GIP receptor antagonist treatment causes weight loss in ovariectomized
high fat diet-fed mice
Abstract
Background and purpose The incretin hormone, glucose-dependent
insulinotropic polypeptide (GIP), secreted by the enteroendocrine
K-cells in the proximal intestine, may regulate lipid metabolism and
adiposity but its exact role in these processes is unclear. Experimental
approach We characterized in vitro and in vivo antagonistic properties
of a novel GIP analogue, mGIPAnt-1. We further assessed the in vivo
pharmacokinetic profile of this antagonist, as well as its ability to
affect high-fat diet (HFD)-induced body weight gain in ovariectomized
mice during an 8-week treatment period. Key results mGIPAnt-1 showed
competitive antagonistic properties to the GIP receptor (GIPR) in vitro
as it inhibited GIP-induced cAMP accumulation in COS-7 cells.
Furthermore, mGIPAnt-1 was capable of inhibiting GIP-induced
glucoregulatory and insulinotropic effects in vivo and has a favourable
pharmacokinetic profile with a half-life of 7.2 hours in C57Bl6 female
mice. Finally, sub-chronic treatment with mGIPAnt-1 in ovariectomized
HFD mice resulted in a reduction of body weight and fat mass. Conclusion
and Implications mGIPAnt-1 successfully inhibited acute GIP-induced
effects in vitro and in vivo and sub-chronically induces resistance to
HFD-induced weight gain in ovariectomized mice. Our results support the
development of GIP antagonists for the therapy of obesity.