Feenstra, M. (2016) The Intestinal Epithelial Barier in severely malnourished mice, and the role of autophagy. thesis, Medicine.
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Abstract
Malnutrition is a leading cause of infant and childhood mortality, and is associated with 45% of all child deaths annually. Enteric dysfunction is one of the leading comorbidities in severe acute malnutrition. The aim of this study was to answer the following research questions. In our animal model is severe malnutrition associated with impaired epithelial barrier function? Is autophagy affected in our animal model of severe malnutrition? Does induction of autophagy improve the epithelial barrier function in our animal model of malnutrition? In our murine model, we see a clear phenotype of enteric dysfunction in severe acute malnutrition consisted of villous blunting in the small intestine, crypt hypoplasia and goblet cells loss in the large intestine. In addition, multiple experiments, ex vivo and in vivo, showed a loss of intestinal epithelial barrier function through tight junction protein loss. Previous studies showed an association between autophagy and improvement in the intestinal epithelial barrier, therefor autophagy was induced to see if autophagy has an effect on the tight junction proteins in severe acute malnutrition. Autophagy is an essential biological pathway in human cells to maintain normal cell homeostasis, and is activated by nutritional stress. When inducing autophagy in our malnourished mice, we saw an increased levels of tight junction proteins. Therefor autophagy could be a possible therapeutic strategy to improve the intestinal barrier function in malnourished children.
| Item Type: | Thesis (Thesis) |
|---|---|
| Supervisor name: | Faculty supervisor: and Lisman, Prof. Dr. J.A. |
| Supervisor name: | Supervisor: and Bandsma, Dr. R. and Physiology & Experimental Medicine Department, The Hospital |
| Faculty: | Medical Sciences |
| Date Deposited: | 25 Jun 2020 11:05 |
| Last Modified: | 25 Jun 2020 11:05 |
| URI: | https://umcg.studenttheses.ub.rug.nl/id/eprint/2480 |
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