As a consequence of the longer WTD feeding in males and the lesions in Ldlr −/− mice being larger than usual, we may have missed detecting a significant increase of hepatocyte-specific G6pc deficiency on atherosclerotic plaques, though we observed a tendency that did not reach statistical significance ( p = 0.10).
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Increased atherosclerosis in a mouse model of glycogen storage disease type 1a.
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