Abstract
Fatty liver haemorrhagic syndrome (FLHS) is a widespread metabolic disease in laying hens that causes a decrease in egg production and even death. Insulin resistance is a major contributor to the pathogenesis of nonalcoholic fatty liver disease. However, the relationship between FLHS and the insulin resistance mechanisms underlying FLHS is not well elucidated. Therefore, we established an FLHS model induced by feeding a high-energy low-protein diet. In the current study, we found that the fasting glucose and insulin concentrations were elevated in the FLHS group compared with the control group during the experimental period. The results of the oral glucose tolerance test (OGTT) and insulin sensitivity test (IST) showed a high level of insulin resistance in the FLHS model. InsR, 4EBP-1, Glut-1 and Glut-3 mRNA expression were decreased, and TOR, S6K1, and FOXO1 were elevated (P < 0.05). Metabolomic analysis with GC/MS identified 46 differentially expressed metabolites between these two groups, and of these, 14 kinds of metabolism molecules and 32 kinds of small metabolism molecules were decreased (P < 0.05). Further investigation showed that glucose, lipid and amino acid metabolism blocks in the progression of FLHS by GO functional and pathway analysis. Overall, these results suggest that insulin resistance participated in FLHS; comprehensively, metabolites participated in the dysregulated biological process.
Highlights
Fatty liver haemorrhagic syndrome (FLHS) is a nutritional and metabolic disease characterized by a lipid metabolism disorder that is harmful to the development of the layer breeding industry[1,2,3]
Insulin binding with insulin receptor (InsR) activates a cascade of molecules collectively known as the PI3K/Akt/TOR signalling pathway, which is responsible for most metabolic actions of insulin[11]
The results of the present study showed that blood glucose and insulin levels of layers in the high-energy low-protein (HELP) group were significantly higher than those of the control group, with signs of hyperinsulinaemia and hyperglycaemia resembling insulin resistance, and these were further confirmed by changes in serum inflammatory factors, including TNF-α and IL-6 in the HELP group[28,29,30]
Summary
Fatty liver haemorrhagic syndrome (FLHS) is a nutritional and metabolic disease characterized by a lipid metabolism disorder that is harmful to the development of the layer breeding industry[1,2,3]. A study by Song and his colleagues showed that abnormal expression of apoAI and apoB100 in the liver was observed in the FLHS model induced by a low-protein high-energy diet[5]. This result suggested that lipid transfer disorder was a component of FLHS. We first established the FLHS model by feeding layers a high-energy low-protein (HELP) diet, and glucose, insulin and insulin resistance and expression of the insulin signalling pathway were measured during the experimental period to analyse the relationship between the insulin resistance and FLHS.
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