Calorie restriction initiated at middle age improved glucose tolerance without affecting age-related impairments of insulin signaling in rat skeletal muscle

Seongjoon Park, Toshimitsu Komatsu, Hiroko Hayashi, Haruyoshi Yamaza, Takuya Chiba, Yoshikazu Higami, Kazunao Kuramoto, Isao Shimokawa

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Calorie restriction (CR) may affect glucose tolerance via modulation of the insulin action in skeletal muscle. The present study investigated the effect of CR initiated at middle age in rats bearing glucose intolerance, in comparison with CR at a younger age. Male F344 rats at 2.5 and 18 months (mo) of age were fed ad libitum (AL) or 30% CR diets for 4-4.5 mo, subjected to glucose tolerance testing, and then sacrificed 15 min after intraperitoneal glucose or saline injection to evaluate glucose-stimulated insulin response and subsequent activation of insulin signaling molecules. The protein abundance of phosphorylated (p) insulin receptors, p-Akt, and p-atypical PKC and the membrane fraction of glucose transporter 4 in quadriceps femoris muscle (QFM) were analyzed by EIA or immunoblotting. CR initiated either at young or middle age improved glucose tolerance with a lower serum insulin response to glucose. However, middle-aged CR did not improve aging-related impairments in insulin signaling in QFM. The present results emphasized the possibilities of CR activation of an insulin-independent mechanism in skeletal muscle and also of the involvement of non-muscle tissues in glucose uptake.

Original languageEnglish
Pages (from-to)837-845
Number of pages9
JournalExperimental Gerontology
Volume41
Issue number9
DOIs
Publication statusPublished - 2006 Sep
Externally publishedYes

Fingerprint

Muscle
Rats
Skeletal Muscle
Insulin
Glucose
Quadriceps Muscle
Bearings (structural)
Chemical activation
Glucose Intolerance
Facilitative Glucose Transport Proteins
Insulin Receptor
Inbred F344 Rats
Immunoblotting
Nutrition
Diet
Aging of materials
Modulation
Tissue
Injections
Membranes

Keywords

  • Aging
  • Calorie restriction
  • Glucose intolerance
  • Insulin resistance
  • Insulin signal
  • Skeletal muscle

ASJC Scopus subject areas

  • Ageing
  • Medicine(all)

Cite this

Calorie restriction initiated at middle age improved glucose tolerance without affecting age-related impairments of insulin signaling in rat skeletal muscle. / Park, Seongjoon; Komatsu, Toshimitsu; Hayashi, Hiroko; Yamaza, Haruyoshi; Chiba, Takuya; Higami, Yoshikazu; Kuramoto, Kazunao; Shimokawa, Isao.

In: Experimental Gerontology, Vol. 41, No. 9, 09.2006, p. 837-845.

Research output: Contribution to journalArticle

Park, Seongjoon ; Komatsu, Toshimitsu ; Hayashi, Hiroko ; Yamaza, Haruyoshi ; Chiba, Takuya ; Higami, Yoshikazu ; Kuramoto, Kazunao ; Shimokawa, Isao. / Calorie restriction initiated at middle age improved glucose tolerance without affecting age-related impairments of insulin signaling in rat skeletal muscle. In: Experimental Gerontology. 2006 ; Vol. 41, No. 9. pp. 837-845.
@article{0e8f39259a104aa5a75b53dab7c1761e,
title = "Calorie restriction initiated at middle age improved glucose tolerance without affecting age-related impairments of insulin signaling in rat skeletal muscle",
abstract = "Calorie restriction (CR) may affect glucose tolerance via modulation of the insulin action in skeletal muscle. The present study investigated the effect of CR initiated at middle age in rats bearing glucose intolerance, in comparison with CR at a younger age. Male F344 rats at 2.5 and 18 months (mo) of age were fed ad libitum (AL) or 30{\%} CR diets for 4-4.5 mo, subjected to glucose tolerance testing, and then sacrificed 15 min after intraperitoneal glucose or saline injection to evaluate glucose-stimulated insulin response and subsequent activation of insulin signaling molecules. The protein abundance of phosphorylated (p) insulin receptors, p-Akt, and p-atypical PKC and the membrane fraction of glucose transporter 4 in quadriceps femoris muscle (QFM) were analyzed by EIA or immunoblotting. CR initiated either at young or middle age improved glucose tolerance with a lower serum insulin response to glucose. However, middle-aged CR did not improve aging-related impairments in insulin signaling in QFM. The present results emphasized the possibilities of CR activation of an insulin-independent mechanism in skeletal muscle and also of the involvement of non-muscle tissues in glucose uptake.",
keywords = "Aging, Calorie restriction, Glucose intolerance, Insulin resistance, Insulin signal, Skeletal muscle",
author = "Seongjoon Park and Toshimitsu Komatsu and Hiroko Hayashi and Haruyoshi Yamaza and Takuya Chiba and Yoshikazu Higami and Kazunao Kuramoto and Isao Shimokawa",
year = "2006",
month = "9",
doi = "10.1016/j.exger.2006.06.055",
language = "English",
volume = "41",
pages = "837--845",
journal = "Experimental Gerontology",
issn = "0531-5565",
publisher = "Elsevier Inc.",
number = "9",

}

TY - JOUR

T1 - Calorie restriction initiated at middle age improved glucose tolerance without affecting age-related impairments of insulin signaling in rat skeletal muscle

AU - Park, Seongjoon

AU - Komatsu, Toshimitsu

AU - Hayashi, Hiroko

AU - Yamaza, Haruyoshi

AU - Chiba, Takuya

AU - Higami, Yoshikazu

AU - Kuramoto, Kazunao

AU - Shimokawa, Isao

PY - 2006/9

Y1 - 2006/9

N2 - Calorie restriction (CR) may affect glucose tolerance via modulation of the insulin action in skeletal muscle. The present study investigated the effect of CR initiated at middle age in rats bearing glucose intolerance, in comparison with CR at a younger age. Male F344 rats at 2.5 and 18 months (mo) of age were fed ad libitum (AL) or 30% CR diets for 4-4.5 mo, subjected to glucose tolerance testing, and then sacrificed 15 min after intraperitoneal glucose or saline injection to evaluate glucose-stimulated insulin response and subsequent activation of insulin signaling molecules. The protein abundance of phosphorylated (p) insulin receptors, p-Akt, and p-atypical PKC and the membrane fraction of glucose transporter 4 in quadriceps femoris muscle (QFM) were analyzed by EIA or immunoblotting. CR initiated either at young or middle age improved glucose tolerance with a lower serum insulin response to glucose. However, middle-aged CR did not improve aging-related impairments in insulin signaling in QFM. The present results emphasized the possibilities of CR activation of an insulin-independent mechanism in skeletal muscle and also of the involvement of non-muscle tissues in glucose uptake.

AB - Calorie restriction (CR) may affect glucose tolerance via modulation of the insulin action in skeletal muscle. The present study investigated the effect of CR initiated at middle age in rats bearing glucose intolerance, in comparison with CR at a younger age. Male F344 rats at 2.5 and 18 months (mo) of age were fed ad libitum (AL) or 30% CR diets for 4-4.5 mo, subjected to glucose tolerance testing, and then sacrificed 15 min after intraperitoneal glucose or saline injection to evaluate glucose-stimulated insulin response and subsequent activation of insulin signaling molecules. The protein abundance of phosphorylated (p) insulin receptors, p-Akt, and p-atypical PKC and the membrane fraction of glucose transporter 4 in quadriceps femoris muscle (QFM) were analyzed by EIA or immunoblotting. CR initiated either at young or middle age improved glucose tolerance with a lower serum insulin response to glucose. However, middle-aged CR did not improve aging-related impairments in insulin signaling in QFM. The present results emphasized the possibilities of CR activation of an insulin-independent mechanism in skeletal muscle and also of the involvement of non-muscle tissues in glucose uptake.

KW - Aging

KW - Calorie restriction

KW - Glucose intolerance

KW - Insulin resistance

KW - Insulin signal

KW - Skeletal muscle

UR - http://www.scopus.com/inward/record.url?scp=33749684748&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33749684748&partnerID=8YFLogxK

U2 - 10.1016/j.exger.2006.06.055

DO - 10.1016/j.exger.2006.06.055

M3 - Article

VL - 41

SP - 837

EP - 845

JO - Experimental Gerontology

JF - Experimental Gerontology

SN - 0531-5565

IS - 9

ER -