–gut–brain interactions, especially in the context of neurological disorders such as autism spectrum disorder and Alzheimer’s disease.