Plasma Lecithin: Cholesterol Acyltransferase Activity in Liver Disease*

Calandra, S.; Martin, Michael; McIntyre, Neil

doi:10.1111/j.1365-2362.1971.tb00642.x

Cited by 82 publications

(11 citation statements)

References 38 publications

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“…The observed decrease in serum phospholipids is supported by two other reports in patients with certain types of malignant tumours (Nydegger & Butler, 1972) and those with advanced liver disease and malignancy (Calandra et al, 1971). Again this observation supports the theory that the presence of cancer affects the metabolic controls within the liver.…”

Section: Resultssupporting

confidence: 83%

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Changes in serum lipids related to the presence of experimental colon cancer

Cruse¹,

Lewin²

1987

Br J Cancer

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Summary People at risk from coronary heart disease and large bowel cancer are drawn from the same urbanised, industrialised Western populations. Whilst changes in blood lipids are well recognised in heart disease, little is known of their role in large bowel cancer. This study investigates serial alterations in blood lipids in the 1,2-dimethylhydrazine (DMH) rat model of colon cancer. Eighty Wistar rats received a 5 weekly regimen of DMH. At week 10, and at 5 weekly intervals until week 40, random groups of 10 rats were killed and blood taken for total and free cholesterol, phospholipids, triglycerides and liver enzymes. All colonic neoplasms were histologically classified either as adenomas or carcinomas with groups being allocated into tumour-free (n = 16) or tumour-bearing (n = 54), the latter group being further sub-divided into animals with adenoma alone (n =8) and those with carcinoma (n = 46). Results were considered both sequentially and according to tumour status. Sequential results showed that with increase in colonic neoplasms with time there were accompanying increases in free and % free cholesterol and in phospholipids (P<0.001). There were no changes in total cholesterol, triglycerides or liver enzymes. Results according to tumour status showed that whilst there was no difference in total cholesterol or triglycerides between tumour-free and tumour-bearing rats, there was a significant increase in free (P<0.01) and % free cholesterol (P<0.001) and a decrease in phospholipids in the tumour-bearing animals (P<0.001). There was no difference in any serum lipid between tumour-free and adenoma-bearing rats. In animals with carcinoma, while there was no difference in total cholesterol or triglycerides, there was an increase in free (P<0.005) and % free cholesterol (P<0.001) and a decrease in phospholipids (P<0.001) compared to tumour-free rats.The data show for the first time a clear relationship between blood lipids and the presence or absence of large bowel cancer.The incidence and mortality rates for large bowel cancer are the second highest of all malignant disease in Western society (American Cancer Society, 1978). Although the cause(s) of colon cancer is unknown, epidemiological studies have implicated dietary fats in the pathogenesis of this disease (Wynder, 1975;Doll, 1978;Wynder & Reddy, 1983). More specifically, cholesterol in the diet has been shown to be co-carcinogenic in animals (Cruse et al., 1978(Cruse et al., ,1982 and there is indirect evidence for a similar role in man (Cruse et al., 1979;Broitman, 1981).Populations at high risk for colorectal cancer (CRC) are similarly at high risk of coronary heart disease (CHD) (Hill, 1975;Wynder & Shigematsu, 1967) and a common factor for both diseases is the high fat intake of the 'at risk' population (Hill, 1975). The familiar direct relationship between serum cholesterol levels and CHD probably reflects a causal role between hypercholesterolaemia and atherosclerosis (Lewis, 1983). Recent evidence also indicates that a direct but inverse relation...

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Section: Resultssupporting

confidence: 83%

“…This enzyme is produced in the liver and it has been reported that in liver disease, (Calandra et al, 1971). The lack of alteration in liver enzymes in this study implied that the function of the liver was unimpaired.…”

Section: Resultsmentioning

confidence: 49%

Changes in serum lipids related to the presence of experimental colon cancer

Cruse¹,

Lewin²

1987

Br J Cancer

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“…IOc). Because in acute hepatitis the synthetic capacity of the liver is not impaired, the low level of Apo A is probably due to an increased catabolism of the apolipoprotein after reduction of LCAT activity described by several authors (Simon and Scheig, 1970;Calandra et al, 1971;Gjone et al, 1971) in acute hepatitis.…”

Section: Resultsmentioning

confidence: 96%

Serum total lipids, lipoprotein cholesterol, and apolipoprotein A in acute viral hepatitis and chronic liver disease.

et al. 1978

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“…Its results are thought to represent activity of the enzyme in vivo (Norum, 1974). There is evidence to suggest that low LCAT activity found in patients with liver disease is usually due to a reduction in enzyme concentration rather than to abnormality of the substrate (Calandra et al, 1971;Simon, 1974). In normal subjects and in patients with obstructive and parenchymal liver disease there is a good correlation between the results of the Stokke & Norum (1971) method and those obtained with the method of Glomset & Wright (1964) (Blomhoff, Skrede & Ritland, 1974); the results of the latter method are thought to depend largely on enzyme concentration (Glomset & Wright, 1964).…”

Section: Methodsmentioning

confidence: 96%

Lecithin—Cholesterol Acyltransferase and the Lipoprotein Abnormalities of Parenchymal Liver Disease

et al. 1979

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1. Detailed studies have been made of the plasma lipoprotein abnormalities in parenchymal liver disease to test the hypothesis that the abnormalities would correlate with plasma lecithin-cholesterol acyltransferase (LCAT) activity. 2. When LCAT was high, very-low-density-lipoproteins (VLDL) were normal in composition and had a normal pre-beta electrophoretic mobility. When LCAT was low, VLDL concentrations were greatly reduced. 3. With high LCAT low-density lipoproteins (LDL) were normal. The LDL particles found with low LCAT activity were of normal size but of abnormal composition, being triglyceride rich and cholesteryl ester poor. Regardless of LCAT activity LDL were present in normal amounts. 4. High-density lipoproteins (HDL) were normal in composition and electron-microscopic appearance when LCAT activity was high. When LCAT activity was low HDL were abnormal in composition and 'stacked discs' were seen on electron microscopy. 5. These results suggest that low LCAT activity may be the cause of at least some of the lipoprotein changes of parenchymal liver disease.

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Plasma Lecithin: Cholesterol Acyltransferase Activity in Liver Disease*

Cited by 82 publications

References 38 publications

Changes in serum lipids related to the presence of experimental colon cancer

Changes in serum lipids related to the presence of experimental colon cancer

Serum total lipids, lipoprotein cholesterol, and apolipoprotein A in acute viral hepatitis and chronic liver disease.

Lecithin—Cholesterol Acyltransferase and the Lipoprotein Abnormalities of Parenchymal Liver Disease

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