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

Hiroko Hayashi, Haruyoshi Yamaza, Toshimitsu Komatsu, Seongjoon Park, Takuya Chiba, Yoshikazu Higami, Takeshi Nagayasu, Isao Shimokawa

Research output: Contribution to journalArticle

12 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)827-832
Number of pages6
JournalExperimental Gerontology
Volume43
Issue number9
DOIs
Publication statusPublished - Sep 2008
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Ageing
  • Molecular Biology
  • Genetics
  • Endocrinology
  • Cell Biology

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