Accompanying the dramatic increase in maternal obesity, the incidence of type I diabetes (T1D) in children is also rapidly increasing. The objective of this study was to explore impacts of maternal obesity on the incidence of T1D in offspring using non-obese diabetic (NOD) mice, a common model for TID. Four-week-old female NOD mice were fed either a control diet (10% energy from fat, CON) or a high fat diet (60% energy from fat, HFD) for 8 weeks before mating. Mice were maintained in their respective diets during pregnancy and lactation. All offspring mice were fed the control diet to 16 weeks. Female offspring (16-wk-old) born to obese dams showed more severe islet lymphocyte infiltration (major manifestation of insulitis) (P < 0.01), concomitant with elevated nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) p65 signaling (P < 0.01) and tumor necrosis factor (TNF) α protein level (P < 0.05) in the pancreas. In addition, maternal obesity resulted in impaired (P < 0.05) glucose tolerance and lower (P < 0.05) serum insulin levels in offspring. In conclusion, maternal obesity resulted in exacerbated insulitis and inflammation in the pancreas of NOD offspring mice, providing a possible explanation for the increased incidence of T1D in children.