Nonshivering Thermogenesis in Winter-Acclimatized King Penguin Chicks

Duchamp, Claude; Barré, Hervé; Delage, Didier; Berne, G.; Brebion, P.; Rouanet, Jean‐Louis

doi:10.1007/978-1-4757-0031-2_6

Cited by 3 publications

(1 citation statement)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The effects of glucagon in birds are similar to those of catecholamines in mammals, leading to suggestions that glucagon could be a potential mediator of avian NST (Freeman, 1970; Barre, Cohen‐Adad & Rouanet, 1987; Duchamp et al ., 1999). Glucagon injection activates NST in birds like ducklings, penguins and pigeons (Barre et al ., 1987; Duchamp et al ., 1993, 1989 a ; Hohtola, Hissa & Saarela, 1977; Carey et al ., 2019), but whether cold exposure increases plasma glucagon levels is not known. The physiological effects of glucagon might partly result from synergistic action with hormones that regulate metabolism and BMR, such as corticosterone and norepinephrine (Filali‐Zegzouti et al ., 2005; Koban & Feist, 1982; Abdelmelek et al ., 2001).…”

Section: Hormonal Regulators Of Cold Adaptation In Birdsmentioning

confidence: 99%

Avian adjustments to cold and non‐shivering thermogenesis: whats, wheres and hows

Pani

Bal

2022

Biological Reviews

View full text Add to dashboard Cite

Avian cold adaptation is hallmarked by innovative strategies of both heat conservation and thermogenesis. While minimizing heat loss can reduce the thermogenic demands of body temperature maintenance, it cannot eliminate the requirement for thermogenesis. Shivering and non-shivering thermogenesis (NST) are the two synergistic mechanisms contributing to endothermy. Birds are of particular interest in studies of NST as they lack brown adipose tissue (BAT), the major organ of NST in mammals. Critical analysis of the existing literature on avian strategies of cold adaptation suggests that skeletal muscle is the principal site of NST. Despite recent progress, isolating the mechanisms involved in avian muscle NST has been difficult as shivering and NST co-exist with its primary locomotory function. Herein, we re-evaluate various proposed molecular bases of avian skeletal muscle NST. Experimental evidence suggests that sarco(endo)plasmic reticulum Ca 2+ -ATPase (SERCA) and ryanodine receptor 1 (RyR1) are key in avian muscle NST, through their mediation of futile Ca 2+ cycling and thermogenesis. More recent studies have shown that SERCA regulation by sarcolipin (SLN) facilitates muscle NST in mammals; however, its role in birds is unclear. Ca 2+ signalling in the muscle seems to be common to contraction, shivering and NST, but elucidating its roles will require more precise measurement of local Ca 2+ levels inside avian myofibres. The endocrine control of avian muscle NST is still poorly defined. A better understanding of the mechanistic details of avian muscle NST will provide insights into the roles of these processes in regulatory thermogenesis, which could further inform our understanding of the evolution of endothermy among vertebrates.

show abstract