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
Subjects:
Animals
Associated diseases and complications
Biological and medical sciences
Blood Glucose - analysis
Brain-Derived Neurotrophic Factor - pharmacology
Carboxy-Lyases - genetics
Diabetes. Impaired glucose tolerance
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Glucokinase - genetics
Glucose-6-Phosphatase - genetics
Glycogen - metabolism
Insulin - blood
Insulin Resistance
Liver - drug effects
Liver - physiopathology
Male
Medical sciences
Metabolic diseases
Obesity
Obesity - physiopathology
Rats
Rats, Zucker
RNA, Messenger - metabolism
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cited_by cdi_FETCH-LOGICAL-c371t-996478e08fc27925680b3eb6e9e11fee78417d6576a991fe134716a9ade17cec3
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creator 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
description 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
doi_str_mv 10.1053/meta.2003.50026
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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 &lt;.05). There was no significant difference in Rd and EGP between the 2 groups under the clamp condition, but the insulin-mediated suppression ratio of endogenous glucose production in BDNF was significantly greater than in vehicle (48.9 ± 22.2 v 22.4% ± 20.6%, P &lt;.05). In BDNF, mRNA expressions of hepatic phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase) were comparable to those of vehicle, while hepatic glucokinase (GK) mRNA expression was significantly higher (1.57 ± 0.33 v 1.03 ± 0.17, P &lt;.05). We conclude that BDNF mainly improves hepatic insulin resistance in obese insulin-resistant rats, probably by affecting the hepatic GK flux. Copyright 2003, Elsevier Science (USA). 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There was no significant difference in Rd and EGP between the 2 groups under the clamp condition, but the insulin-mediated suppression ratio of endogenous glucose production in BDNF was significantly greater than in vehicle (48.9 ± 22.2 v 22.4% ± 20.6%, P &lt;.05). In BDNF, mRNA expressions of hepatic phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase) were comparable to those of vehicle, while hepatic glucokinase (GK) mRNA expression was significantly higher (1.57 ± 0.33 v 1.03 ± 0.17, P &lt;.05). We conclude that BDNF mainly improves hepatic insulin resistance in obese insulin-resistant rats, probably by affecting the hepatic GK flux. Copyright 2003, Elsevier Science (USA). All rights reserved.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>12601633</pmid><doi>10.1053/meta.2003.50026</doi><tpages>6</tpages></addata></record>
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ispartof Metabolism, clinical and experimental, 2003-02, Vol.52 (2), p.203-208
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subjects Animals
Associated diseases and complications
Biological and medical sciences
Blood Glucose - analysis
Brain-Derived Neurotrophic Factor - pharmacology
Carboxy-Lyases - genetics
Diabetes. Impaired glucose tolerance
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Glucokinase - genetics
Glucose-6-Phosphatase - genetics
Glycogen - metabolism
Insulin - blood
Insulin Resistance
Liver - drug effects
Liver - physiopathology
Male
Medical sciences
Metabolic diseases
Obesity
Obesity - physiopathology
Rats
Rats, Zucker
RNA, Messenger - metabolism
title Brain-derived neurotrophic factor ameliorates hepatic insulin resistance in Zucker fatty rats
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