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Excessive lipomobilization increases fat accumulation in liver cells 3 and leads to development of fatty liver (also known as hepatic lipidosis or fatty liver change). Although cattle with mild and moderate fatty liver do not necessarily have clinical signs

Full access
in Journal of the American Veterinary Medical Association

H epatic lipidosis, or fatty liver disease, is the progressive accumulation of triacylglycerols in hepatocytes resulting in hepatocellular dysfunction. 1 It is exceedingly common in reptiles but particularly in the central bearded dragon ( Pogona

Open access
in American Journal of Veterinary Research

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

Haptoglobin (Hp), an acute-phase protein, is detected in serum of cows with hepatic lipidosis (fatty liver). To assess the relevance of Hp in fatty liver, induction of Hp was examined, using conditions similar to those involving development of fatty liver in cows. Induction of Hp was achieved by a combination of dexamethasone administration (0.1 mg/kg of body weight) and 2 days’ starvation. Haptoglobin appearance in serum was not associated with the increase of α1-acid glycoprotein (a marker for inflammation). This treatment increased serum nonesterified fatty acids concentration and decreased serum triglycerides concentration. Protein kinase C activity was decreased in the cytosolic fractions of liver and mononuclear cells. Reduction of protein kinase C-catalyzed endogenous protein phosphorylation also was observed, particularly in the cytosolic fractions of the tissue and cells. Detection of Hp in serum of cows with fatty liver appears to be explained by the fact that Hp is induced by dexamethasone administration and starvation, which are similar to the condition responsible for fatty liver development. The change of protein kinase C-catalyzed phosphorylation was suggested to be involved in the induction of Hp in cows.

Free access
in American Journal of Veterinary Research

Summary

A protein that has 2 subunits with molecular weight of 35,000 and 23,000 was detected in serum of cattle with hepatic lipidosis (fatty liver). The protein was purified from serum obtained from a cow with fatty liver, and was identified as haptoglobin, which is known to have hemoglobin-binding capacity and to be an acute-phase protein. To assess the relevance of haptoglobin in fatty liver, cattle were classified in 3 groups (healthy control, haptoglobin-positive, and haptoglobin-negative); liver triglyceride content and several serum biochemical variables were evaluated for the 3 groups. Compared with the control and haptoglobin-negative cattle, haptoglobin-positive cattle had significantly (P < 0.01) higher liver triglyceride content, serum bilirubin concentration, and aspartate transaminase activity. Serum haptoglobin concentration was high in slaughter cattle (27 of 40 cattle tested), particularly in cows (20/28).

Free access
in American Journal of Veterinary Research

Abstract

Objective

To assess the relevance of hepatic lipidosis (fatty liver) in the development of ketosis and left displacement of the abomasum (LDA).

Sample Population

Sera from 22 healthy cows in early lactation. 21 cows with ketosis, and 19 cows with LDA, and serum and liver specimens from 35 slaughtered cows with or without fatty liver, ketosis, and/or LDA.

Procedure

Apolipoprotein B-100 and A-I concentrations were measured in sera of healthy farm cows and of farm cows with ketosis and LDA. Serum apolipoprotein concentration, together with liver triglyceride content, also were surveyed in a subset of slaughtered cows.

Results

Compared with those in healthy cows or controls, apolipoprotein B-100 and A-I concentrations were decreased in cows with ketosis and LDA.

Conclusions

Decreases in apolipoprotein B-100 and A-I concentrations in cows with ketosis and LDA indicate that the 2 disorders may be intimately associated with fatty liver.

Clinical Relevance

Monitoring of the apolipoprotein B-100 and A-I concentrations during the stages of nonlactation and early lactation is helpful for detecting cows susceptible to ketosis and LDA. (Am J Vet Res 1997;58:121–125)

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
Authors and

Abstract

An elisa was developed to evaluate the concentration of apolipoprotein A-I, a major apoprotein in high-density lipoprotein, in the serum of cattle. Serum apolipoprotein A-I was purified electrophoretically, and antibodies to this protein were raised in rabbits. The specificity of the antiserum was assessed by use of several immunologic techniques including western blotting. The elisa was sensitive (detection limit was 70 ng of apolipoprotein A-I/ml) and reliable (coefficients of variance were in the range of 3.5 to 8.2%). By use of this method, the serum apolipoprotein A-I concentration was higher in 2- to 6-year-old Holstein cows (mean ± SD, 0.580 ± 0.304 mg/ml) than in 7- to 15-month-old heifers (0.339 ± 0.237 mg/ml), 6-month-old heifers (0.238 ± 0.188 mg/ml), and 6-month-old steers (0.173 ± 0.146 mg/ml). The concentration, however, is not largely different in cows in early, middle, and late lactation and in nonlactating stages. Results also indicated that apolipoprotein A-I concentration was decreased in cows with hepatic lipidosis (fatty liver) induced by administration of ethionine, suggesting that this method is a useful tool for the pathophysiologic study of lipid metabolism and its impairment in cattle.

Free access
in American Journal of Veterinary Research

Abstract

Objective

To investigate the involvement of (n-6) essential fatty acids, such as linoleic acid [18:2(n-6)] or γ-linolenic acid [18:3(n-6)], and of prostaglandins on liver lipid accumulation in Japanese quail.

Design

Effects of graded amounts of aspirin, which inhibits prostaglandin synthesis, on liver weight were determined in experiment 1. Experiment 2 was designed to clarify the effect of dietary essential fatty acid sources and inhibition of prostaglandin synthesis on the liver fat and fatty acid profile.

Animals

Female Japanese quail.

Procedure

In experiment 1, from 1 to 3 weeks of age, birds were fed ad libitum the essential fatty acids-free or linoleic acid-adequate (2%) diets with graded amounts of aspirin (0, 0.1, 0.2, and 0.4%). In experiment 2, from 1 to 4 weeks of age, birds were fed the same amount of essential fatty acids-free, linoleic acid-adequate, or γ-linolenic acid (0.4%) diets with (0.2%) or without aspirin.

Results

In experiment 1, in groups given the essential fatty acids-free diet, liver weight increased with an increase in dietary aspirin concentration. In experiment 2, γ-linolenic acid completely prevented liver triacylglycerol and cholesterol accumulation induced by the essential fatty acids-free diet. Aspirin treatment significantly lowered plasma prostaglandin F concentration, but did not affect liver lipid concentrations. In groups fed the essential fatty acids-free diets, however, aspirin treatment increased liver weight and liver triacylglycerol concentration by 20 and 40%, respectively.

Conclusions

γ-Linolenic acid or its metabolites, but not linoleic acid itself, are important factors in reducing fatty liver in Japanese quail with the essential fatty acids-deficient condition.(Am J Vet Res 1996;57:342-345)

Free access
in American Journal of Veterinary Research