25-Hydroxycholecalciferol Improves Cardiac Metabolic Adaption, Mitochondrial Biogenetics, and Redox Status to Ameliorate Pathological Remodeling and Functional Failure in Obese Chickens
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...
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2024-11-01
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| Series: | Antioxidants |
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| Online Access: | https://www.mdpi.com/2076-3921/13/11/1426 |
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| author | 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 |
| author_facet | 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 |
| author_sort | Shih-Kai Chiang |
| collection | DOAJ |
| description | 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 (<i>p</i> < 0.05). 25-OH-D3 mitigated cardiac deficient bioenergetics in Ad-hens by rescuing PGC-1α activation, mitochondrial biogenesis, dynamics, and electron transport chain complex activities, and metabolic adaptions in glucose oxidation, pyruvate/lactate interconversion, TCA cycle, and β-oxidation, as well as in TG and ceramide accumulation to limit lipotoxic development (<i>p</i> < 0.05). Supplemental 25-OH-D3 also sustained Nrf2 activation and relieved MDA accumulation, protein carbonylation, and GSH depletion to potentiate cell survival in the failing heart (<i>p</i> < 0.05). Parts of the redox amendments were mediated via lessened blood hematocrit and heme metabolism, and improved iron status and related gene regulations (<i>p</i> < 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. |
| format | Article |
| id | doaj-art-016d44bf86704381a2be7ae0fd6acc77 |
| institution | OA Journals |
| issn | 2076-3921 |
| language | English |
| publishDate | 2024-11-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Antioxidants |
| spelling | doaj-art-016d44bf86704381a2be7ae0fd6acc772025-08-20T01:53:48ZengMDPI AGAntioxidants2076-39212024-11-011311142610.3390/antiox1311142625-Hydroxycholecalciferol Improves Cardiac Metabolic Adaption, Mitochondrial Biogenetics, and Redox Status to Ameliorate Pathological Remodeling and Functional Failure in Obese ChickensShih-Kai Chiang0Mei-Ying Sin1Jun-Wen Lin2Maraddin Siregar3Gilmour Valdez4Yu-Hui Chen5Thau Kiong Chung6Rosemary L. Walzem7Lin-Chu Chang8Shuen-Ei Chen9Department of Animal Science, National Chung Hsing University, Taichung 40227, TaiwanChinese Medicinal Research and Development Center, China Medical University Hospital, Taichung 40447, TaiwanDepartment of Animal Science, National Chung Hsing University, Taichung 40227, TaiwanDepartment of Animal Science, National Chung Hsing University, Taichung 40227, TaiwanDepartment of Animal Science, National Chung Hsing University, Taichung 40227, TaiwanDepartment of Animal Science, National Chung Hsing University, Taichung 40227, TaiwanDSM Nutritional Products Asia Pacific, Mapletree Business City, Singapore 117440, SingaporeDepartment of Poultry Science, Texas A&M University, College Station, TX 77843, USAChinese Medicinal Research and Development Center, China Medical University Hospital, Taichung 40447, TaiwanDepartment of Animal Science, National Chung Hsing University, Taichung 40227, TaiwanBroiler 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 (<i>p</i> < 0.05). 25-OH-D3 mitigated cardiac deficient bioenergetics in Ad-hens by rescuing PGC-1α activation, mitochondrial biogenesis, dynamics, and electron transport chain complex activities, and metabolic adaptions in glucose oxidation, pyruvate/lactate interconversion, TCA cycle, and β-oxidation, as well as in TG and ceramide accumulation to limit lipotoxic development (<i>p</i> < 0.05). Supplemental 25-OH-D3 also sustained Nrf2 activation and relieved MDA accumulation, protein carbonylation, and GSH depletion to potentiate cell survival in the failing heart (<i>p</i> < 0.05). Parts of the redox amendments were mediated via lessened blood hematocrit and heme metabolism, and improved iron status and related gene regulations (<i>p</i> < 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.https://www.mdpi.com/2076-3921/13/11/1426hensvitamin Dheart failuremetabolic adaptionmitochondriaredox homeostasis |
| spellingShingle | 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 25-Hydroxycholecalciferol Improves Cardiac Metabolic Adaption, Mitochondrial Biogenetics, and Redox Status to Ameliorate Pathological Remodeling and Functional Failure in Obese Chickens Antioxidants hens vitamin D heart failure metabolic adaption mitochondria redox homeostasis |
| title | 25-Hydroxycholecalciferol Improves Cardiac Metabolic Adaption, Mitochondrial Biogenetics, and Redox Status to Ameliorate Pathological Remodeling and Functional Failure in Obese Chickens |
| title_full | 25-Hydroxycholecalciferol Improves Cardiac Metabolic Adaption, Mitochondrial Biogenetics, and Redox Status to Ameliorate Pathological Remodeling and Functional Failure in Obese Chickens |
| title_fullStr | 25-Hydroxycholecalciferol Improves Cardiac Metabolic Adaption, Mitochondrial Biogenetics, and Redox Status to Ameliorate Pathological Remodeling and Functional Failure in Obese Chickens |
| title_full_unstemmed | 25-Hydroxycholecalciferol Improves Cardiac Metabolic Adaption, Mitochondrial Biogenetics, and Redox Status to Ameliorate Pathological Remodeling and Functional Failure in Obese Chickens |
| title_short | 25-Hydroxycholecalciferol Improves Cardiac Metabolic Adaption, Mitochondrial Biogenetics, and Redox Status to Ameliorate Pathological Remodeling and Functional Failure in Obese Chickens |
| title_sort | 25 hydroxycholecalciferol improves cardiac metabolic adaption mitochondrial biogenetics and redox status to ameliorate pathological remodeling and functional failure in obese chickens |
| topic | hens vitamin D heart failure metabolic adaption mitochondria redox homeostasis |
| url | https://www.mdpi.com/2076-3921/13/11/1426 |
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