The seasonal glucocorticoid response of male Rufous-winged Sparrows to acute stress correlates with changes in plasma uric acid, but neither glucose nor testosterone.
We sought to clarify functional relationships between baseline and acute stress-induced changes in plasma levels of the stress hormone corticosterone (CORT) and the reproductive hormone testosterone (T), and those of two main metabolites, uric acid (UA) and glucose (GLU). Acute stress in vertebrates generally stimulates the secretion of glucocorticoids, which in birds is primarily CORT. This stimulation is thought to promote behavioral and metabolic changes, including increased glycemia. However, limited information in free-ranging birds supports the view that acutely elevated plasma CORT stimulates glycemia. Acute stress also often decreases the secretion of reproductive hormones (e.g., T in males), but the role of CORT in this decrease and the contribution of T to the regulation of plasma GLU remain poorly understood. We measured initial (pre-stress) and acute stress-induced plasma CORT and T as well as GLU in adult male Rufous-winged Sparrows, Peucaea carpalis, sampled during the pre-breeding, breeding, post-breeding molt, and non-breeding stages. Stress increased plasma CORT and the magnitude of this increase did not differ across life history stages. The stress-induced elevation of plasma CORT was consistently associated with decreased plasma UA, suggesting a role for CORT in the regulation of plasma UA during stress. During stress plasma GLU either increased (pre-breeding), did not change (breeding), or decreased (molt and non-breeding), and plasma T either decreased (pre-breeding and breeding) or did not change (molt and non-breeding). These data provide only partial support to the hypothesis that CORT secretion during acute stress exerts a hyperglycemic action or is responsible for the observed decrease in plasma T taking place at certain life history stages. They also do not support the hypothesis that rapid changes in plasma T influence glycemia.
School of Life Sciences, Arizona State University, Tempe, AZ 85287-4501, USA. Electronic address: deviche@asu.edu.
Pierre
P
Deviche
School of Life Sciences, Arizona State University, Tempe, AZ 85287-4501, USA.
Shelley
S
Valle
School of Life Sciences, Arizona State University, Tempe, AZ 85287-4501, USA.
Sisi
S
Gao
School of Life Sciences, Arizona State University, Tempe, AZ 85287-4501, USA; Department of Biological Sciences, Virginia Tech, Blacksburg, VA 24061, USA.
Scott
S
Davies
School of Life Sciences, Arizona State University, Tempe, AZ 85287-4501, USA.
Stephanie
S
Bittner
Universite de Poitiers, Faculte des Sciences Fondamentales et Appliquees, Poitiers F-86022, France.
Elodie
E
Carpentier
D000818:Animals; D003345:Corticosterone / Q000097:blood; D005938:Glucocorticoids / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism*; D008297:Male; D012621:Seasons; D046370:Sparrows; D013312:Stress, Physiological / Q000502:physiology*; D013739:Testosterone / Q000097:blood*; D014527:Uric Acid / Q000378:metabolism*
D005938:Glucocorticoids; D014527:Uric Acid; D013739:Testosterone; D005947:Glucose; D003345:Corticosterone
Annual cycle; Antioxidant; Glycemia; Passerine; Seasonality; Sparrow