Physical activity prevented age-related decline in energy metabolism in genetically obese and diabetic rats, but not in control rats

被引:18
作者
Miyasaka, K
Ichikawa, M
Kawanami, T
Kanai, S
Ohta, M
Sato, N
Ebisawa, H
Funakoshi, A
机构
[1] Tokyo Metropolitan Inst Gerontol, Dept Clin Physiol, Itabashi Ku, Tokyo 1730015, Japan
[2] Tokyo Metropolitan Inst Gerontol, Dept Nutr, Itabashi Ku, Tokyo 1730015, Japan
[3] Kyushu Natl Canc Ctr, Dept Gastroenterol, Fukuoka 8111395, Japan
关键词
physical exercise; energy expenditure; insulin; diabetes mellitus; obesity; rats;
D O I
10.1016/S0047-6374(02)00118-5
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Laboratory rats are normally confined to cages that markedly restrict their physical activity. In these rats, the resting energy expenditure accounts for 90% of the total daily energy expenditure, while the daily physical activity in humans consumes 30% of the total daily energy expenditure. Otsuka Long Evans Tokushima Fatty (OLETF) rats have been developed as a model of non-insulin-dependent diabetes mellitus (NIDDM) with mild obesity, and obesity is an important factor that induces diabetes in this strain. We implemented a running-wheel exercise regimen that was the equivalent of normal physical activity to provide light exercise for OLETF rats. The purpose of the study was to determine if light exercise improves the age-related decline in energy metabolism and glucose intolerance in OLETF rats. The effects were also compared in control Long Evans Tokushima (LETO) rats. From 12 to 46 weeks of age, the rats performed a running-wheel exercise (3000 m/day). Energy metabolism was determined at 8-week intervals. The typical increase in body weight was significantly decreased in OLETF rats in response to exercise, while no significant effect was observed in LETO rats. Energy expenditure and basal metabolic rate (BMR) per kilogram body weight (not whole-body weight) were increased by exercise in OLETF rats, but not in LETO rats. At 46 weeks of age, after exercise, the blood glucose and hemoglobin (Hb)Alc levels, as well as the plasma levels of insulin, triglyceride, cholesterol, and leptin significantly decreased in OLETF rats, while only the plasma levels of cholesterol and leptin significantly decreased in LETO rats. Light exercise thus appears to be beneficial for preventing age-related decline in energy metabolism and glucose intolerance in OLETF rats. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:183 / 190
页数:8
相关论文
共 34 条
  • [1] ALLAIN CC, 1974, CLIN CHEM, V20, P470
  • [2] IMMUNOCHEMICAL EVIDENCE OF CHOLECYSTOKININ-LIKE PEPTIDES IN BRAIN
    DOCKRAY, GJ
    [J]. NATURE, 1976, 264 (5586) : 568 - 570
  • [3] FOSSATI P, 1982, CLIN CHEM, V28, P2077
  • [4] EFFECTS OF FEED RESTRICTION AND SWITCHING THE DIET ON PROTEINURIA IN MALE WISTAR RATS
    FUJITA, Y
    ICHIKAWA, M
    KURIMOTO, F
    RIKIMARU, T
    [J]. JOURNALS OF GERONTOLOGY, 1984, 39 (05): : 531 - 537
  • [5] Fujita Yoshiaki, 1993, Japanese Journal of Geriatrics, V30, P568
  • [6] LITTLE OR NO EXPRESSION OF THE CHOLECYSTOKININ-A RECEPTOR GENE IN THE PANCREAS OF DIABETIC RATS (OTSUKA LONG-EVANS TOKUSHIMA FATTY=OLETF RATS)
    FUNAKOSHI, A
    MIYASAKA, K
    JIMI, A
    KAWANAI, T
    TAKATA, Y
    KONO, A
    [J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1994, 199 (02) : 482 - 488
  • [7] AN ANIMAL-MODEL OF CONGENITAL DEFECT OF GENE-EXPRESSION OF CHOLECYSTOKININ (CCK)-A RECEPTOR
    FUNAKOSHI, A
    MIYASAKA, K
    SHINOZAKI, H
    MASUDA, M
    KAWANAMI, T
    TAKATA, Y
    KONO, A
    [J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1995, 210 (03) : 787 - 796
  • [8] Pancreatic endocrine dysfunction in rats not expressing the cholecystokinin-A receptor
    Funakoshi, A
    Miyasaka, K
    Kanai, S
    Masuda, M
    Yasunami, T
    Nagai, T
    Ikeda, S
    Jimi, A
    Kawanami, T
    Kono, A
    [J]. PANCREAS, 1996, 12 (03) : 230 - 236
  • [9] PHYSICAL-ACTIVITY AND REDUCED OCCURRENCE OF NON-INSULIN-DEPENDENT DIABETES-MELLITUS
    HELMRICH, SP
    RAGLAND, DR
    LEUNG, RW
    PAFFENBARGER, RS
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1991, 325 (03) : 147 - 152
  • [10] HILL DR, 1990, J NEUROSCI, V10, P1070