Heat stress alters adipose adrenergic signaling in lactating dairy cows

Wednesday, July 23, 2014
Exhibit Hall AB (Kansas City Convention Center)
Guohao Xie , Virginia Tech, Blacksburg, VA
Laun W. Hall , The University of Arizona, Tucson, AZ
Marie Nearing , The University of Arizona, Tucson, AZ
Lori C Cole , The University of Arizona, Tucson, AZ
Diane M. Spurlock , Iowa State University, Ames, IA
Lance H. Baumgard , Iowa State University, Ames, IA
Robert P Rhoads , Virginia Tech, Blacksburg, VA
Abstract Text: Malnourished animals mobilize adipose tissue to alleviate the impact of energy deficiency on galactopoiesis, but heat-stressed (HS) lactating cows lessen their dependence on this strategy. One possibility is that lipolytic response becomes refractory to adrenergic signaling. To test this hypothesis, multiparous dairy cows (n=6; parity = 4 ± 0.9; 436 ± 93 DIM; 721 ± 39 kg BW) housed in climate chambers were fed a TMR consisting primarily of alfalfa hay and steam-flaked corn and subjected to 2 experimental periods (P): 1) thermoneutral conditions (TN; 18°C, 20% humidity) with ad libitum intake for 9d and 2) HS conditions (cyclical temperature 31–40°C, 20% humidity: min THI = 73, max THI = 86) with ad libitum intake for 9d. Rectal temperature (Tre) was measured thrice daily at 0600, 1400 and 1800h. During each P, cows were administered epinephrine intramuscularly (0.02 mg/kg) twice daily from d 6 to d 9. Before and after epinephrine treatment, adipose biopsies were obtained from contralateral tailhead areas. Adipose lipolysis and lipogenic-related proteins were measured by western immunoblotting. During P2, HS caused a 1.3 °C increase in Tre compared with TN (P < 0.001).  Heat stress reduced DMI by 18% (P < 0.001) and milk yield by 10% (P < 0.01). Epinephrine increased 5’ adenosine monophosphate (AMP)-activated protein kinase (AMPK) (P < 0.1), cyclic-AMP response element-binding protein (CREB) (P < 0.05) and hormone sensitive lipase (HSL) (P < 0.05) phosphorylation abundance during TN but not in HS. Beta2 adrenergic receptor (BAR2) abundance was stable in all periods and treatments. Adipose triglyceride lipase (ATGL) protein expression was blunted (P < 0.05) by epinephrine in TN and HS. Fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC) and phosphorylated ACC protein abundance were decreased (P < 0.05) by HS but did not respond to epinephrine challenge. In contrast, insulin receptor (IR) increased (P < 0.05) in HS regardless of epinephrine administration. Protein kinase B (AKT) phosphorylation tended to increase (P < 0.1) in response to epinephrine during HS. These observations indicate HS may alter adrenergic signaling by blunting lipolytic response in lactating cows. Potential cross talk between epinephrine and insulin may underlie HS adaptation.

Keywords: Heat stress, lactation, catecholamine