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Calorie restriction minimizes activation of insulin signaling in response to glucose: Potential involvement of the growth hormone-insulin-like growth factor 1 axis


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Title: Calorie restriction minimizes activation of insulin signaling in response to glucose: Potential involvement of the growth hormone-insulin-like growth factor 1 axis
Authors: Hayashi, Hiroko / Yamaza, Haruyoshi / Komatsu, Toshimitsu / Park, Seongjoon / Chiba, Takuya / Higami, Yoshikazu / Nagayasu, Takeshi / Shimokawa, Isao
Issue Date: Sep-2008
Publisher: Elsevier BV
Citation: Experimental Gerontology, 43(9), pp.827-832; 2008
Abstract: Calorie restriction (CR) may modulate insulin signaling in response to energy intake through suppression of the growth hormone (GH)-IGF-1 axis. We investigated the glucose-stimulated serum insulin response and subsequent alterations in insulin receptor (IR), Akt, and FoxO1 in the rat liver and quadriceps femoris muscle (QFM). Nine-month-old wild-type (W) male Wistar rats fed ad libitum (AL) or a 30% CR diet initiated at 6 weeks of age and GH-suppressed transgenic (Tg) rats fed AL were killed 15 min after intraperitoneal injection of glucose or saline. In W-AL rats, the serum insulin concentration was elevated by glucose injection. Concomitantly, the phosphorylated (p)-IR and p-Akt levels were increased in both tissues. The active FoxO1 level was decreased in the liver, but not significantly in the QFM. In W-CR and Tg-AL rats, the serum insulin response was lower, and no significant changes were noted for the p-IR, p-Akt, or active FoxO1 levels in the liver. In the QFM, the p-Akt level was increased in W-CR and Tg-AL rats with an insignificant elevation of p-IR levels. The phenotypic similarity of W-CR and Tg-AL rats suggest that CR minimizes activation of insulin signaling in response to energy intake mostly through the GH-IGF-1 axis.
Keywords: Akt / Calorie restriction / FoxO1 / Glucose metabolism / Growth hormone-insulin-like growth factor 1 axis / Insulin signaling
URI: http://hdl.handle.net/10069/18753
ISSN: 05315565
DOI: 10.1016/j.exger.2008.05.011
PubMed ID: 18603396
Rights: Copyright (c) 2008 Elsevier Inc. All rights reserved.
Type: Journal Article
Text Version: author
Appears in Collections:Articles in academic journal

Citable URI : http://hdl.handle.net/10069/18753

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