Differential Effects of Lycopene Supplementation on Adipose Tissue Development and Redox Status in Weanling Offspring of Rats Consuming a High Fat Diet

Abstract

Abstract Objectives Dietary patterns high in fat contribute to the onset of cardiometabolic disease through accrual of adipose tissue (AT). Nevertheless, carotenoids, such as lycopene, may disrupt these metabolic perturbations. The purpose of this study was to evaluate AT development, systemic and AT redox status, and cardiometabolic biomarkers during weaning and post-weaning periods of offspring from mothers fed high fat diets with and without lycopene supplementation. Methods Sprague-Dawley rats arrived on the 2nd day of gestation and were randomized to 25% normal fat diet (NFD) or 50% high fat diet (HFD). Upon delivery, half of HFD mothers were transitioned to HFD supplemented with 1% lycopene (HFDL group). Remaining mothers continued NFD or HFD without supplementation. Four pups/litter were euthanized at postnatal day 25 (P25). Beginning at P25, weanling pups were fed diets of their respective mothers until euthanization at P35 (three pups/litter). Visceral white AT (WAT) and brown AT (BAT) mass was determined, as well as lipid peroxides and antioxidant capacity (AC) of these tissues and serum. Cardiometabolic biomarkers were assessed at P25. Results At each time point, HFD groups had significantly greater (P < 0.05) WAT accrual compared to NFD group, sufficiently representing diet-induced obesity. Compared to the HFD group, the HFDL group exhibited significantly greater BAT at P25 (P = 0.025) with a significant reduction in WAT mass (P = 0.004). Such patterns continued into P35, albeit non-significant. At both time points, serum lipid peroxides were significantly lower in the HFDL group compared to the HFD (P = 0.005, P = 0.003, respectively). In contrast, AT results were starkly different such that the HFDL group exhibited significantly greater (P < 0.05) lipid peroxides in WAT and BAT at P25 and P35 compared to HFD group. No significant differences in systemic or AT AC were observed between groups. Furthermore, serum adiponectin and leptin did not differ significantly between groups despite the aforementioned modifications in AT development. Conclusions Results from this exploratory analysis suggest that lycopene may induce favorable alterations in AT development, yet it differentially influences redox status in serum and AT. Additional research is warranted to elucidate molecular mechanisms by which lycopene influences AT biology and redox status. Funding Sources NIH.