@article{KluthStadionGottmannetal.2019,
  author    = {Kluth, Oliver and Stadion, Mandy and Gottmann, Pascal and Aga-Barfknecht, Heja and J{\"a}hnert, Markus and Scherneck, Stephan and Vogel, Heike and Krus, Ulrika and Seelig, Anett and Ling, Charlotte and Gerdes, Jantje and Sch{\"u}rmann, Annette},
  title     = {Decreased expression of cilia genes in pancreatic islets as a risk factor for type 2 diabetes in mice and humans},
  series = {Cell reports},
  volume    = {26},
  journal   = {Cell reports},
  number    = {11},
  publisher = {Cell Press},
  address   = {Maryland Heights},
  issn      = {2211-1247},
  doi       = {10.1016/j.celrep.2019.02.056},
  pages     = {3027 -- 3036},
  year      = {2019},
  abstract  = {An insufficient adaptive beta-cell compensation is a hallmark of type 2 diabetes (T2D). Primary cilia function as versatile sensory antennae regulating various cellular processes, but their role on compensatory beta-cell replication has not been examined. Here, we identify a significant enrichment of downregulated, cilia-annotated genes in pancreatic islets of diabetes-prone NZO mice as compared with diabetes-resistant B6-ob/ob mice. Among 327 differentially expressed mouse cilia genes, 81 human orthologs are also affected in islets of diabetic donors. Islets of nondiabetic mice and humans show a substantial overlap of upregulated cilia genes that are linked to cell-cycle progression. The shRNA-mediated suppression of KIF3A, essential for ciliogenesis, impairs division of MINE beta cells as well as in dispersed primary mouse and human islet cells, as shown by decreased BrdU incorporation. These findings demonstrate the substantial role of cilia-gene regulation on islet function and T2D risk.},
  language  = {en}
}
@article{AgaBarfknechtSoultoukisStadionetal.2022,
  author    = {Aga-Barfknecht, Heja and Soultoukis, George A. and Stadion, Mandy and Garcia-Carrizo, Francisco and J{\"a}hnert, Markus and Gottmann, Pascal and Vogel, Heike and Schulz, Tim Julius and Sch{\"u}rmann, Annette},
  title     = {Distinct adipogenic and fibrogenic differentiation capacities of mesenchymal stromal cells from pancreas and white adipose tissue},
  series = {International journal of molecular sciences},
  volume    = {23},
  journal   = {International journal of molecular sciences},
  number    = {4},
  publisher = {Molecular Diversity Preservation International},
  address   = {Basel},
  issn      = {1422-0067},
  doi       = {10.3390/ijms23042108},
  pages     = {21},
  year      = {2022},
  abstract  = {Pancreatic steatosis associates with beta-cell failure and may participate in the development of type-2-diabetes. Our previous studies have shown that diabetes-susceptible mice accumulate more adipocytes in the pancreas than diabetes-resistant mice. In addition, we have demonstrated that the co-culture of pancreatic islets and adipocytes affect insulin secretion. The aim of this current study was to elucidate if and to what extent pancreas-resident mesenchymal stromal cells (MSCs) with adipogenic progenitor potential differ from the corresponding stromal-type cells of the inguinal white adipose tissue (iWAT). miRNA (miRNome) and mRNA expression (transcriptome) analyses of MSCs isolated by flow cytometry of both tissues revealed 121 differentially expressed miRNAs and 1227 differentially expressed genes (DEGs). Target prediction analysis estimated 510 DEGs to be regulated by 58 differentially expressed miRNAs. Pathway analyses of DEGs and miRNA target genes showed unique transcriptional and miRNA signatures in pancreas (pMSCs) and iWAT MSCs (iwatMSCs), for instance fibrogenic and adipogenic differentiation, respectively. Accordingly, iwatMSCs revealed a higher adipogenic lineage commitment, whereas pMSCs showed an elevated fibrogenesis. As a low degree of adipogenesis was also observed in pMSCs of diabetes-susceptible mice, we conclude that the development of pancreatic steatosis has to be induced by other factors not related to cell-autonomous transcriptomic changes and miRNA-based signals.},
  language  = {en}
}
@article{StadionSchuermann2020,
  author    = {Stadion, Mandy and Sch{\"u}rmann, Annette},
  title     = {Intermittent fasting},
  series = {Psychotherapeut},
  volume    = {66},
  journal   = {Psychotherapeut},
  number    = {1},
  publisher = {Springer},
  address   = {New York},
  issn      = {0935-6185},
  doi       = {10.1007/s00278-020-00471-5},
  pages     = {23 -- 27},
  year      = {2020},
  abstract  = {A long-term positive energy balance leads to overweight and obesity. Adiposity is the main risk factor for cardiovascular diseases, type 2 diabetes and cancer and is often accompanied by depression. The increasing prevalence creates a major problem for the healthcare system. The conservative management of obesity strives for weight loss by reducing the daily caloric intake and increasing physical activity as well as an improvement in the quality of life supported by psychological interventions. For reducing body weight, intermittent fasting represents an alternative to continuous calorie restriction as it can be easily integrated into daily life. In this form of diet calorie intake is limited in time, i.e. on 2 days in the week or 6-10 h per day. Animal and human studies provide evidence that intermittent fasting over a longer time period is a suitable method to decrease body fat and to improve many metabolic parameters. Fasting alters metabolism and activates specific cellular pathways. These have not only cardioprotective effects but also neuroprotective and antidepressive effects. In this article the currently discussed mechanisms induced by intermittent fasting are highlighted and the essential observations from randomized controlled human trials are presented.},
  language  = {de}
}
@article{StadionSchuermann2020,
  author    = {Stadion, Mandy and Sch{\"u}rmann, Annette},
  title     = {Intermittierendes Fasten},
  series = {Der Diabetologe},
  volume    = {16},
  journal   = {Der Diabetologe},
  number    = {7},
  publisher = {Springer Medizin},
  address   = {Berlin},
  issn      = {1860-9716},
  doi       = {10.1007/s11428-020-00666-z},
  pages     = {641 -- 646},
  year      = {2020},
  abstract  = {Obesity increases the risk of metabolic disorders and can lead to type 2 diabetes. Therefore, the treatment and prevention of obesity represent important medical challenges. Increased physical activity and a reduction in daily caloric intake of 25-30\% are often recommended. Another possibility is intermittent fasting, by limiting dietary caloric content over certain times, i.e. one or more days a week or for more than 14 h a day. Animal and human studies provide evidence that intermittent fasting in obesity leads to a reduction in body fat mass as well as to improvements of metabolic parameters and insulin sensitivity. These positive effects are mediated not only by the decrease in body mass, but also by the activation of metabolic pathways and cellular processes that are specific for fasting conditions. In this article, we describe the current knowledge about the mechanisms induced by intermittent fasting and present results from randomized controlled human trials.},
  language  = {de}
}
@article{QuicletDittbernerGaessleretal.2019,
  author    = {Quiclet, Charline and Dittberner, Nicole and Gaessler, Anneke and Stadion, Mandy and Gerst, Felicia and Helms, Anett and Baumeier, Christian and Schulz, Tim Julius and Schurmann, Annette},
  title     = {Pancreatic adipocytes mediate hypersecretion of insulin in diabetes-susceptible mice},
  series = {Metabolism - Clinical and experimental},
  volume    = {97},
  journal   = {Metabolism - Clinical and experimental},
  publisher = {Elsevier},
  address   = {Philadelphia},
  issn      = {0026-0495},
  doi       = {10.1016/j.metabol.2019.05.005},
  pages     = {9 -- 17},
  year      = {2019},
  abstract  = {Objective: Ectopic fat accumulation in the pancreas in response to obesity and its implication on the onset of type 2 diabetes remain poorly understood. Intermittent fasting (IF) is known to improve glucose homeostasis and insulin resistance. However, the effects of IF on fat in the pancreas and beta-cell function remain largely unknown. Our aim was to evaluate the impact of IF on pancreatic fat accumulation and its effects on islet function. Methods: New Zealand Obese (NZO) mice were fed a high-fat diet ad libitum (NZO-AL) or fasted every other day (intermittent fasting, NZO-IF) and pancreatic fat accumulation, glucose homoeostasis, insulin sensitivity, and islet function were determined and compared to ad libitum-fed B6.V-Lep(ob/ob) (ob/ob) mice. To investigate the crosstalk of pancreatic adipocytes and islets, co-culture experiments were performed. Results: NZO-IF mice displayed better glucose homeostasis and lower fat accumulation in both the pancreas (-32\%) and the liver (-35\%) than NZO-AL mice. Ob/ob animals were insulin-resistant and had low fat in the pancreas but high fat in the liver. NZO-AL mice showed increased fat accumulation in both organs and exhibited an impaired islet function. Co-culture experiments demonstrated that pancreatic adipocytes induced a hypersecretion of insulin and released higher levels of free fatty adds than adipocytes of inguinal white adipose tissue. Conclusions: These results suggest that pancreatic fat participates in diabetes development, but can be prevented by IF. (C) 2019 Published by Elsevier Inc.},
  language  = {en}
}
@article{KehmJaehnertDeubeletal.2020,
  author    = {Kehm, Richard and J{\"a}hnert, Markus and Deubel, Stefanie and Flore, Tanina and K{\"o}nig, Jeannette and Jung, Tobias and Stadion, Mandy and Jonas, Wenke and Sch{\"u}rmann, Annette and Grune, Tilman and H{\"o}hn, Annika},
  title     = {Redox homeostasis and cell cycle activation mediate beta-cell mass expansion in aged, diabetes-prone mice under metabolic stress conditions: role of thioredoxin-interacting protein (TXNIP)},
  series = {Redox Biology},
  volume    = {37},
  journal   = {Redox Biology},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {2213-2317},
  doi       = {10.1016/j.redox.2020.101748},
  pages     = {11},
  year      = {2020},
  abstract  = {Overnutrition contributes to insulin resistance, obesity and metabolic stress, initiating a loss of functional beta-cells and diabetes development. Whether these damaging effects are amplified in advanced age is barely investigated. Therefore, New Zealand Obese (NZO) mice, a well-established model for the investigation of human obesity-associated type 2 diabetes, were fed a metabolically challenging diet with a high-fat, carbohydrate restricted period followed by a carbohydrate intervention in young as well as advanced age. Interestingly, while young NZO mice developed massive hyperglycemia in response to carbohydrate feeding, leading to beta-cell dysfunction and cell death, aged counterparts compensated the increased insulin demand by persistent beta-cell function and beta-cell mass expansion. Beta-cell loss in young NZO islets was linked to increased expression of thioredoxin-interacting protein (TXNIP), presumably initiating an apoptosis-signaling cascade via caspase-3 activation. In contrast, islets of aged NZOs exhibited a sustained redox balance without changes in TXNIP expression, associated with higher proliferative potential by cell cycle activation. These findings support the relevance of a maintained proliferative potential and redox homeostasis for preserving islet functionality under metabolic stress, with the peculiarity that this adaptive response emerged with advanced age in diabetesprone NZO mice.},
  language  = {en}
}