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Brain-derived neurotrophic factor ameliorates hepatic insulin resistance in Zucker fatty rats

Brain-derived neurotrophic factor (BDNF), a member of the neurotrophins, has been reported to ameliorate hyperglycemia in obese diabetic animal models. To elucidate the mechanism of BDNF on glucose metabolism, we determined the glucose turnover under basal and euglycemic hyperinsulinemic (insulin in...

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Published in:Metabolism, clinical and experimental clinical and experimental, 2003-02, Vol.52 (2), p.203-208
Main Authors: Kuroda, Akio, Yamasaki, Yoshimitsu, Matsuhisa, Munehide, Kubota, Minoru, Nakahara, Itsuro, Nakatani, Yoshihisa, Hoshi, Ayumu, Gorogawa, Shin-ichi, Umayahara, Yutaka, Itakura, Yasushi, Nakagawa, Tsutomu, Taiji, Mutsuo, Kajimoto, Yoshitaka, Hori, Masatsugu
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Language:English
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Summary:Brain-derived neurotrophic factor (BDNF), a member of the neurotrophins, has been reported to ameliorate hyperglycemia in obese diabetic animal models. To elucidate the mechanism of BDNF on glucose metabolism, we determined the glucose turnover under basal and euglycemic hyperinsulinemic (insulin infusion rate, 54 pmol · kg−1 · min−1) clamp conditions in obese insulin-resistant rats, male Zucker fatty rats, which had been acutely administered a subcutaneous injection of BDNF (20 mg/kg) (n = 9, BDNF) or vehicle (n = 8, vehicle). Under the basal condition, acute administration of BDNF did not affect the blood glucose level, plasma insulin level, rate of glucose disappearance (Rd), and endogenous glucose production (EGP). Under the clamp condition, the glucose infusion rate (GIR) was significantly higher in BDNF than in vehicle (mean ± SD, 61.4 ± 19.1 v 41.4 ± 4.9 μmol · kg−1 · min−1, P
ISSN:0026-0495
1532-8600
DOI:10.1053/meta.2003.50026