Changes in hepatic lipid parameters and hepatic messenger ribonucleic acid expression following estradiol administration in laying hens (Gallus domesticus)

Abstract

Fatty liver hemorrhagic syndrome (FLHS) is characterized by increased hepatic triacylglycerol content associated with liver hemorrhages and results in a sudden decline in egg production. Genetic, environmental, nutritional, and hormonal factors have all been implicated in the etiology of FLHS, but the exact cause of FLHS is still unknown. Estrogens have been implicated in the development of excess fat content of the liver and in the etiology of FLHS. This study investigated estradiol (E(2)) administration in hens and its effect on lipid metabolism. Hy-Line Brown laying hens were intramuscularly injected with E(2) on a daily basis for 3 wk. The dosages were 0, 0.5, and 1.0 mg/kg of BW, with corn oil injections used as a control. Egg production and quality were measured among the groups, with no significant difference seen in egg production. Liver weights of hens treated with E(2) were greater than those of control hens, but the increase was not statistically significant. Serum glutamic-oxaloacetic transaminase and glutamic-pyruvic transaminase activities and E(2) plasma concentrations increased in a dose-dependent manner, with plasma concentration of E(2) increasing from 6,900 to 19,000 pg/mL. No significant differences in free cholesterol or phospholipids were observed, but there was a significant increase in hepatic triacylglycerol levels. Injection with E(2) showed an increased expression of mRNA for peroxisome proliferator-activated receptor γ (23-fold), but not for peroxisome proliferator-activated receptor α. A statistically significant increase was seen for fatty acid synthase, apolipoprotein B, and adenosine triphosphate citrate lyase, but not for acetyl coenzyme A carboxylase, apolipoprotein VLDL-II, microsomal triglyceride transport protein, or malic enzyme. For proteins involved in the oxidation of E(2), only cytochrome P450 3A37 showed a statistically significant increase. The present results suggest that E(2) upregulates the synthesis of fatty acids and triacylglycerols and the accumulation of hepatic lipids by increasing mRNA expression related to lipid metabolism, and that excess E(2) in the blood leads to activation of E(2) catabolic metabolism (cytochrome P450 3A37)-related mRNA expression.

Bioaccumulation and Toxicity Studies of Lead and Mercury in Laying Hens: Effects on Laying Performance, Blood Metabolites, Egg Quality and Organ Parameters

“…Previous reports demonstrated lead exposure could change lipid metabolism in chickens, increasing liver cholesterol levels that cause fatty liver issues (Lawton and Donaldson, 1991;Bruggeman et al, 1999;Cave et al, 2010). Lipid accumulated in the liver resulted in an imbalance in nutrition and fatty liver syndrome by changing the rate of hepatic lipogenesis in chickens (Lee et al, 2010). In this respect, our results indicate that heavier liver weight resulted from the slight alteration of fat content in the liver.…”

Increasing persistency in lay and stabilising egg quality in longer laying cycles. What are the challenges?

“…Hepatic steatosis in layers tends to occur most often where there is an imbalance in the protein/ energy ratio and causes a drop in egg production and obese hens. Fatty liver haemorrhagic syndrome (FLHS) has also been observed in hens treated with oestrogens (Butler, 1976 ; Lee et al ., 2010 ; Choi et al ., 2012 ). This disease, which is not to be confused with hepatic steatosis, is almost invariably fatal but it can also affect egg production (Walzem et al ., 1993 ; Lee et al ., 2010 ).…”

“…Fatty liver haemorrhagic syndrome (FLHS) has also been observed in hens treated with oestrogens (Butler, 1976 ; Lee et al ., 2010 ; Choi et al ., 2012 ). This disease, which is not to be confused with hepatic steatosis, is almost invariably fatal but it can also affect egg production (Walzem et al ., 1993 ; Lee et al ., 2010 ). The provision of dietary 25 (OH) D3, feed restriction with substitution of carbohydrate by dietary fat, supplementation of choline, inositol, vitamin B12, folic acid and vitamin E in the diet have all been shown to limit the incidence of hepatic steatosis and FLHS in layers (Bouvarel and Nys, 2013 ).…”

The impact ofSalmonellaEnteritidis on lipid accumulation in chicken hepatocytes

“…Our data indicated the secretion of VLDL from SE-infected LMH-2A cells reduced (Figure 4(a)) and the lipid accumulation in hepatocytes increased (Figure 1(a),(b)). Lee et al (2010) indicated that excessive triacylglycerol deposited in the hepatocytes of laying hens reduced egg production. We speculate that SE infection leads to excessive lipid accumulation in the LMH-2A cells and it may then have impact on egg production.…”