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Insulin as a differential regulator of lipid mobilization in fasting northern elephant seals
Fowler, M.A.; Debier, C.; Champagne, C.D.; Crocker, D.E.; Costa, D.P. (2013). Insulin as a differential regulator of lipid mobilization in fasting northern elephant seals. Integrative and Comparative Biology 53: E71-E71
In: Integrative and Comparative Biology. Oxford University Press: McLean, VA. ISSN 1540-7063, more
Peer reviewed article  

Available in  Authors 
Document type: Summary

Authors  Top 
  • Fowler, M.A.
  • Debier, C., more
  • Champagne, C.D.
  • Crocker, D.E.
  • Costa, D.P.

Abstract
    Animals that experience fasting concomitant with metabolically demanding activities are presented with conflicting demands of energy savings and energy expenditure. We aimed to understand 1) understand how fasting, molting northern elephant seals and fasting, lactating northern elephant seals differentially regulate the mobilization of lipid reserves and 2) how milk lipid content is regulated in lactating elephant seals. We sampled 36 lactating females in early lactation, 39 females in late lactation and eight early molt females and six late molt females. Mass, adiposity, circulating non-esterified fatty acids (NEFA), triacylglycerol (TAG), cortisol, insulin and growth hormone levels and milk lipid content were measured. Milk lipid increased from 31% lipid to 51% lipid over ~ 17 days of fasting and lactation. In lactating females increasing cortisol and decreasing insulin were significantly (p<0.05) related to NEFA levels, but in molting seals, only increasing cortisol was significantly (p<0.05) related to circulating NEFA. Milk lipid content varied significantly (p<0.05) with mass, adiposity, NEFA and TAG. Growth hormone was not related to metabolites or milk lipid. Decreasing insulin appears to be the differential regulator of lipolysis in lactating seals versus molting seals, facilitating the additional liberation of stored lipids required for milk synthesis. Milk lipid is strongly impacted by the supply of substrate to the mammary gland, indicating that the regulation of lipid mobilization from adipose reserves may be responsible for changes in milk lipid content.

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