The embryo is critically sensitive to altered environmental conditions in utero, which can subsequently direct fetal growth and influence offspring health in later life. Emerging evidence suggests the father’s pre-conception diet/lifestyle also has a role in regulating fetal development and ultimately alters disease risk in the adult offspring. Defining the early embryonic dynamics that underlie this impact on offspring health is key to improving our understanding of the developmental origins of health and disease. Therefore, the aim of this study was to examine how impaired paternal nutritional status influences early embryo development in a mouse model. Male C57/BL6J mice were fed either a low-protein (LPD: 9% casein, 24% sugar, 10% fat; n=6), Western (WD: 19% casein, 34% sugar, 21% fat; n=7) or control (CD: 18% casein, 21% sugar, 10% fat; n=6) diet for a minimum of 8 weeks, to ensure all periods of spermatogenesis were exposed to dietary factors. Males were mated to virgin 8-12 week old females (n=6-7 per group), with pregnancy confirmed by the presence of a copulation plug and termed embryonic day (E)0.5. Pregnant dams were euthanized on E1.5 and the oviducts flushed to retrieve 2-cell embryos. Embryos were cultured individually in EmbryoMax® KSOM media (37°C; 5% CO2) in an EmbryoScope time-lapse incubator, with images acquired every 10 minutes. Embryo cleavage rate and blastomere/blastocyst area were determined using EmbryoViewer software. Fully expanded blastocysts were fixed in 4% paraformaldehyde and stained for quantification of inner cell mass (Oct4) and trophectoderm (Cdx2) cell numbers. Statistical analysis was performed using IBM SPSS Statistics v25. Data were assessed using a linear mixed model or a one-way ANOVA with Tukey’s post-test where appropriate. The sub-optimal paternal diets did not alter number of embryos per dam (CD: 8.2±1.0, LPD: 8.2±0.2, WD: 8.1±0.3). Embryos generated by WD fed-males demonstrated an increased average blastomere size at the 2-cell stage (2282±31µm2 vs 2108±47µm2, p<0.05) compared to CD. Embryos from both LPD and WD fed males developed through all pre-compaction cell cleavage stages faster than those from CD males (time to 4-cell stage; LPD: 6.0±0.6h, WD: 5.3±0.4h vs CD: 9.8±0.8h; p<0.01, p<0.001 respectively, and to 8-cell stage; LPD: 19.1±1.0h, WD: 19.0±0.5h vs CD: 22.9±0.8h; p<0.01). Post-compaction, no differences were seen between diet groups. Blastocysts from LPD fed males demonstrated a faster time to expansion compared to CD (54.1±1.0h vs 59.5±1.3h, p<0.01 (h= hours from start of culture)), yet were found to have a smaller area than both CD and WD blastocysts (6745±127µm2 vs 7647±278µm2 and 7886±245µm2, p<0.05, P<0.01 respectively). We observed no differences in inner cell mass or trophectoderm cell number. We found patterns of early embryonic development were accelerated in embryos derived from LPD and WD fed males. Whilst this accelerated rate of developed declined post-compaction, differences in blastocyst formation were still observed. Altered rates of early embryonic development have been linked with impaired implantation, and even altered fetal development later in gestation. Our data suggests that a poor paternal pre-conception diet plays a key role in regulating the rate of early embryonic development, which could have implications for the future health of the offspring.