Background: Previous clinical studies have suggested that apolipoprotein M (apoM) is
involved in glucose metabolism and plays a causative role in insulin sensitivity.
Objective: The potential mechanism of apoM on modulating glucose homeostasis is explored and
differentially expressed genes are analyzed by employing ApoM deficient (ApoM-/-
) and wild type
Methods: The metabolism of glucose in the hepatic tissues of high-fat diet ApoM-/- and WT mice was
measured by a glycomics approach. Bioinformatic analysis was applied for analyzing the levels of
differentially expressed mRNAs in the liver tissues of these mice. The insulin sensitivity of ApoM-/-
and WT mice was compared using the insulin tolerance test and the phosphorylation levels of protein
kinase Akt (AKT) and insulin stimulation in different tissues were examined by Western blot.
Results: The majority of the hepatic glucose metabolites exhibited lower concentration levels in the
mice compared with those of the WT mice. Gene Ontology (GO) classification and Kyoto
Encyclopedia of Genes and Genomes (KEGG) enrichment analysis indicated that ApoM deficiency
affected the genes associated with the metabolism of glucose. The insulin tolerance test suggested that
insulin sensitivity was impaired in ApoM-/-
mice. The phosphorylation levels of AKT in muscle and
adipose tissues of ApoM-/-
mice were significantly diminished in response to insulin stimulation compared
with those noted in WT mice.
Conclusion: ApoM deficiency led to the disorders of glucose metabolism and altered genes related to
glucose metabolism in mice liver. In vivo data indicated that apoM might augment insulin sensitivity
by AKT-dependent mechanism.