Introduction: Prevalence of obesity and type 2 diabetes during pregnancy is increasing, and both conditions may adversely influence later health in the developing offspring. The anti-diabetic drug metformin is commonly prescribed for diabetes during pregnancy, and is considered safe for the developing fetus. However, it’s uncertain whether metformin during pregnancy affects risk of disease in the offspring in adult life. Aims: To investigate the effects of metformin treatment of obese mouse dams during pregnancy on their adult offspring glucose metabolism and adiposity.Methods: Female C57/BL6J mice (n=18) were fed a control diet (C, 7% kcal fat) or a high-fat diet (HF, 45% kcal fat) 6 weeks prior to mating and through pregnancy. A subset of pregnant dams on C or HF diet were given metformin hydrochloride in drinking water (250mg/kg bodyweight per day) through pregnancy and lactation. Female offspring were weaned onto C or HF diet, creating 8 groups (n=5-8 per group): from untreated dams C/C, C/HF, HF/C, & HF/HF and from metformin-treated dams Cm/C, Cm/HF, HFm/C, & HFm/HF. Glucose tolerance in 28 week old offspring was assessed by 2 hour intraperitoneal glucose tolerance test. Fasting concentrations and area under the curve (AUCs) are reported. At 30 weeks of age, offspring body fat percentage (BF%) was assessed by µ-CT scan. Data reported as means ± SEM, or fold differences. Statistical analysis was performed by two-way ANOVA.Results: Offspring bodyweight at 30 weeks of age was significantly increased in C/HF and HF/HF compared to C/C (24.71±0.53g vs 34.13±1.07g, p<0.001, and 44.14 ± 1.67g, p<0.001, respectively). Maternal metformin during pregnancy increased bodyweight in Cm/HF vs C/HF (39.9±1g vs 34.13±1.07g, p< 0.01) but not in HFm/HF relative to HF/HF animals. Fasting blood glucose (FBG) was significantly higher by 1.34-fold (p<0.05) and 1.53-fold (p<0.05) in C/HF and HF/HF offspring groups respectively compared with C/C mice. FBG in HFm/HF offspring was significantly reduced vs HF/HF (0.72-fold, p<0.05). Glucose intolerance (AUC) was raised in C/HF offspring by 1.48-fold (p<0.01) and 2.16-fold (p<0.0001) in HF/HF compared with C/C animals. Metformin treatment did not improve glucose tolerance in Cm/HF and HFm/HF offspring. µ-CT scan showed that BF% in C/HF, HF/C and HF/HF was increased relative to C/C by 1.66-fold (p<0.001), 1.34-fold (p<0.01) and 1.87-fold (p<0.001), respectively. Maternal metformin treatment decreased BF% by 0.83-fold (p<0.05) in HFm/C compared to HF/C animals.Conclusions: Maternal metformin treatment in the obese mother protected female offspring from increased adiposity and reduced their fasting blood glucose. Maternal metformin treatment may therefore reduce the long-term effects of maternal obesity during pregnancy on offspring metabolic health.