@article{LiLuTsuprykovetal.2018,
  author    = {Li, Jian and Lu, Yong-Ping and Tsuprykov, Oleg and Hasan, Ahmed Abdallah Abdalrahman Mohamed and Reichetzeder, Christoph and Tian, Mei and Zhang, Xiao Li and Zhang, Qin and Sun, Guo-Ying and Guo, Jingli and Gaballa, Mohamed Mahmoud Salem Ahmed and Peng, Xiao-Ning and Lin, Ge and Hocher, Berthold},
  title     = {Folate treatment of pregnant rat dams abolishes metabolic effects in female offspring induced by a paternal pre-conception unhealthy diet},
  series = {Diabetologia : journal of the European Association for the Study of Diabetes (EASD)},
  volume    = {61},
  journal   = {Diabetologia : journal of the European Association for the Study of Diabetes (EASD)},
  number    = {8},
  publisher = {Springer},
  address   = {New York},
  issn      = {0012-186X},
  doi       = {10.1007/s00125-018-4635-x},
  pages     = {1862 -- 1876},
  year      = {2018},
  abstract  = {Aims/hypothesis Paternal high-fat diet prior to mating programmes impaired glucose tolerance in female offspring. We examined whether the metabolic consequences in offspring could be abolished by folate treatment of either the male rats before mating or the corresponding female rats during pregnancy. Methods Male F0 rats were fed either control diet or high-fat, high-sucrose and high-salt diet (HFSSD), with or without folate, before mating. Male rats were mated with control-diet-fed dams. After mating, the F0 dams were fed control diet with or without folate during pregnancy.},
  language  = {en}
}
@article{TsuprykovChenHocheretal.2018,
  author    = {Tsuprykov, Oleg and Chen, Xin and Hocher, Carl-Friedrich and Skoblo, Roman and Yin, Lianghong and Hocher, Berthold},
  title     = {Why should we measure free 25(OH) vitamin D?},
  series = {The Journal of Steroid Biochemistry and Molecular Biology},
  volume    = {180},
  journal   = {The Journal of Steroid Biochemistry and Molecular Biology},
  publisher = {Elsevier},
  address   = {Oxford},
  issn      = {0960-0760},
  doi       = {10.1016/j.jsbmb.2017.11.014},
  pages     = {87 -- 104},
  year      = {2018},
  abstract  = {Vitamin D, either in its D-2 or D-3 form, is essential for normal human development during intrauterine life, kidney function and bone health. Vitamin D deficiency has also been linked to cancer development and some auto immune diseases. Given this huge impact of vitamin Don human health, it is important for daily clinical practice and clinical research to have reliable tools to judge on the vitamin D status. The major circulating form of vitamin D is 25-hydroxyvitamin D (25(OH)D), although it is not the most active metabolite, the concentrations of total 25-hydroxyvitamin D in the serum are currently routinely used in clinical practice to assess vitamin D status. In the circulation, vitamin D - like other steroid hormones - is bound tightly to a special carrier - vitamin D-binding protein (DBP). Smaller amounts are bound to blood proteins - albumin and lipoproteins. Only very tiny amounts of the total vitamin D are free and potentially biologically active. Currently used vitamin D assays do not distinguish between the three forms of vitamin D - DBP-bound vitamin D, albumin-bound vitamin D and free, biologically active vitamin D. Diseases or conditions that affect the synthesis of DBP or albumin thus have a huge impact on the amount of circulating total vitamin D. DBP and albumin are synthesized in the liver, hence all patients with an impairment of liver function have alterations in their total vitamin D blood concentrations, while free vitamin D levels remain mostly constant. Sex steroids, in particular estrogens, stimulate the synthesis of DBP. This explains why total vitamin D concentrations are higher during pregnancy as compared to nonpregnant women, while the concentrations of free vitamin D remain similar in both groups of women. The vitamin D-DBP as well as vitamin D-albumin complexes are filtered through the glomeruli and re-uptaken by megalin in the proximal tubule. Therefore, all acute and chronic kidney diseases that are characterized by a tubular damage, are associated with a loss of vitamin D-DBP complexes in the urine. Finally, the gene encoding DBP protein is highly polymorphic in different human racial groups. In the current review, we will discuss how liver function, estrogens, kidney function and the genetic background might influence total circulating vitamin D levels and will discuss what vitamin D metabolite is more appropriate to measure under these conditions: free vitamin D or total vitamin D.},
  language  = {en}
}