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Background and aims: Individuals with type 2 diabetes (T2D) have a higher risk of cardiovascular disease, compared with those without T2D. The serum T50 test captures the transformation time of calciprotein particles in serum. We aimed to assess whether serum T50 predicts cardiovascular mortality in T2D patients, independent of traditional risk factors. Methods: We analyzed 621 individuals with T2D in this prospective cohort study. Cox regression models were performed to test the association between serum T50 and cardiovascular and all‐cause mortality. Causes of death were categorized according to ICD‐10 codes. Risk prediction improvement was assessed by comparing Harrell's C for models without and with T50. Results: The mean age was 64.2 ± 9.8 years, and 61% were male. The average serum T50 time was 323 ± 63 min. Higher age, alcohol use, high‐sensitive C‐reactive protein, and plasma phosphate were associated with lower serum T50 levels. Higher plasma triglycerides, venous bicarbonate, sodium, magnesium, and alanine aminotransferase were associated with higher serum T50 levels. After a follow‐up of 7.5[5.4–10.7] years, each 60 min decrease in serum T50 was associated with an increased risk of cardiovascular (fully adjusted HR 1.32, 95% CI 1.08–1.50, and p = 0.01) and all‐cause mortality (HR 1.15, 95%CI 1.00–1.38, and p = 0.04). Results were consistent in sensitivity analyses after exclusion of individuals with estimated glomerular filtration rate <45 or <60 mL/min/1.73 m2 and higher plasma phosphate levels. Conclusions: Serum T50 improves prediction of cardiovascular and all‐cause mortality risk in individuals with T2D. Serum T50 may be useful for risk stratification and to guide therapeutic strategies aiming to reduce cardiovascular mortality in T2D. [ABSTRACT FROM AUTHOR]

Background: Cardiovascular disease (CVD) is the major cause of mortality in type 1 diabetes (T1D). The objective of this study is to evaluate fibroblast growth factor 23 (FGF23) and calcium‐phosphate metabolism in relation to cardiovascular risk factors in adults with and without T1D. Methods: A case–control study was conducted using data from patients with T1D and age‐ and sex matched controls without T1D from the Lifelines Cohort Study. Results: We included 302 adults in the T1D group and 302 adults in the control group. Median age was 42 years. Median glycosylated hemoglobin (HbA1c) in the T1D group was 7.8%. FGF23 of all patients with T1D was not significantly different from controls. Females with T1D had significantly higher FGF23 than males with T1D (83.3 vs 69.3 U/mL, p = 0.002), this was not observed in controls. Serum phosphate, calcium, and alkaline phosphatase were higher and parathyroid hormone was lower in patients with T1D, compared to controls (all p <.001), all within normal range. In the T1D group, FGF23 was positively correlated with serum phosphate (p <.001), alkaline phosphatase (p =.01), and calcium (p =.030), these correlations were not observed in controls. Median FGF23 was significantly higher in current smokers than in nonsmokers with T1D (84.9 vs 73.5 U/mL, p <.05). Conclusions: Serum calcium, phosphate, and alkaline phosphatase were higher in patients with T1D than in controls and were positively correlated to FGF23 in patients with T1D. Current smokers with T1D had higher FGF23 than nonsmokers with T1D. These findings may contribute to the increased risk of CVD in patients with T1D. [ABSTRACT FROM AUTHOR]

Objective This work aimed to study whether fibroblast growth factor 23 (FGF23) is predictive for incident posttransplant diabetes mellitus (PTDM) in kidney transplant recipients (KTRs). Methods We repeatedly analyzed plasma C-terminal FGF23 concentrations in 170 KTRs enrolled in the TransplantLines Biobank and Cohort Study. Associations of time-updated plasma FGF23 with incident PTDM were studied by Cox regression. Results A total of 170 KTRs (46% female, aged 54.4 ± 12.4 years) with 540 FGF23 measurements were included. Plasma FGF23 concentrations at transplantation were 31.1 (0.76-2576) pmol/L. During a follow-up of 24 (12-24) months, 38 patients developed PTDM. The highest FGF23 tertile (compared to the lowest) was associated with an increased risk for PTDM (fully adjusted hazard ratio 20.9; 95% CI, 3.4-130.0; P <.001). Conclusion In KTRs without diabetes at baseline, the highest tertile of FGF23, compared to the lowest, is predictive for development of PTDM. [ABSTRACT FROM AUTHOR]

The impact of pre-transplant parathyroid hormone (PTH) levels on early or long-term kidney function after kidney transplantation is subject of debate. We assessed whether severe hyperparathyroidism is associated with delayed graft function (DGF), deathcensored graft failure (DCGF), or all-cause mortality. In this single-center cohort study, we studied the relationship between PTH and other parameters related to bone and mineral metabolism, including serum alkaline phosphatase (ALP) at time of transplantation with the subsequent risk of DGF, DCGF and all-cause mortality using multivariable logistic and Cox regression analyses. In 1,576 kidney transplant recipients (51.6 ± 14.0 years, 57.3% male), severe hyperparathyroidism characterized by pre-transplant PTH ≥771 pg/ mL (>9 times the upper limit) was present in 121 patients. During 5.2 [0.2--30.0] years follow-up, 278 (15.7%) patients developed DGF, 150 (9.9%) DCGF and 432 (28.6%) died. A higher pre-transplant PTH was not associated with DGF (HR 1.06 [0.90--1.25]), DCGF (HR 0.98 [0.87--1.13]), or all-cause mortality (HR 1.02 [0.93--1.11]). Results were consistent in sensitivity analyses. The same applied to other parameters related to bone and mineral metabolism, including ALP. Severe pre-transplant hyperparathyroidism was not associated with an increased risk of DGF, DCGF or all-cause mortality, not supporting the need of correction before kidney transplantation to improve graft or patient survival. [ABSTRACT FROM AUTHOR]

Higher betaine is associated with lower incidence of microvascular complications in type 2 diabetes (Zodiac-61) Betaine serves as a methyl donor in a reaction catalysed by betaine homocysteine methyltransferase, which converts homocysteine to methionine.[1] Betaine is thus required for the remethylation of homocysteine to methionine, a precursor of the universal methyl donor S-adenosylmethionine (SAM), with an essential role in many body processes. Keywords: betaine; microvascular complications; type 2 diabetes EN betaine microvascular complications type 2 diabetes 1 3 3 12/15/22 20230101 NES 230101 Abbreviations NMR Nuclear magnetic resonance T2D Type 2 diabetes SAM S-adenosylmethionine VEGF Vascular endothelial growth factor ZODIAC Zwolle Outpatient Diabetes project Integrating Available Care Betaine (N,N,N-trimethylglycine) is a gut microbiome-derived osmolyte, and its concentration in plasma is in part dependent on dietary intake.[1] Dietary sources include shellfish, wheat, beets and spinach. [Extracted from the article]