title: Physical activity prevented age-related decline in energy metabolism in genetically obese and diabetic rats, but not in control rats.
abstract: 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)A1c 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.
authors.affiliation: Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology, 35-2 Sakaecho Itabashiku, Tokyo 173-0015, Japan. miyasaka@tmig.or.jp
authors.forename: Kyoko
authors.initials: K
authors.lastname: Miyasaka
authors.forename: Mineko
authors.initials: M
authors.lastname: Ichikawa
authors.forename: Takako
authors.initials: T
authors.lastname: Kawanami
authors.forename: Setsuko
authors.initials: S
authors.lastname: Kanai
authors.forename: Minoru
authors.initials: M
authors.lastname: Ohta
authors.forename: Norikazu
authors.initials: N
authors.lastname: Sato
authors.forename: Hidemichi
authors.initials: H
authors.lastname: Ebisawa
authors.forename: Akihiro
authors.initials: A
authors.lastname: Funakoshi
mesh_terms: D000375:Aging / Q000378:metabolism*; D000818:Animals; D001786:Blood Glucose; D001835:Body Weight; D002784:Cholesterol / Q000097:blood; D003920:Diabetes Mellitus / Q000235:genetics / Q000378:metabolism*; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics / Q000378:metabolism*; D004734:Energy Metabolism / Q000502:physiology*; D006442:Glycated Hemoglobin / Q000378:metabolism; D007328:Insulin / Q000097:blood; D008297:Male; D009043:Motor Activity / Q000502:physiology*; D009765:Obesity; D009929:Organ Size; D051381:Rats; D020334:Rats, Inbred OLETF; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D002784:Cholesterol; D006442:Glycated Hemoglobin; D007328:Insulin; D014280:Triglycerides