Cell Biology

Sugar Sabotage

See allHide authors and affiliations

Science  10 Jan 2014:
Vol. 343, Issue 6167, pp. 119
DOI: 10.1126/science.343.6167.119-c

In patients with diabetes, too much of a good thing—glucose—in the bloodstream causes the debilitating loss of biological functions and can eventually lead to death. Scientists continue to home in on the precise mechanisms by which this occurs, in hope of mitigating the damage. Warren et al. have found a mechanism by which excess glucose can alter the functions of vascular endothelial cells, one of the main sites of complications in diabetes. In mouse endothelial cells, too much glucose leads to the overproduction of reactive oxygen species (ROS) in the mitochondria. This excess of ROS causes the phosphorylation of the receptor for vascular endothelial growth factor (VEGF) within the Golgi, rendering the receptor vulnerable to proteolysis. This reduces the levels of VEGF receptor at the cell surface, where it would be able to detect circulating VEGF. Thus, cells chronically exposed to excess glucose become less responsive to VEGF, which is necessary for the proper growth, function, and survival of endothelial cells.

Sci. Signal. 7, ra1 (2014).

Navigate This Article