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Effect of Heat Stress on Pig Skeletal Muscle Metabolism
Author(s) -
Zhao Lidan,
McMillan Ryan,
Zhang Zhenhe,
Xie Guohao,
Baumgard Lance,
ElKadi Samer,
Selsby Joshua,
Ross Jason,
Gabler Nicholas,
Hulver Matthew,
Rhoads Robert
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.755.7
Subject(s) - medicine , endocrinology , lipolysis , skeletal muscle , citrate synthase , chemistry , acetyl coa carboxylase , beta oxidation , metabolism , carnitine , adipose tissue , fatty acid , pyruvate carboxylase , biochemistry , biology , enzyme
Hyperthermic pigs differ metabolically, including altered insulin profiles, reduced lipolysis, and compromised intestinal integrity, leading to lower lean tissue and elevated adipose tissue mass. This is distinct from thermal neutral pigs on a similar plane of nutrition. To delineate between direct and indirect (via feed intake changes) HS effects, skeletal muscle substrate metabolism was assessed. Pigs (35 ± 0.8 kg) were assigned to three treatments: thermal neutral fed ad libitum (TN, 21°C, n=8), heat stress fed ad libitum (HS, 35°C, n=8), and thermal neutral, pair‐fed to HS intake (PF, n=8) for 7 days. Body temperature (TB) and feed intake (FI) were recorded daily. Longissimus dorsi muscle was biopsied on day ‐2, 3, and 7 relative to start of treatments for metabolic assays. Heat stress increased TB and decreased FI (P < 0.05). Heat stress tended to decrease acid soluble metabolites (P = 0.07), and did not alter glucose oxidation. Metabolic flexibility decreased in HS versus TN and PF (P < 0.05). Total fatty acid oxidation and pyruvate dehydrogenase (PDH) activity increased in PF (P < 0.05), however, TN and HS did not differ. Heat stress inhibited citrate synthase and beta hydroxyacyl‐CoA dehydrogenase (BHAD) activities (P < 0.05). Heat stress did not alter PDH phosphorylation or carnitine palmitoyltransferase 1 abundances, but reduced acetyl‐CoA carboxylase (ACC) protein abundance (P < 0.05). In conclusion, HS altered skeletal muscle fatty acid oxidation and metabolic flexibility, likely involving BHAD and ACC regulation.