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Investigating the role of miR-152 and miR-130a in Glucose-Stimulated Insulin Secretion

Ofori, Jones (2013) MOBN19 20122
Degree Projects in Molecular Biology
Abstract
Investigating the role of miRNAs in Glucose-Stimulated Insulin Secretion

MicroRNAs have emerged as important players in many aspects of fundamental biological processes including regulation of pancreatic β-cell functions. Failure in beta cell functions, specifically with regards to glucose-stimulated insulin secretion (GSIS), contributes in the pathogenesis of type-2 diabetes (T2D). Previous studies in a T2D rodent model, Goto-Kakizaki (GK) rat, implicated dysregulated microRNAs as contributing factors in impaired GSIS.

Here, we investigated two such miRNAs in two clonal beta cell lines which display diametrically opposite phenotypes: INS1-832/13 which readily responds to glucose stimulation and secretes high amount of insulin and... (More)
Investigating the role of miRNAs in Glucose-Stimulated Insulin Secretion

MicroRNAs have emerged as important players in many aspects of fundamental biological processes including regulation of pancreatic β-cell functions. Failure in beta cell functions, specifically with regards to glucose-stimulated insulin secretion (GSIS), contributes in the pathogenesis of type-2 diabetes (T2D). Previous studies in a T2D rodent model, Goto-Kakizaki (GK) rat, implicated dysregulated microRNAs as contributing factors in impaired GSIS.

Here, we investigated two such miRNAs in two clonal beta cell lines which display diametrically opposite phenotypes: INS1-832/13 which readily responds to glucose stimulation and secretes high amount of insulin and INS1-832/2, which exhibit very low insulin secretion upon glucose stimulation.

Quantification of miRNAs using qRT-PCR shows that both miRNAs are up-regulated in INS1-832/2 cells reflecting the findings in the pancreatic islets of T2D model GK rat. Overexpression of both miRNAs in INS1-832/13 cells reduces insulin secretion by down-regulating important metabolic enzymes necessary for β-cell function during GSIS.

We conclude that these miRNAs play important roles in cellular functions necessary for insulin secretion.



Advisor: Jonathan Esguerra
Master´s Degree Project 45 credits in Molecular Biology, Molecular Genetics 2013
Department of Biology, Lund University (Less)
Please use this url to cite or link to this publication:
author
Ofori, Jones
supervisor
organization
course
MOBN19 20122
year
type
H2 - Master's Degree (Two Years)
subject
language
English
id
3631998
date added to LUP
2013-04-09 12:29:03
date last changed
2013-04-10 09:26:55
@misc{3631998,
  abstract     = {Investigating the role of miRNAs in Glucose-Stimulated Insulin Secretion

MicroRNAs have emerged as important players in many aspects of fundamental biological processes including regulation of pancreatic β-cell functions. Failure in beta cell functions, specifically with regards to glucose-stimulated insulin secretion (GSIS), contributes in the pathogenesis of type-2 diabetes (T2D). Previous studies in a T2D rodent model, Goto-Kakizaki (GK) rat, implicated dysregulated microRNAs as contributing factors in impaired GSIS. 

Here, we investigated two such miRNAs in two clonal beta cell lines which display diametrically opposite phenotypes: INS1-832/13 which readily responds to glucose stimulation and secretes high amount of insulin and INS1-832/2, which exhibit very low insulin secretion upon glucose stimulation.

Quantification of miRNAs using qRT-PCR shows that both miRNAs are up-regulated in INS1-832/2 cells reflecting the findings in the pancreatic islets of T2D model GK rat. Overexpression of both miRNAs in INS1-832/13 cells reduces insulin secretion by down-regulating important metabolic enzymes necessary for β-cell function during GSIS.

We conclude that these miRNAs play important roles in cellular functions necessary for insulin secretion.



Advisor: Jonathan Esguerra
Master´s Degree Project 45 credits in Molecular Biology, Molecular Genetics 2013
Department of Biology, Lund University},
  author       = {Ofori, Jones},
  language     = {eng},
  note         = {Student Paper},
  title        = {Investigating the role of miR-152 and miR-130a in Glucose-Stimulated Insulin Secretion},
  year         = {2013},
}