25-Hydroxycholecalciferol Improves Cardiac Metabolic Adaption, Mitochondrial Biogenetics, and Redox Status to Ameliorate Pathological Remodeling and Functional Failure in Obese Chickens
Shih-Kai Chiang,
Mei-Ying Sin,
Jun-Wen Lin,
Maraddin Siregar,
Gilmour Valdez,
Yu-Hui Chen,
Thau Kiong Chung,
Rosemary L. Walzem,
Lin-Chu Chang,
Shuen-Ei Chen
Affiliations
Shih-Kai Chiang
Department of Animal Science, National Chung Hsing University, Taichung 40227, Taiwan
Mei-Ying Sin
Chinese Medicinal Research and Development Center, China Medical University Hospital, Taichung 40447, Taiwan
Jun-Wen Lin
Department of Animal Science, National Chung Hsing University, Taichung 40227, Taiwan
Maraddin Siregar
Department of Animal Science, National Chung Hsing University, Taichung 40227, Taiwan
Gilmour Valdez
Department of Animal Science, National Chung Hsing University, Taichung 40227, Taiwan
Yu-Hui Chen
Department of Animal Science, National Chung Hsing University, Taichung 40227, Taiwan
Thau Kiong Chung
DSM Nutritional Products Asia Pacific, Mapletree Business City, Singapore 117440, Singapore
Rosemary L. Walzem
Department of Poultry Science, Texas A&M University, College Station, TX 77843, USA
Lin-Chu Chang
Chinese Medicinal Research and Development Center, China Medical University Hospital, Taichung 40447, Taiwan
Shuen-Ei Chen
Department of Animal Science, National Chung Hsing University, Taichung 40227, Taiwan
Broiler breeder hens allowed ad libitum (Ad) feed intake developed obesity and cardiac pathogenesis and thereby were susceptible to sudden death. A supplement of 69 µg 25-hydroxycholecalciferol (25-OH-D3)/kg feed rescued the livability of feed-restricted (R) and Ad-hens (mortality; 6.7% vs. 8.9% and 31.1% vs. 48.9%). Necropsy with the surviving counterparts along the time course confirmed alleviation of myocardial remodeling and functional failure by 25-OH-D3, as shown by BNP and MHC-β expressions, pathological hypertrophy, and cardiorespiratory responses (p p p p < 0.05). In conclusion, 25-OH-D3 ameliorates cardiac pathological remodeling and functional compromise to rescue the livability of obese hens through metabolic flexibility and mitochondrial bioenergetics, and by operating at antioxidant defense, and heme and iron metabolism, to maintain redox homeostasis and sustain cell viability.
