Controls energy balance and peripheral insulin action. Involved in the regulation of feeding behavior particularly in the ventromedial nucleus of hypothalamus (VMH) regulation of food intake. Has a role in the regulation of metabolic rate and insulin sensitivity or resistance via effects on brown adipogenesis, sympathetic nervous outflow to brown adipose tissue, spontaneous activity and energy expenditure in skeletal muscle. In case of murine coronavirus (MHV) infection, does probably not serve as functional receptor for the virus. Isoform 2 may be an adhesion molecule contributing to cell to cell adhesion between elongating spermatids and Sertoli cells within the seminiferous epithelium. Interacts weakly with MHV spike protein in tissue culture. Localizes to sites on the plasma membrane of elongating spermatids where Sertoli cells make contact. Isoform 2 is detected in elongating spermatids within the seminiferous epithelium (at protein level). Expressed in kidney, colon, uterus, gut mononuclear cells, crypt epithelia of intestinal tissues, and to a lesser extent, in spleen. Expressed in brain including VMH, globus pallidus, ventral pallidum, striatum, olfactory bulb and hippocampus. Also detected in rectal carcinoma cell line CMT93. Isoform 2 and isoform 3 are expressed in testis. Isoform 2 is detected in seminiferous tubule, not detected in epididymal spermatozoa. Also not observed on spermatogonia, spermatocytes, round spermatids or somatic Sertoli cells. During stages I-VII of spermatogenesis, detected on the elongating spermatids. At spermiation (stage VIII) and subsequent stages IX-XII, levels are drastically reduced or absent in the seminiferous tubules. Sometimes weakly detected in the apical region of stage-VIII seminiferous epithelium. Isoform 2 level is very low in stomach, kidney, intestine, liver and spleen. Expressed throughout embryonic development. Isoform 2 first appears faintly in the testis 3 weeks into postnatal development and its expression level increases after 5 weeks. Levels in brain increase at fasting and decrease at 4 and 7 hours of refeeding. 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. The human orthologous protein seems not to exist. In mice, both Ceacam1 and Ceacam2 are the paralogs of human CEACAM1. Belongs to the immunoglobulin superfamily. CEA family.