The human glucagon-like peptide-1 analogue liraglutide preserves pancreatic beta cells via regulation of cell kinetics and suppression of oxidative and endoplasmic reticulum stress in a mouse model of diabetes

Pancreatic Islets
DOI: 10.1007/s00125-011-2069-9 Publication Date: 2011-02-21T16:47:01Z
ABSTRACT
We investigated the molecular mechanism by which human glucagon-like peptide-1 analogue liraglutide preserves pancreatic beta cells in diabetic db/db mice. Male and m/m mice aged 10 weeks received or vehicle for 2 days weeks. In addition to morphological biochemical analysis of islets, gene expression profiles islet core area were laser capture microdissection real-time RT-PCR. Liraglutide treatment improved metabolic variables insulin sensitivity also increased glucose-stimulated secretion (GSIS) content both mouse strains reduced triacylglycerol Expression genes involved cell differentiation proliferation was regulated liraglutide, which, mice, downregulated pro-apoptosis, endoplasmic reticulum (ER) stress lipid synthesis, upregulated related anti-apoptosis anti-oxidative stress. day experiment, slightly but GSIS, not affected. associated with differentiation, anti-apoptosis, suppressed pro-apoptosis; it had no effect on oxidative ER Morphometric results proliferation, apoptosis islets consistent analysis. increases mass only directly regulating kinetics, suppressing stress, secondary amelioration glucolipotoxicity.
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