Objective To employ the Abi3bp gene deletion mouse model for the detection of postnatal changes in body weight and glucose metabolism. Additionally, It also suggests a different method for low birth weight mice models. Methods A mouse model with the Abi3bp gene deletion was developed using CRISPR/Cas9 technology, followed by breeding and identification processes. To produce Abi3bp gene knockout homozygotes (Abi3bp-/-), heterozygotes (Abi3bp+/-), and wild type (WT) mice, heterozygotes were mated. Adult mice from all three groups were evaluated for glucose metabolism markers such as fasting blood glucose levels, glucose tolerance, and insulin tolerance, in addition to body weight at various postnatal time periods including the weight ratio of critical organs in adulthood. Results Gene identification confirmed successful knockout of the Abi3bp gene in Abi3bp-/- mice, with RT-qPCR analysis demonstrating significantly reduced Abi3bp expression in Abi3bp-/- mice compared to WT mice. Notably, the birth weight of Abi3bp-/- mice (1.25±0.08g) was markedly lower than that of WT mice (1.34±0.12g) (P<0.05). Conversely, the weight of adult (120d) Abi3bp-/- mice (27.70±1.93g) was significantly higher than that of WT mice (23.64±1.34g) (P<0.01). The ratio of key organs to body weight did not exhibit significant differences between the groups (P>0.05). Fasting blood glucose and insulin tolerance tests showed no significant variations between the groups. However, glucose tolerance tests indicated that Abi3bp-/- animals displayed lower blood glucose levels (15.68±7.04mmol/L) compared to WT mice（23.01±5.75 mmol/L）. Conclusion Deletion of the Abi3bp gene results in mice with low birth weight, growth recuperation, and inadequate glucose tolerance in adulthood similar to clinical growth traits of low birth weight neonates, thus presenting a promising choice for low birth weight mouse models.