Relationship between Garcinia cambogia-Induced Impairment of Spermatogenesis and Meiosis-Activating Sterol Production in Rat Testis

  • Kiyose Chikako
    Division of Food Science, Incorporated Administrative Agency, National Institute of Health and Nutrition
  • Ogino Satomi
    Division of Food Science, Incorporated Administrative Agency, National Institute of Health and Nutrition
  • Kubo Kazuhiro
    Division of Food Science, Incorporated Administrative Agency, National Institute of Health and Nutrition
  • Takeuchi Masaya
    Sapporo General Pathology Laboratory, Co., Ltd.
  • Saito Morio
    Division of Food Science, Incorporated Administrative Agency, National Institute of Health and Nutrition

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Dietary supplements for body fat reduction have become popular, particularly in developed countries. Garcinia cambogia (GA) is one such supplement, and its active component is (−)-hydroxycitric acid ((−)-HCA), a competitive inhibitor of ATP citrate lyase, which is responsible for producing acetyl CoA from citric acid. Recently we have found that administration of (−)-HCA-containing GA markedly reduces testis weight in male Zucker obese rats. In particular, histopathological examinations revealed testicular atrophy and impairment of spermatogenesis. In the present study, we investigated the cause of the impaired spermatogenesis after ingestion of GA containing (−)-HCA at 102 mmol/kg diet in young Fischer 344 male rats. Among hormones related to spermatogenesis, the serum level of inhibin-B was significantly lower and that of follicle-stimulating hormone (FSH) was higher in the GA group. The level of testis meiosis-activating sterol (T-MAS), which is an intermediate in cholesterol biosynthesis from acetyl CoA and is presumed to transmit a signal for spermatogenesis, was statistically lower in the testes of rats administered GA. We hypothesize from these results that (−)-HCA-mediated inhibition of ATP citrate lyase in rats fed GA leads to diminished accumulation of MAS substances, thus resulting in impairment of spermatogenesis.<br>

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