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The enteroinsular axis in glucose dependent insulinotropic polypeptide receptor knockout (GIPR-/-) miee Pamir, Nathalie

Abstract

The incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagonlike peptide-1 (GLP-1), are gut hormones that act via the enteroinsular axis to potentiate insulin secretion from the pancreas in a glucose-dependent manner. Both GLP-1 and GIP receptor knockout mice (GLP-1 R-/- and GIPR-/- respectively) have been generated to investigate the physiological importance of this axis. Studies in this thesis were carried out on GIP receptor knockout mice (GIPR-/-). Although reduced GIP action is a component of type 2 diabetes, GIP receptor-deficient mice exhibit only moderately impaired glucose tolerance. Thus, the present thesis was directed at investigating possible compensatory mechanisms that take place within the enteroinsular axis in the absence of GIP action. Fasting and 20t h minute OGTT serum GIP levels as well as duodenojejunal GIP content were altered in GIPR-/- mice. Total serum GLP-1 levels and serum DPIV activity in GIPR knockout mice were not significantly different from those in control animals, either before or during a glucose tolerance test. However, insulin responses to GLP-1 in pancreas perfusions and static islet incubations were significantly greater in GIPR -/- than in +/+ mice (P

Item Metadata

Title
The enteroinsular axis in glucose dependent insulinotropic polypeptide receptor knockout (GIPR-/-) miee
Creator
Pamir, Nathalie
Publisher
University of British Columbia
Date Issued
2002
Description
The incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagonlike peptide-1 (GLP-1), are gut hormones that act via the enteroinsular axis to potentiate insulin secretion from the pancreas in a glucose-dependent manner. Both GLP-1 and GIP receptor knockout mice (GLP-1 R-/- and GIPR-/- respectively) have been generated to investigate the physiological importance of this axis. Studies in this thesis were carried out on GIP receptor knockout mice (GIPR-/-). Although reduced GIP action is a component of type 2 diabetes, GIP receptor-deficient mice exhibit only moderately impaired glucose tolerance. Thus, the present thesis was directed at investigating possible compensatory mechanisms that take place within the enteroinsular axis in the absence of GIP action. Fasting and 20t h minute OGTT serum GIP levels as well as duodenojejunal GIP content were altered in GIPR-/- mice. Total serum GLP-1 levels and serum DPIV activity in GIPR knockout mice were not significantly different from those in control animals, either before or during a glucose tolerance test. However, insulin responses to GLP-1 in pancreas perfusions and static islet incubations were significantly greater in GIPR -/- than in +/+ mice (P
Extent
4800014 bytes
Genre
Thesis/Dissertation
Type
Text
File Format
application/pdf
Language
eng
Date Available
2009-09-29
Provider
Vancouver : University of British Columbia Library
Rights
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.
DOI
10.14288/1.0099678
URI
http://hdl.handle.net/2429/13341
Degree (Theses)
Master of Science - MSc
Program (Theses)
Psychology
Affiliation
Arts, Faculty of; Psychology, Department of
Degree Grantor
University of British Columbia
Graduation Date
2002-05
Campus
UBCV
Scholarly Level
Graduate
Aggregated Source Repository
DSpace

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For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.