CMP-Neu5Ac Hydroxylase Null Mice as a Model for Studying Metabolic Disorders Caused by the Evolutionary Loss of Neu5Gc in Humans

Figure 1

Cmah-null mice show impaired insulin secretion in response to glucose. (a) Liver abnormality in Cmah-null mice. The number of Kupffer cells was significantly higher in Cmah-null mouse-derived liver tissues than in WT. Bar: 100 μm. (b) Immunofluorescence staining of Cmah-null-derived liver tissue to detect expression of Kupffer cells using F4/80 antibody. (c) Body and liver weights of WT and Cmah-null mice. (d) Quantity of glucose (mL/dL), FFA (μEq/L), and insulin (μU/mL) in sera of WT and Cmah-null mice. Significant differences are indicated by value.

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