| 26367 | Q925P2 | CEAM2_MOUSE | Carcinoembryonic antigen-related cell adhesion molecule 2 (CEA-related cell adhesion molecule 2) (Biliary glycoprotein 2) (BGP-2) | DISRUPTION PHENOTYPE | Sexually dimorphic effect. Homozygous null mutant female mice exhibit obesity that results from hyperphagia and reduced energy expenditure. Hyperphagia leads to peripheral insulin resistance. Insulin action is normal in liver but is compromised in skeletal muscle; the mice have incomplete fatty acid oxidation and impaired glucose uptake and disposal. Hyperphagia appears to result partly from increased hyperinsulinemia-induced hypothalamic fatty acid synthase levels and activity. Hyperinsulinemia is caused by increased insulin secretion. Homozygous null mutant male mice show total fat mass reduction, which ows to the hypermetabolic state despite hyperphagia. They also exhibit insulin sensitivity with elevated beta-oxidation in skeletal muscle, which is likely to offset the effects of increased food intake. Both males and females have increased brown adipogenesis. However, only males have increased activation of sympathetic tone regulation of adipose tissue and increased spontaneous activity. {ECO:0000269|PubMed:20381490, ECO:0000269|PubMed:22159884}. |