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Rôles des facteurs de croissance dans la prolifération de la cellule β-pancréatique en réponse à un excès de nutriments : étude du facteur de croissance HB-EGF et du récepteur à l’EGF
| Content Provider | Semantic Scholar |
|---|---|
| Author | Benterki, Isma |
| Copyright Year | 2015 |
| Abstract | Type 2 diabetes (T2D) results from insulin resistance in peripheral tissues and impaired insulin secretion from the pancreatic β-cell. Over the time, compensation of the β cell islets for insulin resistance fails, and therefore leads to a gradual decline in β-cell function. Several factors may contribute to β-cell compensation. However, the cellular and molecular mechanisms underlying βcell compensation remain unknown. The purpose of this thesis was to identify what mechanism could lead to β cell compensation in response to nutrients excess and specifically the increase in proliferation and β-cell mass. Thus, with increasing insulin resistance and circulating factors in the 6 month rats infused with glucose + intralipid, the hypothesis was made and confirmed in our study that the growth factor HB-EGF would activate the EGF receptor, and subsequent signaling pathways such as mTOR and FoxM1, both involved in the proliferation of the pancreatic beta-cell. Collectively, these results allow us to understand better the molecular mechanisms involved in the β cell compensation in the insulin resistance state and may serve as a potential new therapeutic approach to prevent or delay T2D development. |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | https://papyrus.bib.umontreal.ca/xmlui/bitstream/handle/1866/13131/Isma_Benterki_2015_memoire.pdf?isAllowed=y&sequence=2 |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
