@misc{ReichetzederPutraLietal.2016,
  author    = {Reichetzeder, Christoph and Putra, Sulistyo Emantoko Dwi and Li, Jian and Hocher, Berthold},
  title     = {Developmental Origins of Disease - Crisis Precipitates Change},
  series = {Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry and pharmacology},
  volume    = {39},
  journal   = {Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry and pharmacology},
  publisher = {Karger},
  address   = {Basel},
  issn      = {1015-8987},
  doi       = {10.1159/000447801},
  pages     = {919 -- 938},
  year      = {2016},
  abstract  = {The concept of developmental origins of diseases has gained a huge interest in recent years and is a constantly emerging scientific field. First observations hereof originated from epidemiological studies, linking impaired birth outcomes to adult chronic, noncommunicable disease. By now there is a considerable amount of both epidemiological and experimental evidence highlighting the impact of early life events on later life disease susceptibility. Albeit far from being completely understood, more recent studies managed to elucidate underlying mechanisms, with epigenetics having become almost synonymous with developmental programming. The aim of this review was to give a comprehensive overview of various aspects and mechanisms of developmental origins of diseases. Starting from initial research foci mainly centered on a nutritionally impaired intrauterine environment, more recent findings such as postnatal nutrition, preterm birth, paternal programming and putative interventional approaches are summarized. The review outlines general underlying mechanisms and particularly discusses mechanistic explanations for sexual dimorphism in developmental programming. Furthermore, novel hypotheses are presented emphasizing a non-mendelian impact of parental genes on the offspring's phenotype.},
  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}
}
@misc{YangDarkoHuangetal.2017,
  author    = {Yang, Xiaoping and Darko, Kwame Oteng and Huang, Yanjun and He, Caimei and Yang, Huansheng and He, Shanping and Li, Jianzhong and Li, Jian and Hocher, Berthold and Yin, Yulong},
  title     = {Resistant starch regulates gut microbiota},
  series = {Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry and pharmacology},
  volume    = {42},
  journal   = {Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry and pharmacology},
  number    = {1},
  publisher = {Karger},
  address   = {Basel},
  issn      = {1015-8987},
  doi       = {10.1159/000477386},
  pages     = {306 -- 318},
  year      = {2017},
  abstract  = {Starch is one of the most popular nutritional sources for both human and animals. Due to the variation of its nutritional traits and biochemical specificities, starch has been classified into rapidly digestible, slowly digestible and resistant starch. Resistant starch has its own unique chemical structure, and various forms of resistant starch are commercially available. It has been found being a multiple-functional regulator for treating metabolic dysfunction. Different functions of resistant starch such as modulation of the gut microbiota, gut peptides, circulating growth factors, circulating inflammatory mediators have been characterized by animal studies and clinical trials. In this mini-review, recent remarkable progress in resistant starch on gut microbiota, particularly the effect of structure, biochemistry and cell signaling on nutrition has been summarized, with highlights on its regulatory effect on gut microbiota.},
  language  = {en}
}
@misc{TianReichetzederLietal.2019,
  author    = {Tian, Mei and Reichetzeder, Christoph and Li, Jian and Hocher, Berthold},
  title     = {Low birth weight, a risk factor for diseases in later life, is a surrogate of insulin resistance at birth},
  series = {Journal of hypertension},
  volume    = {37},
  journal   = {Journal of hypertension},
  number    = {11},
  publisher = {Kluwer},
  address   = {Philadelphia},
  issn      = {0263-6352},
  doi       = {10.1097/HJH.0000000000002156},
  pages     = {2123 -- 2134},
  year      = {2019},
  abstract  = {Low birth weight (LBW) is associated with diseases in adulthood. The birthweight attributed risk is independent of confounding such as gestational age, sex of the newborn but also social factors. The birthweight attributed risk for diseases in later life holds for the whole spectrum of birthweight. This raises the question what pathophysiological principle is actually behind the association. In this review, we provide evidence that LBW is a surrogate of insulin resistance. Insulin resistance has been identified as a key factor leading to type 2 diabetes, cardiovascular disease as well as kidney diseases. We first provide evidence linking LBW to insulin resistance during intrauterine life. This might be caused by both genetic (genetic variations of genes controlling glucose homeostasis) and/or environmental factors (due to alterations of macronutrition and micronutrition of the mother during pregnancy, but also effects of paternal nutrition prior to conception) leading via epigenetic modifications to early life insulin resistance and alterations of intrauterine growth, as insulin is a growth factor in early life. LBW is rather a surrogate of insulin resistance in early life - either due to inborn genetic or environmental reasons - rather than a player on its own.},
  language  = {en}
}