Abnormal histopathology, fat percent and hepatic apolipoprotein A I and apolipoprotein B100 mRNA expression in fatty liver hemorrhagic syndrome and their improvement by soybean lecithin

Abstract

To investigate the etiopathogenesis of fatty liver hemorrhagic syndrome (FLHS) and the protective effects of soybean lecithin against FLHS in laying hens, 135 healthy 300-day-old Hyline laying hens were randomly divided into groups: control (group 1), diseased (group 2), and protected (group 3). Each group contained 45 layers with 3 replicates. The birds in these 3 groups were fed a control diet, a high-energy/low-protein (HELP) diet or the HELP diet supplemented with 3% soybean lecithin instead of maize. The fat percent in the liver was calculated. Histopathological changes in the liver were determined by staining, and the mRNA expression levels of apolipoproteinA I (apoA I) and apolipoprotein B100 (apoB100) in the liver were determined by RT-PCR. The results showed that the fat percent in the liver of group 2 was much higher (P < 0.01) than that of group 1 and group 2 on d 30 and 60. The histology of the liver in group 2 on d 30 and 60 displayed various degrees of liver lesions, while the hepatocytes showed a normal structure in group 3 with mild microvesicular steatosis in the liver cell on d 30 and 60. The mRNA expression levels of apoA I and apoB100 in the livers were variable throughout the experiment. The expression level of apoA I in group 2 significantly decreased on d 60 (P < 0.05); the expression level of apoB100 slightly increased on d 30 in group 2, while it sharply decreased on d 60. Compared to group 1, the expression level of apoB100 showed no significant difference in group 3 (P < 0.05). This study indicated that FLHS induced pathological changes and abnormal expression of apoA I and apoB100 in the livers of laying hens and that soybean lecithin alleviated these abnormal changes.

Effects of a high energy and low protein diet on hepatic and plasma characteristics and Cidea and Cidec mRNA expression in liver and adipose tissue of laying hens with fatty liver hemorrhagic syndrome

“…Analysis of the liver by tissue sectioning and H&E staining further showed that the HELP diet induced micro‐vesicular steatosis in the layers, which indicated that FLHS successfully occurred in experimental group. The results were also supported by previous studies (Song et al., ; Trott et al., ; Yang et al., ; Zhang, Chen, Yu, & Wang, ). It was thought that high‐energy intake caused increased fatty acids in plasma, furthering an elevated level of lipogenesis in the liver, which leaded to TG accumulation in the liver and then the occurrence of FLHS (Whitehead, ).…”

“…Nutritional and genetic factors, feeding methods, environmental conditions, toxic substances, and hormones all contribute to the occurrence of this syndrome (Butler, ; Choi et al., ; Hansen & Walzem, ; Polin & Wolford, ; Schuman, Squires, & Leeson, ; Squires & Leeson, ; Zhu et al., ), whereas nutrition is the major factor in current poultry industry. Recently some studies reported that a HELP diet successfully induced FLHS in laying hens (Song et al., ; Yang et al., ). The HELP diet was also reported as a natural cause of FLHS (Rozenboim et al., ).…”

“…Wolford and Polin reported over consumption of energy would appear to be related because excessive food intake has been observed to result in liver hemorrhages characteristic of FLHS (Wolford & Polin, ). Recently, some studies also reported that a high‐energy low‐protein (HELP) diet induced FLHS model successfully (Jiang, Cheng, Cui, Zhou, & Hou, ; Rozenboim, Mahato, Cohen, & Tirosh, ; Song et al., ; Yang et al., ).…”

Insulin resistance and metabonomics analysis of fatty liver haemorrhagic syndrome in laying hens induced by a high-energy low-protein diet

“…FLHS is a widespread metabolic disease in laying hens that causes adult deaths and a sudden drop in egg production 2,5 . However, the molecular mechanisms underlying FLHS are still poorly understood.…”

“…FLHS is characterized by excessive ectopic fat deposition in the liver and abdominal cavity along with a haemorrhagic and fragile liver. A study by Song and his colleagues showed that abnormal expression of apoAI and apoB 100 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.…”