Gravidas with obesity and diabetes (diabesity) may transmit this syndrome to their children through genetic and non-genetic mechanisms. Here, we used the Lepr^db/+ diabese mouse to examine the magnitude of these transmission modes, focusing on adipose tissue (AT). We compared six groups: wild-type (+/+) offspring from +/+ and db/+ dams (different early-life environment) and db/+ offspring from db/+ dams, fed a standard or high-fat diet. Weight gain (0-8 weeks) was higher in +/+ offspring from db/+ vs. +/+ mothers, and even higher in db/+ vs. +/+ offspring from db/+ mothers. In addition, we observed a stepwise increase in AT and adipocyte size in +/+ from +/+ mice, +/+ from db/+ mice and db/+ mice at 8 weeks. Differences in weight and adiposity between +/+ offspring from db/+ vs. +/+ dams were more pronounced in males than in females. Leptin and apelin mRNA levels in white and brown AT were higher in +/+ offspring from db/+ vs. +/+ dams; however, leptin, apelin and tumor necrosis factor- expression were boosted more robustly in db/+ offspring. The high-fat diet amplified AT differences between db/+ vs. +/+ offspring from db/+ dams, but not between +/+ offspring from db/+ vs. +/+ dams. Moreover, db/+ but not +/+ offspring from db/+ mothers were insulin-resistant and hyperinsulinemic after a glucose challenge. In conclusion, the genetic transmission of the diabesity phenotype clearly prevailed, but the early-life diabesity environment had discernible effects on postnatal weight gain as well as on adipocyte size and adipokine expression at a postpubertal age.