Jia Xu1, Fan Wang1, Ivan Jakovlić2, Wassana Prisingkorn1, Jun-Tao Li3, Wei-Min Wang1, Yu-Hua Zhao4. 1. College of Fisheries Huazhong Agricultural University, Key Lab of Freshwater Animal Breeding, Ministry of Agriculture, Key Lab of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education, Freshwater Aquaculture Collaborative Innovation Center of Hubei Province, Wuhan, 430070, People's Republic of China. 2. Bio-Transduction Lab, Wuhan, 430075, People's Republic of China. 3. Institute of Tropical Bioscience and Biotechnology, Haikou, 570102, People's Republic of China. 4. College of Fisheries Huazhong Agricultural University, Key Lab of Freshwater Animal Breeding, Ministry of Agriculture, Key Lab of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education, Freshwater Aquaculture Collaborative Innovation Center of Hubei Province, Wuhan, 430070, People's Republic of China. zhaoyuhua2005@mail.hzau.edu.cn.
Abstract
BACKGROUND: High-carbohydrate diets (HCD) are favoured by the aquaculture industry for economic reasons, but they can produce negative impacts on growth and induce hepatic steatosis. We hypothesised that the mechanism behind this is the reduction of hepatic betaine content. OBJECTIVE: We further explored this mechanism by supplementing betaine (1%) to the diet of a farmed fish Megalobrama amblycephala. METHODS: Four diet groups were designed: control (CD, 27.11% carbohydrates), high-carbohydrate (HCD, 36.75% carbohydrates), long-term betaine (LBD, 35.64% carbohydrates) and short-term betaine diet (SBD; 12 weeks HCD + 4 weeks LBD). We analysed growth performance, body composition, liver condition, and expression of genes and profiles of metabolites associated with betaine metabolism. RESULTS: HCD resulted in poorer growth and liver health (compared to CD), whereas LBD improved these parameters (compared to HCD). HCD induced the expression of genes associated with glucose, serine and cystathionine metabolisms, and (non-significantly, p = .20) a betaine-catabolizing enzyme betaine-homocysteine-methyltransferase; and decreased the content of betaine, methionine, S-adenosylhomocysteine and carnitine. Betaine supplementation (LBD) reversed these patterns, and elevated betaine-homocysteine-methyltransferase, S-adenosylmethionine and S-adenosylhomocysteine (all p ≤ .05). CONCLUSION: We hypothesise that HCD reduced the content of hepatic betaine by enhancing the activity of metabolic pathways from glucose to homocysteine, reflected in increased glycolysis, serine metabolism, cystathionine metabolism and homocysteine remethylation. Long-term dietary betaine supplementation improved the negative impacts of HCD, inculding growth parameters, body composition, liver condition, and betaine metabolism. However, betaine supplementation may have caused a temporary disruption in the metabolic homeostasis.
BACKGROUND: High-carbohydrate diets (HCD) are favoured by the aquaculture industry for economic reasons, but they can produce negative impacts on growth and induce hepatic steatosis. We hypothesised that the mechanism behind this is the reduction of hepatic betaine content. OBJECTIVE: We further explored this mechanism by supplementing betaine (1%) to the diet of a farmed fish Megalobrama amblycephala. METHODS: Four diet groups were designed: control (CD, 27.11% carbohydrates), high-carbohydrate (HCD, 36.75% carbohydrates), long-term betaine (LBD, 35.64% carbohydrates) and short-term betaine diet (SBD; 12 weeks HCD + 4 weeks LBD). We analysed growth performance, body composition, liver condition, and expression of genes and profiles of metabolites associated with betaine metabolism. RESULTS:HCD resulted in poorer growth and liver health (compared to CD), whereas LBD improved these parameters (compared to HCD). HCD induced the expression of genes associated with glucose, serine and cystathionine metabolisms, and (non-significantly, p = .20) a betaine-catabolizing enzyme betaine-homocysteine-methyltransferase; and decreased the content of betaine, methionine, S-adenosylhomocysteine and carnitine. Betaine supplementation (LBD) reversed these patterns, and elevated betaine-homocysteine-methyltransferase, S-adenosylmethionine and S-adenosylhomocysteine (all p ≤ .05). CONCLUSION: We hypothesise that HCD reduced the content of hepatic betaine by enhancing the activity of metabolic pathways from glucose to homocysteine, reflected in increased glycolysis, serine metabolism, cystathionine metabolism and homocysteine remethylation. Long-term dietary betaine supplementation improved the negative impacts of HCD, inculding growth parameters, body composition, liver condition, and betaine metabolism. However, betaine supplementation may have caused a temporary disruption in the metabolic homeostasis.
Authors: Randolph P Matthews; Kristin Lorent; Rafael Mañoral-Mobias; Yuehua Huang; Weilong Gong; Ian V J Murray; Ian A Blair; Michael Pack Journal: Development Date: 2009-03 Impact factor: 6.868