Bacterial Regulation of Host Pancreatic Beta Cell Development
Diabetes is a metabolic disease characterized by the loss of functional pancreatic beta cells. The incidence of diabetes has risen rapidly in recent decades, which has been attributed at least partially to alterations in host-associated microbial communities, or microbiota. It is hypothesized that t...
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ndltd-uoregon.edu-oai-scholarsbank.uoregon.edu-1794-231402019-01-06T05:41:28Z Bacterial Regulation of Host Pancreatic Beta Cell Development Hill, Jennifer Guillemin, Karen BefA Beta cells Development Diabetes Microbiota Zebrafish Diabetes is a metabolic disease characterized by the loss of functional pancreatic beta cells. The incidence of diabetes has risen rapidly in recent decades, which has been attributed at least partially to alterations in host-associated microbial communities, or microbiota. It is hypothesized that the loss of important microbial functions from the microbiota of affected host populations plays a role in the mechanism of disease onset. Because the immune system also plays a causative role in diabetes progression, and it is well documented that immune cell development and function are regulated by the microbiota, most diabetes microbiota research has focused on the immune system. However, microbial regulation is also required for the development of many other important tissues, including stimulating differentiation and proliferation. We therefore explored the possibility that the microbiota plays a role in host beta cell development. Using the larval zebrafish as a model, we discovered that sterile or germ free (GF) larvae have a depleted beta cell mass compared to their siblings raised in the presence of bacteria and other microbes. This dissertation describes the discovery and characterization of a rare and novel bacterial gene, whose protein product is sufficient to rescue this beta cell developmental defect in the GF larvae. Importantly, these findings suggest a possible role for the microbiota in preventing or prolonging the eventual onset of diabetes through induction of robust beta cell development. Furthermore, the loss of rare bacterial products such as the one described herein could help to explain why low diversity microbial communities are correlated with diabetes. 2018-04-10T15:02:35Z 2018-04-10 Electronic Thesis or Dissertation http://hdl.handle.net/1794/23140 en_US All Rights Reserved. University of Oregon |
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BefA Beta cells Development Diabetes Microbiota Zebrafish |
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BefA Beta cells Development Diabetes Microbiota Zebrafish Hill, Jennifer Bacterial Regulation of Host Pancreatic Beta Cell Development |
description |
Diabetes is a metabolic disease characterized by the loss of functional pancreatic beta cells. The incidence of diabetes has risen rapidly in recent decades, which has been attributed at least partially to alterations in host-associated microbial communities, or microbiota. It is hypothesized that the loss of important microbial functions from the microbiota of affected host populations plays a role in the mechanism of disease onset. Because the immune system also plays a causative role in diabetes progression, and it is well documented that immune cell development and function are regulated by the microbiota, most diabetes microbiota research has focused on the immune system. However, microbial regulation is also required for the development of many other important tissues, including stimulating differentiation and proliferation. We therefore explored the possibility that the microbiota plays a role in host beta cell development. Using the larval zebrafish as a model, we discovered that sterile or germ free (GF) larvae have a depleted beta cell mass compared to their siblings raised in the presence of bacteria and other microbes. This dissertation describes the discovery and characterization of a rare and novel bacterial gene, whose protein product is sufficient to rescue this beta cell developmental defect in the GF larvae. Importantly, these findings suggest a possible role for the microbiota in preventing or prolonging the eventual onset of diabetes through induction of robust beta cell development. Furthermore, the loss of rare bacterial products such as the one described herein could help to explain why low diversity microbial communities are correlated with diabetes. |
author2 |
Guillemin, Karen |
author_facet |
Guillemin, Karen Hill, Jennifer |
author |
Hill, Jennifer |
author_sort |
Hill, Jennifer |
title |
Bacterial Regulation of Host Pancreatic Beta Cell Development |
title_short |
Bacterial Regulation of Host Pancreatic Beta Cell Development |
title_full |
Bacterial Regulation of Host Pancreatic Beta Cell Development |
title_fullStr |
Bacterial Regulation of Host Pancreatic Beta Cell Development |
title_full_unstemmed |
Bacterial Regulation of Host Pancreatic Beta Cell Development |
title_sort |
bacterial regulation of host pancreatic beta cell development |
publisher |
University of Oregon |
publishDate |
2018 |
url |
http://hdl.handle.net/1794/23140 |
work_keys_str_mv |
AT hilljennifer bacterialregulationofhostpancreaticbetacelldevelopment |
_version_ |
1718806998519119872 |