Sublethal insecticide exposure can affect pest fitness beyond direct mortality, but the effects of dinotefuran on offspring fitness and molecular responses in Sogatella furcifera remain unclear. In this study, third-instar nymphs were exposed for 48 h to dinotefuran concentrations corresponding to the 72-h LC10, LC25, and LC50 values. Adult longevity, fecundity, and molecular responses were assessed in surviving F0 insects, and offspring fitness was evaluated using an age-stage, two-sex life table. Dinotefuran reduced adult longevity and fecundity in the parental (F0) generation, with female fecundity decreasing by 17.22–45.45% across treatments. In F1 offspring, some developmental periods were prolonged, while survival and reproductive performance were reduced. The intrinsic rate of increase (r), finite rate of increase (λ), and net reproductive rate (R0) were lower than in the control, with significant reductions only at LC50. Over 60 d, projected population abundance was lower in treated groups, indicating slower growth relative to the control. At the molecular level, dinotefuran reduced the transcript levels of genes associated with TOR signaling, juvenile hormone (JH) biosynthesis and signaling, and vitellogenesis in F0 females, with SfVg transcript levels decreasing by 73.34–86.40%. Relative mtDNA copy number also decreased by 27.08%, 37.60%, and 44.69% at LC10, LC25, and LC50, respectively. These molecular responses may be associated with altered reproductive regulation and mitochondrial homeostasis. Incorporating such sublethal and transgenerational effects into insecticide evaluation can improve ecological risk assessment and support the rational integration of chemical control into sustainable rice pest management.
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