4.5 Article

Can offsetting the energetic cost of hibernation restore an active season phenotype in grizzly bears (Ursus arctos horribilis)?

Journal

JOURNAL OF EXPERIMENTAL BIOLOGY
Volume 224, Issue 12, Pages -

Publisher

COMPANY BIOLOGISTS LTD
DOI: 10.1242/jeb.242560

Keywords

Bear; Hibernation; Metabolism; Circadian rhythm; Cell culture; Adipocyte

Categories

Funding

  1. International Association for Bear Research and Management [WSU003675]
  2. Washington State University endowments: Raili Korkka Brown Bear Fund
  3. Bear Research and Conservation Fund
  4. Nutritional Ecology Fund

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Feeding glucose to hibernating bears partially restores metabolic parameters to active season levels, with some indicators remaining incomplete due to the suppression of circulating free fatty acids. The study provides a controlled model to examine the relationship between nutrient availability and metabolism on the hibernation phenotype in bears.
Hibernation is characterized by depression of many physiological processes. To determine if this state is reversible in a non-food caching species, we fed hibernating grizzly bears (Ursus arctos horribilis) dextrose for 10 days to replace 53% or 100% of the estimated minimum daily energetic cost of hibernation. Feeding caused serum concentrations of glycerol and ketones (beta-hydroxybutyrate) to return to active season levels irrespective of the amount of glucose fed. By contrast, free fatty acids (FFAs) and indices of metabolic rate, such as general activity, heart rate, strength of heart rate circadian rhythm, and insulin sensitivity were restored to approximately 50% of active season levels. Body temperature was unaffected by feeding. To determine the contribution of adipose to the metabolic effects observed after glucose feeding, we cultured bear adipocytes collected at the beginning and end of the feeding and performed metabolic flux analysis. We found a similar to 33% increase in energy metabolism after feeding. Moreover, basal metabolism before feeding was 40% lower in hibernation cells compared with fed cells or active cells cultured at 37 degrees C, thereby confirming the temperature independence of metabolic rate. The partial depression of circulating FFAs with feeding likely explains the incomplete restoration of insulin sensitivity and other metabolic parameters in hibernating bears. Further depression of metabolic function is likely to be an active process. Together, the results provide a highly controlled model to examine the relationship between nutrient availability and metabolism on the hibernation phenotype in bears.

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