@article{DwiPutraReichetzederHasanetal.2020,
  author    = {Dwi Putra, Sulistyo Emantoko and Reichetzeder, Christoph and Hasan, Ahmed Abdallah Abdalrahman Mohamed and Slowinski, Torsten and Chu, Chang and Kr{\"a}mer, Bernhard K. and Kleuser, Burkhard and Hocher, Berthold},
  title     = {Being born large for gestational age is associated with increased global placental DNA methylation},
  series = {Scientific Reports},
  volume    = {10},
  journal   = {Scientific Reports},
  number    = {1},
  publisher = {Springer Nature},
  address   = {London},
  issn      = {2045-2322},
  doi       = {10.1038/s41598-020-57725-0},
  pages     = {1 -- 10},
  year      = {2020},
  abstract  = {Being born small (SGA) or large for gestational age (LGA) is associated with adverse birth outcomes and metabolic diseases in later life of the offspring. It is known that aberrations in growth during gestation are related to altered placental function. Placental function is regulated by epigenetic mechanisms such as DNA methylation. Several studies in recent years have demonstrated associations between altered patterns of DNA methylation and adverse birth outcomes. However, larger studies that reliably investigated global DNA methylation are lacking. The aim of this study was to characterize global placental DNA methylation in relationship to size for gestational age. Global DNA methylation was assessed in 1023 placental samples by LC-MS/MS. LGA offspring displayed significantly higher global placental DNA methylation compared to appropriate for gestational age (AGA; p<0.001). ANCOVA analyses adjusted for known factors impacting on DNA methylation demonstrated an independent association between placental global DNA methylation and LGA births (p<0.001). Tertile stratification according to global placental DNA methylation levels revealed a significantly higher frequency of LGA births in the third tertile. Furthermore, a multiple logistic regression analysis corrected for known factors influencing birth weight highlighted an independent positive association between global placental DNA methylation and the frequency of LGA births (p=0.001).},
  language  = {en}
}
@article{BaerFegerFajoletal.2018,
  author    = {B{\"a}r, Ludmilla and Feger, Martina and Fajol, Abul and Klotz, Lars-Oliver and Zeng, Shufei and Lang, Florian and Hocher, Berthold and F{\"o}ller, Michael},
  title     = {Insulin suppresses the production of fibroblast growth factor 23 (FGF23)},
  series = {Proceedings of the National Academy of Sciences of the United States of America},
  volume    = {115},
  journal   = {Proceedings of the National Academy of Sciences of the United States of America},
  number    = {22},
  publisher = {National Acad. of Sciences},
  address   = {Washington},
  issn      = {0027-8424},
  doi       = {10.1073/pnas.1800160115},
  pages     = {5804 -- 5809},
  year      = {2018},
  abstract  = {Fibroblast growth factor 23 (FGF23) is produced by bone cells and regulates renal phosphate and vitamin D metabolism, as well as causing left ventricular hypertrophy. FGF23 deficiency results in rapid aging, whereas high plasma FGF23 levels are found in several disorders, including kidney or cardiovascular diseases. Regulators of FGF23 production include parathyroid hormone (PTH), calcitriol, dietary phosphate, and inflammation. We report that insulin and insulin-like growth factor 1 (IGF1) are negative regulators of FGF23 production. In UMR106 osteoblast-like cells, insulin and IGF1 down-regulated FGF23 production by inhibiting the transcription factor forkhead box protein O1 (FOXO1) through phosphoinositide 3-kinase (PI3K)/protein kinase B (PKB)/Akt signaling. Insulin deficiency caused a surge in the serum FGF23 concentration in mice, which was reversed by administration of insulin. In women, a highly significant negative correlation between FGF23 plasma concentration and increase in plasma insulin level following an oral glucose load was found. Our results provide strong evidence that insulin/IGF1dependent PI3K/PKB/Akt/FOXO1 signaling is a powerful suppressor of FGF23 production in vitro as well as in mice and in humans.},
  language  = {en}
}
@article{TaoSuXuetal.2018,
  author    = {Tao, Ting and Su, Qiongli and Xu, Simeng and Deng, Jun and Zhou, Sichun and Zhuang, Yu and Huang, Yanjun and He, Caimei and He, Shanping and Peng, Mei and Hocher, Berthold and Yang, Xiaoping},
  title     = {Down-regulation of PKM2 decreases FASN expression in bladder cancer cells through AKT/mTOR/SREBP-1c axis},
  series = {Journal of cellular physiology},
  volume    = {234},
  journal   = {Journal of cellular physiology},
  number    = {3},
  publisher = {Wiley},
  address   = {Hoboken},
  issn      = {0021-9541},
  doi       = {10.1002/jcp.27129},
  pages     = {3088 -- 3104},
  year      = {2018},
  abstract  = {Fatty acid synthase (FASN) catalyzing the terminal steps in the de novo biogenesis of fatty acids is correlated with low survival and high disease recurrence in patients with bladder cancer. Pyruvate kinase M2 (PKM2) regulates the final step of glycolysis levels and provides a growth advantage to tumors. However, it is unclear whether the change of PKM2 has an effect on FASN and what is the mechanisms underlying. Here we describe a novel function of PKM2 in control of lipid metabolism by mediating transcriptional activation of FASN, showing the reduced expression of sterol regulatory element binding protein 1c (SREBP-1c). We first discovered that PKM2 physically interacts with the SREBP-1c using biochemical approaches, and downregulation of PKM2 reduced the expression of SREBP-1c by inactivating the AKT/mTOR signaling pathway, which in turn directly suppressed the transcription of major lipogenic genes FASN to reduce tumor growths. Furthermore, either PKM2 inhibitor-Shikonin or FASN inhibitor-TVB-3166 alone induced a strong antiproliferative and anticolony forming effect in bladder cancer cell line. The combination of both inhibitors exhibits a super synergistic effect on blocking the bladder cancer cells growth. It provides a new target and scientific basis for the treatment of bladder cancer.},
  language  = {en}
}
@misc{LiTsuprykovYangetal.2016,
  author    = {Li, Jian and Tsuprykov, Oleg and Yang, Xiaoping and Hocher, Berthold},
  title     = {Paternal programming of offspring cardiometabolic diseases in later life},
  series = {Journal of hypertension},
  volume    = {34},
  journal   = {Journal of hypertension},
  publisher = {Wiley-Blackwell},
  address   = {Philadelphia},
  issn      = {0263-6352},
  doi       = {10.1097/HJH.0000000000001051},
  pages     = {2111 -- 2126},
  year      = {2016},
  language  = {en}
}