Role of estrogen as a cause of fatty liver hemorrhagic syndrome.

Fatty liver-hemorrhagic syndrome (FLHS), a nutritional disorder previously reported only in laying chickens was induced in immature male and female chickens, 11 weeks of age, of broiler and egg-laying breeds. Force-feeding three times a day for 21 days, amounts of feed equal to 125% and 150% of ad libitum intake, produced a gradient response in hepatic steatosis (measured by percentage of fat in the liver, and the ratio of fat to the fat-free dry weight), but not FLHS. Intramuscular injection of beta-estradiol-17-dipropionate at 2 mg/kg body weight, three times weekly for 21 days, produced a gradient response in hemorrhagic score and an increase in ad libitum feed intake. There was no significant difference between sex or breed in the score values used to evaluate FLHS, but females of both breeds accumulated significantly more fat in the liver than males. Testosterone dipropionate at 25 mg/kg of body weight, injected three times per week in immature females force-fed at the 150% level, produced increases in food intake and liver fat as did estrogen, but no hepatic hemorrhaging. The data implicate estrogen as a factor in the production of FLHS along with the necessity for the chicken to be in a positive energy balance creating sufficient hepatic fat for FLHS to occur.