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  • Author or Editor: Eiji Uchida x
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Summary

Ethionine, an analogue of methionine, induces fatty liver in rats by inhibiting protein synthesis, including that of apolipoproteins in liver. Ethionine was administered to cows to elucidate the participation in fatty liver development of impaired triglyceride secretion from liver attributable to decreased apolipoprotein synthesis. The administration resulted in a significant increase of liver triglyceride contents. Several apolipoproteins were found to have decreased concentrations. In particular, apolipoprotein B-100 in very low-density (0.95 to 1.006 g/ml) lipoprotein and in low-density (1.006 to 1.063 g/ml) lipoprotein fractions was greatly reduced. The decreases of apolipoprotein B-100 concentrations in the 2 lipoprotein fractions were at least partly correlated to the decreased triglyceride concentrations in the respective fractions. Decreased concentrations of apolipoprotein A-I in high-density (1.063 to 1.210 g/ml) lipoprotein were also observed, although not as distinctly as with apolipoprotein B-100. Total cholesterol and phospholipid concentrations in low- and high-density lipoprotein fractions were decreased. The decrease in cholesterol was attributed to reduced concentrations of cholesteryl esters. It was suggested that the impaired lipid secretion from liver attributable to the decreased apolipoprotein concentrations has a role in ethionine-induced fatty liver of cows.

Free access
in American Journal of Veterinary Research

Summary

Estradiol was administered to 3 steers (0.12 mg/kg of body weight/d for 14 consecutive days), followed by 2 days of nonfeeding (starvation). During estradiol administration, liver nuclear estrogen receptor and serum apolipoprotein B-100 (apoB-100), as well as serum triglycerides concentrations were increased, compared with values before administration. Starvation, together with interruption of estradiol administration, resulted in rapid decreases of the receptor, serum apoB-100, and serum triglycerides concentrations, and increase of nonesterified fatty acids concentration. Of the 3 steers, 2 had higher liver triglyceride content, compared with values before treatment. In the control group (3 steers that received vehicle alone, then starved similarly), these concentrations, except for serum nonesterified fatty acids and triglycerides concentrations after starvation, were not changed. In another experiment, serum apoB-100 concentration in dairy cows was significantly (P< 0.05) lower at parturition than values before and after parturition. These results indicate that estradiol may be involved in development of fatty liver in cattle.

Free access
in American Journal of Veterinary Research

Summary

Parenchymal cells were isolated from the liver of male calves, and monolayer cultures formed were treated with glucocorticoids to examine whether haptoglobin, appearance of which is associated with hepatic lipidosis (fatty liver) in cattle, is induced by steroid hormones. Without addition of dexamethasone, only trace amounts of haptoglobin were detected in culture medium. With addition of dexamethasone (10−12 to 10−4 M), considerable amounts of haptoglobin were released into the medium. Maximal release was observed at concentrations of 10−8 to 10−6 M dexamethasone. Haptoglobin release was similarly induced by Cortisol, although the effect was less potent than that of dexamethasone. Actinomycin D (a known protein synthesis inhibitor) dose-dependently reduced amounts of haptoglobin released in response to 10−8 M dexamethasone. Dexamethazone also induced annexin I, which is known to be synthesized in response to glucocorticoids. Dexamethasone treatment resulted in reduced protein kinase C activity in the cell cytosol, which has been shown to be an early event in dexamethasone-treated cells. Other than glucocorticoids, estradiol induced haptoglobin release, whereas progesterone was less effective. The association of haptoglobin with hepatic lipidosis can be reasonably explained by the fact that haptoglobin production by the liver is induced by glucocorticoids and estradiol, and these steroid hormones are triggers for development of hepatic lipidosis in cattle.

Free access
in American Journal of Veterinary Research