Maternal Obesity Prolongs the Adolescent Growth Spurt in Rat Offspring and Increases Weight Gain in a Sex-Specific Manner.

BACKGROUND: Maternal obesity affects offspring (F1) development, particularly postnatal growth trajectory and adult adiposity in a sex-dependent manner. However, there is no generalized model that allows identification of critical points in development. METHODS: Male and female F1 Wistar rats born to control (C; fed a chow diet) or obese (MO; fed a high-fat diet) mothers were weaned onto a chow diet and weighed weekly from postnatal day (PND) 21-110, to analyze their growth trajectories. F1 body weight (F1 BW) was fitted to a Gompertz function to estimate the growth spurt (GS, period of maximal growth rate) and timing, maximal predicted weight (MPW), peak spurt velocity (PSV), growth acceleration (GA) and growth deceleration (GD) points. RESULTS: F1 MO had lower BW during puberty and adolescence, prolonged GS, and increased MPW compared to C rats. GA was delayed in F1 MO males, but not females. At PND 110, F1 MO exhibited higher adiposity and similar BW compared to C. Adiposity positively correlated with MPW, PSV, and GD in both sexes, suggesting that delayed and extended growth are linked to increased adiposity. CONCLUSION: The Gompertz model showed that maternal obesity programs GS and MPW in a sex-specific manner. These sex-dependent shifts in growth dynamics were associated with increased adiposity. This approach identifies critical windows shaping developmental growth trajectories and highlights periods of vulnerability. It also provides opportunities to develop sex-specific interventions to prevent long-term metabolic alterations, including increased adiposity and obesity-related metabolic dysfunction, in the offspring of obese mothers.