Lycopene improves bone quality and regulates AGEs/RAGE/NF-kB signaling pathway in high-fat diet-induced obese mice

Authors: XIA, BINGKE - Beijing University Of Chinese Medicine; ZHU, RUYUAN - Beijing University Of Chinese Medicine; ZHANG, HAO - Beijing University Of Chinese Medicine; CHEN, BEIBEI - Beijing University Of Chinese Medicine; LIU, YAGE - Beijing University Of Chinese Medicine; DAI, XUAN - Beijing University Of Chinese Medicine; YE, ZIMENGWEI - Beijing University Of Chinese Medicine; ZHAO, DANDAN - Beijing University Of Chinese Medicine; MO, FANGFANG - Beijing University Of Chinese Medicine; GAO, SIHUA - Beijing University Of Chinese Medicine; WANG, XIANG-DONG - Jean Mayer Human Nutrition Research Center On Aging At Tufts University; BROMME, DIETER - University Of British Columbia; WANG, LILI - Beijing University Of Chinese Medicine; WANG, XINXIANG - Beijing University Of Chinese Medicine; ZHANG, DONGWIE - Beijing University Of Chinese Medicine

Submitted to: Oxidative Medicine and Cellular Longevity
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/28/2022
Publication Date: 2/17/2022
Citation: Xia, B., Zhu, R., Zhang, H., Chen, B., Liu, Y., Dai, X., Ye, Z., Zhao, D., Mo, F., Gao, S., Wang, X., Bromme, D., Wang, L., Wang, X., Zhang, D. 2022. Lycopene improves bone quality and regulates AGEs/RAGE/NF-kB signaling pathway in high-fat diet-induced obese mice. Oxidative Medicine and Cellular Longevity. https://doi.org/10.1155/2022/3697067.
DOI: https://doi.org/10.1155/2022/3697067

Interpretive Summary: Lycopene may prevent bone loss in obese people but the potential underlying mechanisms are unclear. We examined the protective effects of lycopene on bone quality in high-fat diet (HFD)-induced obese mice. We observed that lycopene feeding inhibited HFD-associated oxidative stress generation and abnormal bone remodeling as well as metabolic syndrome-related signaling pathway involving bone microarchitecture. The study suggest that lycopene consumption may be beneficial for the management of obesity-induced osteoporosis.

Technical Abstract: Objective: This study was aimed at examining the effects of lycopene on bone metabolism in high-fat diet (HFD)- induced obese mice and to identify the potential underlying mechanisms. Methods: Mice were fed a HFD for 12 weeks and then continue with or without lycopene intervention (15 mg/kg) for additional 10 weeks. The effects of lycopene on blood glucose and lipid metabolism, as well as serum levels of total antioxidant capacity (T-AOC), superoxide dismutase (SOD), and malondialdehyde (MDA) were determined by biochemical assays. Bone histomorphological features and osteoclast activity were assessed by hematoxylin/eosin and tartrate-resistant acid phosphatase staining. Bone microstructure at the proximal tibial metaphysis and diaphysis was determined by microcomputed tomography. Tibial biomechanical strength and material profiles were measured by a three-point bending assay and Fourier transform infrared spectroscopy. Protein expressions involved in the AGE/RAGE/NF-kappa B signaling pathway were determined by western blot and/or immunohistochemical staining. Results: Lycopene consumption reduced body weight gain and improved blood glucose and lipid metabolism in HFD-induced obese mice. In addition, lycopene treatment preserved bone biomechanical strength, material profiles, and microarchitecture in obese mice. Moreover, these alterations were associated with an increase in serum levels of T-AOC and SOD, and a decline in serum levels of MDA, as well as a reduction of AGEs, RAGE, cathepsin K, and p-NF-kappa Bp65 and NF-kappa Bp65 expressions in the femurs and tibias of obese mice. Conclusion: Lycopene may improve bone quality through its antioxidant properties, which may be linked with the regulation of the AGE/RAGE/NF-kappa B signaling pathway in obese mice. These results suggest that lycopene consumption may be beneficial for the management of obesity-induced osteoporosis.