Objective To employ a mouse model of ABI3BP gene deletion for the detection of postnatal changes in body weight and glucose metabolism and establish a different method of creating a mouse model of low birth weight. Methods Heterozygote mice were mated to produce ABI3BP gene knockout homozygote (ABI3BP^-/-) mice, heterozygote (ABI3BP ^{+ /-}) mice, and wild-type (WT) mice. Adult mice from all three groups were evaluated for glucose metabolism markers, including the fasting blood glucose level, glucose tolerance, and insulin tolerance. Additionally, body weight was measured at various postnatal time periods, and the weight ratio of critical organs in adulthood was calculated. Results The gene sequencing result of the polymerase chain reaction product of ABI3BP^-/- mice showed that frameshift mutations occurred in the knockout region, with quantitative reverse-transcription polymerase chain reaction analysis demonstrating significantly reduced ABI3BP expression in ABI3BP^-/- mice compared with that in WT mice. Notably, the birth weight of ABI3BP^-/- mice (1.25 ± 0.08 g) was markedly lower than that of WT mice (1.34 ± 0.12 g) (P<0.05). Conversely, the weight of adult (120 d) ABI3BP^-/- mice (27.70 ± 1.93 g) was significantly higher than that of WT mice (23.64 ± 1.34 g) (P<0.01). The ratios of key organ weights to body weight were not significantly different 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^-/- mice had lower blood glucose levels (15.68 ± 7.04 mmol/L) than WT mice (23.01 ± 5.75 mmol/L). Conclusions Deletion of the ABI3BP gene result in mice with low birth weight, poor growth recuperation, and inadequate glucose tolerance in adulthood, similar to the clinical growth traits of low-birth-weight human neonates. Therefore, this mouse model is a promising choice for the study of low birth weight.