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GLP-1 analogue semaglutide regulates pancreatic beta-cell proliferation via PDX-1 expression control
- 1 University of Cambridge
- 2 The Houde Academy
- 3 Westover school
- 4 Hanvos-Kent school Ningbo Campus,
* Author to whom correspondence should be addressed.
Abstract
Semaglutide as an agonist of glucagon-like peptide-1 receptor was shown to potentiate insulin release and suppress food motivation targeting pancreatic islet beta cells and brain region including subfornical organ and hypothalamus, which effectively treats type 2 diabetes and obesity. The investigation of prolonged response with semaglutide on beta cells triggering proliferation and apoptotic resistance is yet to be confirmed. Previous research findings have shown that glucagon-like peptide-1 and liraglutide as agonists for glucagon-like peptide-1 receptors on beta cells result in proliferation through upregulation of PDX-1 transcription factor. Semaglutide is investigated to show whether long-term beta cell survival regulation is achieved through the same downstream signalling pathways. Both in vivo and in vitro methods were designed to show the proliferation effect of the semaglutide in C57BL/6 mice using tissue imaging, cell counting and immunosorbent assay for quantitative analysis of PDX-1 expression. The proliferation effect would broaden the application of semaglutide from insulin augmentation to the sustained benefit of beta cell survival.
Keywords
glucagon-like peptide-1; diabetes; beta-cell; PDX-1
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Cite this article
Ming,L.;Sun,J.;Chu,X.;Wang,C. (2024). GLP-1 analogue semaglutide regulates pancreatic beta-cell proliferation via PDX-1 expression control . Theoretical and Natural Science,46,46-54.
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The datasets used and/or analyzed during the current study will be available from the authors upon reasonable request.
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