Abstract
Maternal metabolic disorders in ewes induced by energy deficiency have a detrimental effect on the maternal health and lambs. However, the dynamic processes of metabolic disorders are unknown. Therefore, this study attempted to explore the dynamic changes of maternal metabolism based on metabolomics approach during energy deficiency in pregnant ewes. Twenty pregnant Hu sheep were fed a basic diet or a 70% restricted basic diet. The HPLC-MS platform was applied to identify blood metabolites. Principal component analysis of blood samples based on their metabolic profile showed that blood samples of feed restriction group differed after the treatment. In particular, when comparing both groups, there were 120, 129, and 114 differential metabolites at day 5, day 10, and day 114 between the two groups, respectively. Enrichment analysis results showed that four metabolic pathways (glycerophospholipid metabolism, linoleic acid metabolism, arginine and proline metabolism, and aminoacyl-tRNA biosynthesis) at day 5, four metabolic pathways (aminoacyl-tRNA biosynthesis, aminoacyl-tRNA biosynthesis, glycerophospholipid metabolism, and citrate cycle) at day 10, and nine metabolic pathways (aminoacyl-tRNA biosynthesis, synthesis and degradation of ketone bodies, glycerophospholipid metabolism, butanoate metabolism, linoleic acid metabolism, citrate cycle, alanine, aspartate and glutamate metabolism, valine, leucine and isoleucine biosynthesis, and arginine and proline metabolism) at day 15 were significantly enriched between the two groups. These findings revealed temporal changes of metabolic disorders in pregnant ewes caused by severe feed restriction, which may provide insights into mitigation measures.
Highlights
Previous studies show that fatty acids stored in adipose tissue in the form of triglycerides are released and transported into mitochondria for β-oxidation to produce acetyl-CoA [1,2]
The body undergoes adaptive metabolism to maintain the balance of blood glucose, which is important for organs to function normally
Acetyl-CoA produced by fatty acids β-oxidation produces a large amount of ketone bodies, which can be cytotoxic at high concentrations [3]
Summary
Previous studies show that fatty acids stored in adipose tissue in the form of triglycerides are released and transported into mitochondria for β-oxidation to produce acetyl-CoA [1,2]. Acetyl-CoA produced by fatty acids β-oxidation produces a large amount of ketone bodies which can be cytotoxic at high concentrations [3]. Previous results showed that severe feed restriction (FR). Liver metabolic profiling results suggested that severe FR caused disorders of liver lipid metabolism and impaired liver metabolic function [5]. Previous studies mainly focused on the effects of maternal energy deficiency on offspring [6,7], but there are few studies focused on the mechanism of maternal body metabolic disorders and pathogenesis
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