AbstractObesity is chronic disease, leads to fatty liver, its abnormal function tests and hyperlipidemia, exercise improved the lipid profile, liver histomorphology and functions, herbs were frequently included in obesity management, this study aimed to investigate effects of swimming and mixture of garlic and lemon juice on lipid profile, liver function and losing of weight as well. twenty adult male albino rats of about 240 ± 10 gram body weight & 12 weeks old were used and were randomly divided into four experimental groups, during 28 days of experiments first group fed the standard pellet diet, second group fed with the high formulated diet (HFD) , third group fed with the HFD , with orally administration of 28 ml of mixture of garlic and lemon, last group fed with the HFD, and doing swimming 30 minute/day, body weight, lipid profile and serum levels of AST, ALP, ALP were measured as well as evaluation of liver histopathology, all indicated loose of body weight, significantly decreased liver function test parameters and serum levels of cholesterol, triglycerides, LDL and increase of HDL in exercise and treated groups (P value ≤0.01), beside preserving histology of liver compared to fatty liver in model group, the study concluded that obesity can induces fatty liver and deteriorate its functions, accompanied by hyperlipidemia, in other hands swimming and administration mixture of allium sativum and Citrus limon significantly decrease the cholesterol, TG, LDL, and liver function test parameters while increasing HDL and ameliorate the liver histopathological lesions as well.

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.

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.

Protein kinase (PK) C activity in the liver of cattle with fatty liver syndrome was evaluated and compared with that in liver of healthy cattle. The PKC activities in cytosolic and particulate fractions were reduced in fatty livers, compared with those in livers from healthy cattle. The decrease of PKC activity was more distinct in cytosolic (P = 0.0016) than particulate (P = 0.069) fractions. Protein kinase activities other than PKC were not substantially changed. Seemingly, PKC was involved in the pathogenesis of fatty liver syndrome in cattle.

Concentrations of 3 alpha-hydroxylated bile acids were measured in serum and urine of clinically normal (healthy) cats (n = 6), cats with severe hepatic lipidosis (n = 9), and cats with complete bile duct occlusion (n = 4). Bile acid concentrations were measured by use of a gradient flow high-performance liquid chromatography procedure with an acetonitrile and ammonium phosphate mobile phase and an in-line postanalytic column containing 3 alpha-hydroxysteroid dehydrogenase and a fluorescence detector. Specific identification of all bile acid peaks was not completed; unidentified moieties were represented in terms of their elution time (in minutes). Significant differences in serum and urine bile acid concentrations, quantitative and proportional, were determined among groups of cats. Cats with hepatic lipidosis and bile duct occlusion had significantly (P greater than or equal to 0.05) greater total serum and urine bile acids concentrations than did healthy cats. The proportion of hydrophobic bile acids in serum, those eluting at greater than or equal to 400 minutes, was 1.9% for healthy cats, 3.3% for cats with lipidosis, and 5.4% for bile duct-obstructed cats. Both groups of ill cats had a broader spectrum of unidentified late-eluting serum bile acids than did healthy cats; the largest spectrum developed in bile duct-occluded cats. The trihydroxy-to-dihydroxy serum bile acids ratio was 8.8:1 for healthy cats; 24.1:1 for cats with lipidosis: and 20:1 for cats with bile duct obstruction. There was a paucity of glycine-conjugated bile acids in all cats and small quantities of secondary bile acids in ill cats. A significantly (P < 0.05) smaller proportion of unconjugated primary bile acids was detected in sera from ill cats. Serum taurolithocholic acid was detected only in small quantities in cats of each group. There was significantly increased quantity, but lower proportion, of trihydroxy-cholestanoic acid in serum from ill cats, compared with healthy cats. A significantly (P < 0.05) greater proportional amount of unidentified moieties eluting at 130 and 277 minutes was detected in urine of cats with hepatic lipidosis; we believe that the unidentified moiety eluting at 277 minutes is tau- tauroallocholic acid. Large proportional amounts of taurocholic and cholic acids were detected in urine of all cats, but ill cats had significantly (P < 0.05) greater quantities (quantitatively and proportional). Ill cats had significantly (P < 0.05) more taurocholic than cholic acid in urine. Because taurine is an essential amino acid for cats and is a necessary daily dietary constituent, large urinary losses of taurine in conjugated bile acids may further compromise the health of anorectic cats with severe hepatic lipidosis.

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 alpha 1-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.

A 5-year-old intact female Persian cat was referred with anorexia and vomiting. Physical examination revealed icterus in the pinna, oral mucosa, and sclera. Ultrasonography revealed several findings including uniformly hyperechoic hepatic parenchyma compared to adjacent falciform fat, increased attenuation of the ultrasound beam, and poor visualization of intrahepatic vessel borders. Computed tomography revealed hypoattenuation of the hepatic parenchyma with a radiodensity value of-60 Hounsfield units. The adjacent intrahepatic vessels appeared hyperattenuated relative to the hepatic parenchyma as if the vessels were contrast-enhanced. Based on ultrasonography and computed tomography results, the cat was tentatively diagnosed as feline hepatic lipidosis.