In humans, natural exposure of Ad36 is cross-sectionally and longitudinally linked with markers of better glycemic control.
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In animals, experimental infection by Ad36 improves glycemic control even in the presence of high fat diet.
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In vitro studies indicate that the E4orf1 gene of Ad36 is necessary and sufficient to influence cellular glucose disposal..
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The ability of E4orf1 may be harnessed to reduce hyperglycemia, provided it improves glycemic control in vivo.
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This study provides proof of concept that Ad36 E4orf1 reproducibly improves glycemic control in mice on a high fat diet.
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Further characterization is needed to determine the safety and efficacy of E4orf1 in improving glycemic control.
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