Hormonal responses to extreme fasting in subantarctic fur seal (Arctocephalus tropicalis) pups
Identifieur interne : 005B86 ( Main/Exploration ); précédent : 005B85; suivant : 005B87Hormonal responses to extreme fasting in subantarctic fur seal (Arctocephalus tropicalis) pups
Auteurs : Delphine Verrier [Australie, France] ; Shannon Atkinson [États-Unis] ; Christophe Guinet [France] ; Rene Groscolas [France] ; John P. Y. Arnould [Australie]Source :
- American journal of physiology. Regulatory, integrative and comparative physiology [ 0363-6119 ] ; 2012.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Surviving prolonged fasting implies closely regulated alterations in fuel provisioning to meet metabolic requirements, while preserving homeostasis. Little is known, however, of the endocrine regulations governing such metabolic adaptations in naturally fasting free-ranging animals. The hormonal responses to natural prolonged fasting and how they correlate to the metabolic adaptations observed, were investigated in subantarctic fur seal (Arctocephalus tropicalis) pups, which, because of the intermittent pattern of maternal attendance, repeatedly endure exceptionally long fasting episodes throughout their development (1-3 mo). Phase I fasting was characterized by a dramatic decrease in plasma insulin, glucagon, leptin, and total L-thyroxine (T4) associated with reductions in mass-specific resting metabolic rate (RMR), plasma triglycerides, glycerol, and urea-to-creatine ratio, while nonesterified fatty acids (NEFA) and β-OHB increased. In contrast, the metabolic steady-state of phase II fasting reached within 6 days was associated with minimal concentrations of insulin, glucagon, and leptin; unchanged cortisol and triiodothyronine (T3); and moderately increased T4. The early fall in insulin and leptin may mediate the shift to the strategy of energy conservation, protein sparing, and primary reliance on body lipids observed in response to the cessation of feeding. In contrast to the typical mammalian starvation response, nonelevated cortisol and minimal glucagon levels may contribute to body protein preservation and downregulation of catabolic pathways, in general. Furthermore, thyroid hormones may be involved in a process of energy conservation, independent of pups' nutritional state. These original hormonal settings might reflect an adaptation to the otariid repeated fasting pattern and emphasize the crucial importance of a tight physiological control over metabolism to survive extreme energetic constraints.
Affiliations:
- Australie, France, États-Unis
- Alaska, Alsace (région administrative), Grand Est, Victoria (État)
- Melbourne, Strasbourg
- Université de Melbourne
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Regulatory, integrative and comparative physiology</title><title level="j" type="abbreviated">Am. j. physiol., Regul. integr. comp. physiol.</title><idno type="ISSN">0363-6119</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptation</term><term>Alteration</term><term>Animal</term><term>Development</term><term>Fasting</term><term>Glucagon</term><term>Homeostasis</term><term>Insulin</term><term>Intermittent</term><term>Mammalia</term><term>Plasma</term><term>Prolonged</term><term>Requirement</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Jeûne alimentaire</term><term>Prolongé</term><term>Altération</term><term>Exigence</term><term>Homéostasie</term><term>Adaptation</term><term>Animal</term><term>Intermittent</term><term>Développement</term><term>Plasma</term><term>Insuline</term><term>Glucagon</term><term>Mammalia</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Surviving prolonged fasting implies closely regulated alterations in fuel provisioning to meet metabolic requirements, while preserving homeostasis. Little is known, however, of the endocrine regulations governing such metabolic adaptations in naturally fasting free-ranging animals. The hormonal responses to natural prolonged fasting and how they correlate to the metabolic adaptations observed, were investigated in subantarctic fur seal (Arctocephalus tropicalis) pups, which, because of the intermittent pattern of maternal attendance, repeatedly endure exceptionally long fasting episodes throughout their development (1-3 mo). Phase I fasting was characterized by a dramatic decrease in plasma insulin, glucagon, leptin, and total <sub>L</sub>-thyroxine (T<sub>4</sub>) associated with reductions in mass-specific resting metabolic rate (RMR), plasma triglycerides, glycerol, and urea-to-creatine ratio, while nonesterified fatty acids (NEFA) and β-OHB increased. In contrast, the metabolic steady-state of phase II fasting reached within 6 days was associated with minimal concentrations of insulin, glucagon, and leptin; unchanged cortisol and triiodothyronine (T<sub>3</sub>); and moderately increased T<sub>4</sub>. The early fall in insulin and leptin may mediate the shift to the strategy of energy conservation, protein sparing, and primary reliance on body lipids observed in response to the cessation of feeding. In contrast to the typical mammalian starvation response, nonelevated cortisol and minimal glucagon levels may contribute to body protein preservation and downregulation of catabolic pathways, in general. Furthermore, thyroid hormones may be involved in a process of energy conservation, independent of pups' nutritional state. These original hormonal settings might reflect an adaptation to the otariid repeated fasting pattern and emphasize the crucial importance of a tight physiological control over metabolism to survive extreme energetic constraints.</div></front></TEI><affiliations><list><country><li>Australie</li><li>France</li><li>États-Unis</li></country><region><li>Alaska</li><li>Alsace (région administrative)</li><li>Grand Est</li><li>Victoria (État)</li></region><settlement><li>Melbourne</li><li>Strasbourg</li></settlement><orgName><li>Université de Melbourne</li></orgName></list><tree><country name="Australie"><region name="Victoria (État)"><name sortKey="Verrier, Delphine" sort="Verrier, Delphine" uniqKey="Verrier D" first="Delphine" last="Verrier">Delphine Verrier</name></region><name sortKey="Arnould, John P Y" sort="Arnould, John P Y" uniqKey="Arnould J" first="John P. Y." last="Arnould">John P. Y. Arnould</name></country><country name="France"><region name="Grand Est"><name sortKey="Verrier, Delphine" sort="Verrier, Delphine" uniqKey="Verrier D" first="Delphine" last="Verrier">Delphine Verrier</name></region><name sortKey="Groscolas, Rene" sort="Groscolas, Rene" uniqKey="Groscolas R" first="Rene" last="Groscolas">Rene Groscolas</name><name sortKey="Guinet, Christophe" sort="Guinet, Christophe" uniqKey="Guinet C" first="Christophe" last="Guinet">Christophe Guinet</name></country><country name="États-Unis"><region name="Alaska"><name sortKey="Atkinson, Shannon" sort="Atkinson, Shannon" uniqKey="Atkinson S" first="Shannon" last="Atkinson">Shannon Atkinson</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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