Background and aims: Olfactomedin 2 (OLFM2; also known as noelin 2) is a pleiotropic protein that plays a major role in olfaction and Olfm2 null mice exhibit reduced olfactory sensitivity, as well as abnormal motor coordination and anxiety-related behavior. Here, we investigated the possible metabolic role of OLFM2.
Methods: Olfm2 null mice were metabolically phenotyped. Virogenetic modulation of central OLFM2 was also performed.
Results: Our data showed that, the global lack of OLFM2 in mice promoted anorexia and increased energy expenditure due to elevated brown adipose tissue (BAT) thermogenesis and browning of white adipose tissue (WAT). This phenotype led to resistance to high fat diet (HFD)-induced obesity. Notably, virogenetic overexpression of Olfm2 in the lateral hypothalamic area (LHA) induced weight gain associated with decreased BAT thermogenesis.
Conclusion: Overall, this evidence first identifies central OLFM2 as a new molecular actor in the regulation of whole-body energy homeostasis.
Keywords: Brown adipose tissue; Browning; Lateral hypothalamic area; Obesity; Olfactomedin 2; Thermogenesis.
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