Different adaptive traits to cold exposure in young senescence-accelerated mice

• Published in: Biogerontology (Dordrecht) 2005-03, Vol.6 (2), p.133-139
• Main Authors: YAMASHITA, Yoshinori, CHIBA, Yoichi, CHEN XIA, HIRAYOSHI, Kazunori, SATOH, Mamoru, SAITOH, Yuko, SHIMADA, Atsuyoshi, NAKAMURA, Eitaro, HOSOKAWA, Masanori
• Format: Article
• Language: English
• Subjects: Adaptation, Physiological - physiology; Adipose Tissue, Brown - physiology; Aging - physiology; Animals; Biological and medical sciences; Body Temperature Regulation - physiology; Carrier Proteins - physiology; Cold; Cold Temperature; Injuries of the abdomen. Foreign bodies of the digestive system; Ion Channels; Male; Medical sciences; Membrane Proteins - physiology; Mice; Mice, Inbred Strains; Mitochondrial Proteins; Motor Activity - physiology; Rodents; Species Specificity; Traumas. Diseases due to physical agents; Uncoupling Protein 1
• ISSN: 1389-5729; 1573-6768
• DOI: 10.1007/s10522-005-3499-x

A reduced adaptation to cold is a prominent feature in aged mammals, including humans. The accelerated senescence-prone strain of mice (SAMP) has been studied as an animal model for several age-associated disorders and in the acceleration of senescence. Recent studies revealed that SAMP strains have dysfunctional hyperactive mitochondria and are under a higher oxidative stress status from a young age. To investigate whether young SAMP mice show impaired cold adaptation abilities, we performed cold-exposure experiments. There were no strain differences in baseline body temperature and lowest reached temperature during cold exposure. SAMP1 mice took longer times to reach their lowest temperature in comparison to SAMR1 mice. SAMR1 mice showed an elevation in temperature following cold exposure, whereas SAMP1 mice did not. Behavioral observations demonstrated that SAMP1 mice moved more actively than SAMR1 during cold exposure. However, mRNA levels of uncoupling protein 1 (UCP1), a heat generating protein, as well as plasma norepinephrine levels, were higher in SAMP1 than in SAMR1 mice. This newly found physiological phenotype in SAMP1 mice provides us with a tool to clarify the genetic mechanism which accelerates the senescence process and helps us develop medical means which will bring mankind to a healthy old age.