Lycopene ameliorates diabetic osteoporosis via anti-inflammatory, anti-oxidation, and increasing Osteoprotegerin/RANKL expression ratio
[Display omitted] •Lycopene increases the bone mineral density of diabetic rats.•Lycopene prevents diabetic induced bone loss via anti-inflammatory, anti-oxidation, and regulating abnormal bone turnover.•This study provides a basis for the application of lycopene in the prevention of diabetic osteop...
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Veröffentlicht in: | Journal of functional foods 2021-08, Vol.83, p.104539, Article 104539 |
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Sprache: | eng |
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•Lycopene increases the bone mineral density of diabetic rats.•Lycopene prevents diabetic induced bone loss via anti-inflammatory, anti-oxidation, and regulating abnormal bone turnover.•This study provides a basis for the application of lycopene in the prevention of diabetic osteoporosis.
Diabetic osteoporosis (DOP) is one of the complications of diabetes, with high morbidity, and high disability rate. Here, we established a diabetic rat model and administered lycopene to observe its effect on DOP. Our results showed that ten weeks lycopene treatment lowered blood glucose, improved diabetic induced polydipsia, overeating and body weight loss. Lycopene treatment also enhanced bone mineral density, restored bone mechanical and bone Micro-CT parameters of diabetic rats. Subsequently, lycopene decreased serum inflammatory cytokines levels and increased serum anti-oxidant indicators levels. Moreover, lycopene reduced the number of bone marrow adipocytes, and osteoclasts numbers of diabetic rats. The serum bone turnover markers levels were down-regulated after lycopene treatment. Meanwhile, the bone and serum OPG, RUNX 2 expression levels were up-regulated by lycopene in diabetic rats, and the OPG/RANKL ratio was also up-regulated. This study showed that lycopene could ameliorate diabetic induced bone loss via anti-inflammatory, anti-oxidation, and increasing OPG/RANKL ratio in diabetic rats. Lycopene could be used for nutritional intervention in patients with diabetic osteoporosis. |
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ISSN: | 1756-4646 2214-9414 |
DOI: | 10.1016/j.jff.2021.104539 |