Genistein prevents bone loss in type 2 diabetic rats induced by streptozotocin

  • Rongrong Lu Department of Nutrition, School of Public Health, Sun Yat-Sen University, Guangzhou, People’s Republic of China
  • Zicong Zheng Department of Nutrition, School of Public Health, Sun Yat-Sen University, Guangzhou, People’s Republic of China
  • Yimin Yin Department of Nutrition, School of Public Health, Sun Yat-Sen University, Guangzhou, People’s Republic of China
  • Zhuoqin Jiang Department of Nutrition, School of Public Health, Sun Yat-Sen University, Guangzhou, People’s Republic of China
Keywords: genistein;, diabetic osteoporosis;, inflammation;, osteoclasts;, adipocytes


Background: Diabetic osteoporosis has become a severe public health problem in the aging societies. Genistein has been reported to play an important role in preventing and treating metabolic diseases via its anti-inflammatory, antioxidant, anti-estrogenic, and estrogen-like functions.

Objective: We aimed to investigate whether genistein exerts bone-protective effect on diabetic rats induced by 35 mg/kg streptozotocin (STZ) plus a 4-week high-fat diet.

Design: Sprague–Dawley rats were randomly divided into four groups: (1) control group, (2) type 2 diabetes mellitus (T2DM) model group, (3) T2DM with 10 mg/kg genistein, and (4) T2DM with 30 mg/kg genistein. After an 8-week treatment with genistein, the femurs, tibias, and blood were collected from all rats for further analysis.

Results: Genistein at 10 mg/kg showed little effect on diabetic osteoporosis, whereas genistein at 30 mg/kg significantly improved glucose and bone metabolisms compared with diabetic rats. Our results showed that 30 mg/ kg genistein significantly increased bone mineral density, serum osteocalcin, and bone alkaline phosphatase. Genistein also effectively lowered fasting blood glucose, tartrate-resistant acid phosphatase 5b, tumor necrosis factor-α, interleukin-6, and numbers of adipocytes and osteoclasts. Compared with the T2DM group, protein levels of receptor activator of nuclear factor κB ligand (RANKL) and peroxisome proliferator-activated receptor- γ (PPAR-γ) were decreased, while protein levels of osteoprotegerin (OPG), β-catenin, and runt-related transcription factor 2 (Runx-2) were increased after genistein intervention.

Conclusion: Genistein could effectively improve abnormal bone metabolism in STZ-induced diabetic rats; the underlying molecular mechanisms might be related to OPG/RANKL, PPAR-γ, and β-catenin/Runx-2 pathways.


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Author Biography

Zhuoqin Jiang, Department of Nutrition, School of Public Health, Sun Yat-Sen University, Guangzhou, People’s Republic of China

A professor in Department of Nutrition, School of Public Health, Sun Yat-Sen University.


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How to Cite
Lu, R., Zheng, Z., Yin, Y., & Jiang, Z. (2020). Genistein prevents bone loss in type 2 diabetic rats induced by streptozotocin. Food & Nutrition Research, 64.
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