@article{SunOrtegaTanetal.2018,
  author    = {Sun, Ping and Ortega, Gabriela and Tan, Yan and Hua, Qian and Riederer, Peter F. and Deckert, J{\"u}rgen and Schmitt-B{\"o}hrer, Angelika G.},
  title     = {Streptozotocin impairs proliferation and differentiation of adult hippocampal neural stem cells in vitro-correlation with alterations in the expression of proteins associated with the insulin system},
  series = {Frontiers in Aging Neuroscience},
  volume    = {10},
  journal   = {Frontiers in Aging Neuroscience},
  number    = {145},
  doi       = {10.3389/fnagi.2018.00145},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-176741},
  year      = {2018},
  abstract  = {Rats intracerebroventricularily (icv) treated with streptozotocin (STZ), shown to generate an insulin resistant brain state, were used as an animal model for the sporadic form of Alzheimer's disease (sAD). Previously, we showed in an in vivo study that 3 months after STZ icv treatment hippocampal adult neurogenesis (AN) is impaired. In the present study, we examined the effects of STZ on isolated adult hippocampal neural stem cells (NSCs) using an in vitro approach. We revealed that 2.5 mM STZ inhibits the proliferation of NSCs as indicated by reduced number and size of neurospheres as well as by less BrdU-immunoreactive NSCs. Double immunofluorescence stainings of NSCs already being triggered to start with their differentiation showed that STZ primarily impairs the generation of new neurons, but not of astrocytes. For revealing mechanisms possibly involved in mediating STZ effects we analyzed expression levels of insulin/glucose system-related molecules such as the glucose transporter (GLUT) 1 and 3, the insulin receptor (IR) and the insulin-like growth factor (IGF) 1 receptor. Applying quantitative Real time-PCR (qRT-PCR) and immunofluorescence stainings we showed that STZ exerts its strongest effects on GLUT3 expression, as GLUT3 mRNA levels were found to be reduced in NSCs, and less GLUT3-immunoreactive NSCs as well as differentiating cells were detected after STZ treatment. These findings suggest that cultured NSCs are a good model for developing new strategies to treat nerve cell loss in AD and other degenerative disorders.},
  language  = {en}
}
@article{StraussMoskalenkoTiurbeetal.2012,
  author    = {Strauss, Armin and Moskalenko, Vasily and Tiurbe, Christian and Chodnevskaja, Irina and Timm, Stephan and Wiegering, Verena A. and Germer, Chrioph Thomas and Ulrichs, Karin},
  title     = {Goettingen Minipigs (GMP): Comparison of Two Different Models for Inducing Diabetes},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-75119},
  year      = {2012},
  abstract  = {Purpose: Preclinical experiments on large animals are indispensable for evaluating the effectiveness of diabetes therapies. Miniature swine are well suited for such studies due to their physiological and pathophysiological responses. Methods: We compare two methods for inducing diabetes in Goettingen minipigs (GMP), in five with the beta cell toxin streptozotocin (STZ) and in five other GMP by total pancreatectomy (PE). Glucose homeostasis was assessed with the intravenous glucose-tolerance test (IVGTT) and continual monitoring of interstitial glucose levels. At conclusion of the observation period, the pancreata were examined histologically. Three non-diabetic GMP served as control group. Results: The IVGTT revealed markedly diabetic profiles in both GMP groups. STZ-GMP were found to harbor residual C-peptides and scattered insulin-positive cells in the pancreas. PE-GMP survived the total pancreatectomy only with intensive postoperative care. Conclusions: Although both methods reliably induced diabetes in GMP, the PE-GMP clearly had more health problems and required a greater expenditure of time and resources. The PE-GMP model, however, was better at eliminating endogenous insulin and C-peptide than the STZ-GMP model.},
  subject      = {G{\"o}ttingen},
  language  = {en}
}