NPY signalling in early osteoblasts controls glucose homeostasis.

ABSTRACT:

Objective

The skeleton has recently emerged as an additional player in the control of whole-body glucose metabolism; however, the mechanism behind this is not clear.

Methods

Here we employ mice lacking neuropeptide Y, Y1 receptors solely in cells of the early osteoblastic lineage (Y1f3.6Cre), to examine the role of osteoblastic Y1 signalling in glycaemic control.

Results

Y1f3.6Cre mice not only have a high bone mass phenotype, but importantly also display altered glucose homeostasis; significantly decreased pancreas weight, islet number and pancreatic insulin content leading to elevated glucose levels and reduced glucose tolerance, but with no effect on insulin induced glucose clearance. The reduced glucose tolerance and elevated bone mass was corrected in Y1f3.6Cre m

SUBMITTER: Lee NJ 

PROVIDER: S-EPMC4338316 | biostudies-literature | 2015 Mar

REPOSITORIES: biostudies-literature