In humans, natural exposure of Ad36 is cross-sectionally and longitudinally linked with markers of better glycemic control.

In animals, experimental infection by Ad36 improves glycemic control even in the presence of high fat diet.

In vitro studies indicate that the E4orf1 gene of Ad36 is necessary and sufficient to influence cellular glucose disposal..

The ability of E4orf1 may be harnessed to reduce hyperglycemia, provided it improves glycemic control in vivo.

This study provides proof of concept that Ad36 E4orf1 reproducibly improves glycemic control in mice on a high fat diet.

Further characterization is needed to determine the safety and efficacy of E4orf1 in improving glycemic control.