Lipids in liver

Zaborowska, Z., Uchman, W., Bilska, A., Jelen, H., Rudzinska, M., Wqsowicz, E. and Kummerow, F.A. (2001). Effect of storage on oxidation of cholesterol and lipids in liver pate type sausage, Electron. J. Polish Agricu. Universities, Series Food Sci. TechnoL, 4, 2. 

G7. Gjone, E., and Norum, K. R., Plasma lecithin-cholesterol acyltransferase and erythrocyte lipids in liver disease. Acta Med. Scand. 187, 153-161 (1970). 

Inhalation of bromotrichloromethane by rats increased total lipids in liver and stimulated hepatic lipid peroxidation. After intragastric administration, liver steatosis was observed. Rats injected with 0.26 mmol bromotrichloromethane died after massive accumulation of neutral lipids and necrosis of the liver. 

Fdee Kand Kiechgessnee M (1996a) Effects of zinc deficiency on concentrations of lipids in liver and plasma of rats. Trace Flements and Electrolytes 13 60-65. 

Table 3.222 Simple distribution of lipids in livers from three mammals (g/kg fresh weight) (data from Long, 1961)...

The thesis advanced by Epstein (1932) that lipid in liver cells and kidney epithelium results from passive infiltration, while glial cells, ganglion cells, and histiocytes store lipid actively, has been convincingly repudiated by Letterer (1939, 1947). 

For example, altered lipids in liver tissue samples from NAFLD patients in comparison to normal controls were determined by GC [2], It was found that the mean levels (nmol/g of tissue) of DAG (normal/NAFLD 1922/4947) and TAG (13,609/128,585) were increased significantly in NAFLD, but the levels of NEFA remained unaltered (5533/5929). The study showed that there existed a stepwise increase in the mean TAG/DAG ratio from normal to NAFLD (7/26, p < 0.001). The total PC content decreased in NAFLD. The ratio of free cholesterol/PC increased progressively (0.34/0.69, p <0.008). Taken together, NAFLD is associated with numerous changes in cellular lipidome of the liver. 

Birkenfeld, C., J. Doberenz, H. Kluge and K. Eder, 2006b. Effect of l-camitine supplementation of sows on l-camitine status, body composition and concentrations of lipids in liver and plasma of their piglets at birth and during the suckling period. Anim. Feed Sci. Technol. 129, 23-38. 

Solutions in contact with polyvinyl chloride can become contaminated with trace amounts of lead, titanium, tin, zinc, iron, magnesium or cadmium from additives used in the manufacture and moulding of PVC. V-Phenyl-2-naphthylamine is a contaminant of solvents and biological materials that have been in contact with black rubber or neoprene (in which it is used as an antioxidant). Although it was only an artefact of the separation procedure it has been isolated as an apparent component of vitamin K preparations, extracts of plant lipids, algae, livers, butter, eye tissue and kidney tissue [Brown Chem Br 3 524 1967]. 

Yellow phosphorus was the first identified liver toxin. It causes accumulation of lipids in the liver. Several liver toxins such as chloroform, carbon tetrachloride, and bromobenzene have since been identified. I he forms of acute liver toxicity are accumulation of lipids in the liver, hepartxiellular necrosis, iii-trahepatic cholestasis, and a disease state that resembles viral hepatitis. The types of chrome hepatotoxicity are cirrhosis and liver cancer. 

Accumulation of lipids in the liver (steatosis) is one possible mechanism for liver toxicity. Several compounds causing necrosis of hepatocytes also cause steatosis. There are, however, some doubts that steatosis would be the primary cause of liver injury. Several compounds cause steatosis (e.g., puro-mycin, cycloheximide) without causing liver injury. Most of the accumulated lipids are triglycerides. In steatosis, the balance between the synthesis and excretion of these lipids has been disturbed (see Table 5.13). 

The livers and intestines of animals are the primary sources of circulating lipids. Chylomicrons carry triacylglycerol and cholesterol esters from the intestines to other tissues, and VLDLs carry lipid from liver, as shown in Figure 25.38. At... 

In addition to the described lipid pathways mainly operative in macrophages, two further ABC-transporteis, ABCG5 and ABCG8 have been implicated in the efflux of dietary sterols from intestinal cells back into the gut lumen and from liver to the bile duct (Fig 1). Both ABC-transporters form a functional heterodimer with highest expression levels in liver and intestine and are regulated... 

The distribution of endosulfan and endosulfan sulfate was evaluated in the brains of cats given a single intravenous injection of 3 mg/kg endosulfan (Khanna et al. 1979). Peak concentrations of endosulfan in the brain were found at the earliest time point examined (15 minutes after administration) and then decreased. When tissue levels were expressed per gram of tissue, little differential was observed in distribution among the brain areas studied. However, if endosulfan levels were expressed per gram of tissue lipid, higher initial levels were observed in the cerebral cortex and cerebellum than in the spinal cord and brainstem. Loss of endosulfan was most rapid from those areas low in Upid. Endosulfan sulfate levels peaked in the brain at 1 hour postadministration. In contrast, endosulfan sulfate levels in liver peaked within 15 minutes postadministration. The time course of neurotoxic effects observed in the animals in this study corresponded most closely with endosulfan levels in the central nervous system tissues examined. 

Peroxidation of lipids is another factor which must be considered in the safety evaluation of liposome administration. Smith and coworkers (1983) demonstrated that lipid peroxides can play an important role in liver toxicity. Allen et al. (1984) showed that liposomes protected by an antioxidant caused less MPS impairment than liposomes subjected to mild oxidizing conditions. From the study of Kunimoto et al. (1981) it can be concluded that the level of peroxidation in freshly prepared liposome preparations and those on storage strongly depends both on the phospholipid fatty acid composition and on the head group of the phospholipid. Addition of appropriate antioxidants to liposomes composed of lipids which are liable to peroxidation and designed for use in human studies is therefore necessary. 

For a variety of reasons, lipid—mainly as triacylglycerol—can accumulate in the hver (Figure 25—6). Extensive accumulation is regarded as a pathologic condition. When accumulation of lipid in the Ever becomes chronic, fibrotic changes occur in the cells that progress to cirrhosis and impaired liver function. 

Esterbauer, LI. (1985). Lipid peroxidation products formation, chemical properties and biological activation. In Free Radicals in Liver Injury (eds. G. Poli, K. Cheeseman, M.U. Dianzani and T. Slater) pp. 29-47, IRL Press, Oxford. 

Pederson, T.C., Buege, J.A. and Aust, S.D. (1973). Microsomal electron transport. The role of reduced nicotinamide dinucleotide phosphateliver microsomal lipid peroxidation. J. Biol. Chem. 248, 7134—7141. 

There is very little data on ROM production in haemochromatosis in humans. Increases in thiobarbituric acid reactants in plasma were associated with increases in non-transferrin-bound free iron. However, other indices of lipid peroxidation were no different from controls (Peters eta/., 1985). There are no studies of in vivo lipid peroxidation in humans. It is also of interest that levels of antioxidant defences in liver biopsies from patients with haemochromatosis are normal (Selden et /., 1980). 

Niacin (vitamin B3) has broad applications in the treatment of lipid disorders when used at higher doses than those used as a nutritional supplement. Niacin inhibits fatty acid release from adipose tissue and inhibits fatty acid and triglyceride production in liver cells. This results in an increased intracellular degradation of apolipoprotein B, and in turn, a reduction in the number of VLDL particles secreted (Fig. 9-4). The lower VLDL levels and the lower triglyceride content in these particles leads to an overall reduction in LDL cholesterol as well as a decrease in the number of small, dense LDL particles. Niacin also reduces the uptake of HDL-apolipoprotein A1 particles and increases uptake of cholesterol esters by the liver, thus improving the efficiency of reverse cholesterol transport between HDL particles and vascular tissue (Fig. 9-4). Niacin is indicated for patients with elevated triglycerides, low HDL cholesterol, and elevated LDL cholesterol.3... 

Experiments with monkeys given intramuscular injections of a mineral oil emulsion with [l-14C] -hexa-decane tracer provide data illustrating that absorbed C-16 hydrocarbon (a major component of liquid petrolatum) is slowly metabolized to various classes of lipids (Bollinger 1970). Two days after injection, substantial portions of the radioactivity recovered in liver (30%), fat (42%), kidney (74%), spleen (81%), and ovary (90%) were unmetabolized -hexadecane. The remainder of the radioactivity was found as phospholipids, free fatty acids, triglycerides, and sterol esters. Essentially no radioactivity was found in the water-soluble or residue fractions. One or three months after injection, radioactivity still was detected only in the fat-soluble fractions of the various organs, but 80-98% of the detected radioactivity was found in non-hydrocarbon lipids. 

JR Williamson, SK Joseph, KE Coll, AP Thomas, A Verhoeven, M Prentki. (1986). Hormone-induced inositol lipid breakdown and calcium-mediated cellular responses in liver. In G Poste, ST Crooke, eds. New Insights into Cell and Membrane Transport Processes. New York Plenum Press, pp 217-247. 

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