Obesity is a growing public health burden that heralds significant morbidity and mortality. Maternal obesity is of particular concern as suboptimal intrauterine conditions may predispose offspring to disease in adulthood by instigating pathophysiological changes during foetal development. Exposure to obesity during gestation is associated with an increased risk of obesity and diseases such as diabetes and chronic kidney disease (CKD) in the offspring. It is not well established if maternal preconception weight reduction reduces this risk. This study aims to clarify whether treatment with the glucagon—like peptide-1 (GLP-1) receptor agonist, liraglutide, or diet modification facilitates improved renal outcomes in the offspring of obese dams, and to determine whether there is a temporal aspect to the efficacy of maternal weight loss interventions. Using a mouse model of maternal obesity, we investigated the impact of maternal weight loss interventions (pharmacological versus dietary) commenced during and prior to pregnancy on offspring renal outcomes (n=6-10). Kidney health was evaluated by quantification of gene expression of renal damage markers indicating inflammation, oxidative stress, dyslipidemia, and fibrosis, and immunohistochemical analysis assessed protein expression. Histological stains assessed structural changes, and serum measures assessed renal functionality. Our results showed that maternal obesity did not deleteriously impact offspring kidney health at adolescence (postnatal week 13). Maternal weight loss with liraglutide induced the activation of inflammatory (p<0.05, p<0.01) and oxidative stress (p<0.05) markers in the offspring kidneys in late adolescence. There was no significant difference in offspring kidney outcomes regardless of the timing of the maternal weight loss intervention at adolescence. The upregulation of inflammation and oxidative stress markers seen in the offspring kidneys of mothers with preconception liraglutide suggests a physiological attempt to circumvent the obesity-induced pathophysiological pathways of inflammation and oxidative stress implicated in adverse renal outcomes.