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Am J Physiol Regul Integr Comp Physiol (June 11, 2008). doi:10.1152/ajpregu.00629.2007
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Submitted on September 24, 2007
Accepted on June 3, 2008

Effects of age on thermoregulatory responses during cold exposure in a non-human primate, Microcebus murinus

Jeremy Terrien1*, Philippe Zizzari2, Marie-Therese Bluet-Pajot2, Pierre-Yves Henry1, Martine Perret1, Jacques Epelbaum2, and Fabienne Aujard1

1 UMR CNRS/MNHN 7179, BRUNOY, France
2 U549, Inserm, Paris, France

* To whom correspondence should be addressed. E-mail: terrien{at}mnhn.fr.

Cold resistance appears altered with aging. Among existing hypothesis, the impaired capacity in response to cold could be related to an altered regulation of plasma insulin-like growth factor-1 (IGF-1) concentration. The combined effects of age and cold exposure were studied in a short-living primate, the gray mouse lemur (Microcebus murinus) which adjusts its energy balance using a daily torpor phase, to avoid high energy cost of normothermia maintenance. Changes in body mass, core temperature, locomotor activity and caloric intake were monitored under 9-day exposures to 25 °C and 12 °C in captive animals in winter conditions. Short-term (after 2 days) and long-term (after 9 days) cold-induced changes in IGF-1 levels were also evaluated. In thermoneutral conditions (25 °C), general characteristics of the daily rhythm of core temperature were preserved with age. At 12 °C, age-related changes were mainly characterized by a deeper hypothermia and an increased frequency of torpor phases, associated with a loss of body mass. A short-term cold-induced decrease in plasma IGF-1 levels was observed. IGF-1 levels returned to basal values after 9 days of cold exposure. No significant effect of age could be evidenced on IGF-1 response. However, IGF-1 levels of cold-exposed aged animals were negatively correlated with the frequency of daily torpor. Responses exhibited by aged mouse lemurs exposed to cold revealed difficulties in the maintenance of normothermia and energy balance, and might involve modulations of IGF-1 levels.







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