Inactivation of β-catenin results in the reduction of postnatal body weight gain

• We model the perinatal conditional knockout of β-catenin mice by CamKIIα-Cre.
• We observe reduced body weight gain in β-catenin CKO mice from P8.
• Data suggest the deficiency of food intake in β-catenin CKO mice from P8.
• The level of mRNA expression of NPY increases in β-catenin CKO mice at P15.
• The level of mRNA expression of POMC decreases in β-catenin CKO mice at P15.

Arcuate nucleus of hypothalamus (ARH) is the core component in the regulation circuits of food intake and energy homeostasis. ARH projections to other parts of the hypothalamus and to extrahypothalamic areas are established in the postnatal two weeks, which is a pivotal stage for individual development. β-Catenin, a cell adhesion protein and also the mediator of canonical Wnt signaling pathway, plays an important role in embryonic development and adult homeostasis. However, whether β-catenin plays any roles in the development of hypothalamus is not clear. Here, we report that perinatal conditional knockout of β-catenin by CamKIIα-Cre in forebrain reduces body weight gain from P8 and dramatically shortens life span. Quantitative PCR and in situ hybridization results showed the expression of NPY mRNA in the ARH of β-catenin CKO mice at P15 is obviously increased compared with that of littermate controls, whereas the expression of POMC mRNA is significantly decreased, which suggested the reduction of postnatal body weight gain might be due to the deficiency of food intake. Together, β-catenin might play an important role in the regulation of food intake and postnatal body weight gain probably through affecting the development of ARH circuits.