Abstract
Dietary threonine (Thr) deficiency increases hepatic triglyceride accumulation in Pekin ducks, which results in fatty liver disease and impairs hepatic function. However, the underlying molecular mechanisms altered by dietary Thr deficiency are still unknown. To identify the underlying molecular changes, 180 one-day-old ducklings were divided into three groups, including Thr deficiency group (Thr-D), Thr sufficiency group (Thr-S), and pair-fed group (Pair-F) that was fed with a Thr-sufficient diet but with reduced daily feed intake. The results showed that feed intake was similar between Thr-D and Pair-F groups, but weight gain rate and final body weight in the Thr-D group were lower than those in the Pair-F group. Feed intake, weight gain, and body weight in Thr-D and Pair-F groups were lower than those in the Thr-S group. The Thr-D diet reduced abdominal fat percentage but increased hepatic triglyceride content when compared with that of the Thr-S and Pair-F groups. The Pair-F reduced hepatic levels of C15:0, C17:0, C18:0, C20:0, C20:4n6, and C22:0 and also reduced total fatty acid, saturated fatty acid, and unsaturated fatty acid content when compared with those of the Thr-D and Thr-S groups. The Thr-D diet increased hepatic content of C6:0, C17:1, C18:3n6, C20:0, C20:1n9, and C22:2, as well as reduced the content of C18:2n6t and C23:0 when compared with those of the Thr-S group. Transcriptome analysis in the liver indicated that the Thr-D diet upregulated genes related to fatty acid and triglyceride synthesis and downregulated genes related to fatty acid oxidation and triglyceride transport. Gene ontology analysis showed that more genes related to lipid metabolism processes and molecular function were differentially expressed in the Thr-D group relative to Thr-S and Pair-F groups than in the Pair-F group relative to the Thr-S group. KEGG pathway analysis showed that differentially expressed genes were enriched in signal transduction, immune, hormone, lipid, and amino acid metabolism pathways. Our findings indicated that the Thr-D diet increased hepatic triglyceride and fatty acid accumulation via increasing fatty acid and triglyceride synthesis and reducing fatty acid oxidation and triglyceride transport. These findings provide novel insights into our understanding of the molecular mechanisms underlying fat accumulation in the liver caused by dietary threonine deficiency.
Highlights
Nonalcoholic fatty liver disease (NAFLD) is an increasingly prevalent disease worldwide that leads to chronic hepatic injury (Loomba and Sanyal, 2013)
We have shown that the expression of several hepatic genes related to lipid uptake, fatty acid synthesis, β-oxidation, ketogenesis, and triglyceride transport is affected by dietary Thr levels in Pekin ducks (Jiang et al, 2019)
The gain/feed ratio was lower in the Thr deficiency diet (Thr-D) group than that in the paired fed group (Pair-F) group (P < 0.03)
Summary
Nonalcoholic fatty liver disease (NAFLD) is an increasingly prevalent disease worldwide that leads to chronic hepatic injury (Loomba and Sanyal, 2013). Lipid accumulation in the liver of people who drink little or no alcohol is the main characteristic of NAFLD. Such a fatty liver is more susceptible to inflammatory cytokines and oxidative stress (Browning and Horton, 2004; Cohen et al, 2011) and may gradually develop into steatohepatitis, liver fibrosis, and hepatocellular carcinoma (Chalasani et al, 2012). We demonstrated that dietary Thr deficiency increases hepatic lipid deposition and reduces abdominal fat levels in ducks (Jiang et al, 2017)
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