Serum lipoproteins of rats bearing transplanted morris hepatoma 7777

Ka, Narayan; Hp, Morris

doi:10.1002/ijc.2910050316

Cited by 10 publications

(6 citation statements)

References 5 publications

(8 reference statements)

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“…2 m-r). This was in sharp contrast to results obtained with rats bearing hepatoma 7777 (Narayan and Morris, 1970). Haven and Bloor (1956) have explained that hyperlipemia observed in tumor-bearing animals may be due to increased mobilization of lipids from the fat depots.…”

Section: Figurecontrasting

confidence: 66%

“…Therefore, in a subsequent experiment, where a diet deficient in essential fatty acids (EFA) was used, the serum lipoproteins were analysed by classical ultracentrifugal procedures. This study showed that the serum concentrations of three major classes of lipoproteins, including HDL, were increased in tumor-bearing, EFA-deficient rats (Narayan, 1970~). However, several questions remained partially or fully unanswered: Would a diet containing EFA and FAA induce similar quantitative changes in rat serum lipoproteins?…”

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confidence: 84%

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Rat serum lipoproteins during carcinogenesis of the liver in the preneoplastic and the neoplastic state

Narayan

1971

Intl Journal of Cancer

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The serum lipoproteins of rats during carcinogenesis of the liver, induced by N-2jhorenylacetamide, were investigated by disc electrophoresis, preparative ultracentrifugation and lipid and protein analyses. In the case of rats with preneoplastic livers, the very low-density lipoproteins increased by about 100 %, whereas both low-density and high-density lipoproteins increased by about 200 % as compared with control rats. 269 139 105The livers were composed of hyperplastic nodules. Lipoproteins isolated from pooled sera of 8 animals for each group.Expressed as cholesterol oleate, because the ester form of cholesterol is predominant in rat serum.Diet restricted to only IOg/rat/day, whereas control and carcinogen group were given 20g/rat/day.

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Section: Figurecontrasting

confidence: 66%

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confidence: 84%

Rat serum lipoproteins during carcinogenesis of the liver in the preneoplastic and the neoplastic state

Narayan

1971

Intl Journal of Cancer

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“…However, hypertriglyceridemia cannot be considered a constant change associated with the growth of tumor. In fact, in the blood plasma of host rats bearing 7777 Morris hepatoma, Grigor et al (22) found a decrease of TG associated with a rise of free and esterified cholesterol, and Narayan and Morris (25) reported an increase of cholesterol-rich high density lipoproteins. As far as plasma FFA are concerned, Bizzi et al (24) found an increased level of plasma FFA in fed animals bearing different tumors, including Yoshida hepatoma AH130, when compared to the controls under the same feeding conditions.…”

Section: From the Examination Ofmentioning

confidence: 99%

“…Numerous laboratories have studied the lipid composition of tumors (9)(10)(11). However, only in a few cases have tumor lipids been analyzed concomitantly with lipids of both host and normal animal tissues (12)(13)(14), although there are specific studies on the lipid changes induced by tumor growth on host tissues (15)(16)(17)(18)(19)(20)(21) and fluids (22)(23)(24)(25)(26)(27)(28)(29).…”

Section: Introductionmentioning

confidence: 99%

Lipid composition of yoshida ascites hepatoma and of livers and blood plasma from host and normal rats

Ruggieri

Fallani

1979

Lipids

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The lipid composition of Yoshida ascites hepatoma cells was analyzed together with that of ascitic plasma and of livers and blood plasma from host and normal rats. In comparison to normal livers, host livers showed no significant differences in the content of the various lipid classes, but contained a higher percentage of palmitic acid and a lower proportion of arachidonic acid in the major phospholipid classes. In addition, tumor growth induced a marked hypertriglyceridemia in host animals; changes in the concentration of other plasma lipid classes were not statistically significant. The ascitic plasma contained small amounts of lipids mainly constituted by cholesteryl esters and phospholipids. Yoshida hepatoma cells contained less phospholipids in comparison to both host and normal liver, while the increased level of triglycerides and the decrease of free fatty acids were not statistically significant. Hepatoma cells showed appreciable amounts of ether-linked lipids associated in part to neutral lipids (as glyceryl ether diesters) and, in part, to ethanolamine and choline phosphoglycerides. The alkyl groups in GEDE as well as in ethanolamine and choline phosphoglycerides were mainly constituted by C16:0 and C18:0 followed by C18:1. The alk-1-enyl groups in ethanolamine and choline phosphoglycerides were C16:0 and C18:0 with only a minor proportion of C18:1. In comparison to both host and normal liver, Yoshida hepatoma cells showed significant changes in the fatty acid composition of neutral lipids and phospholipids. Some of the major changes consisted of an increase of monoenoic acids associated with a decrease of arachidonic and docosahexaenoic acids in phosphatidylethanolamine, phosphatidylcholine, and phosphatidylinositol.

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“…The Morris hepatoma 7777 (McA-RH7777) is an extensively studied rat liver tumor that is poorly differentiated and grows rapidly when implanted in the flanks of Buffalo rats and is one of the hepatomas that can cause paraneoplastic hypercholesterolemia in host animals. 5,8 Using this model, we demonstrated that cholesterol efflux from the tumor was accelerated by the upregulation of the ATP-binding cassette transporters A1 and G1 (ABCA1 and ABCG1). In addition, this upregulation was a consequence of overexpression of the SREBP processing system in McA-RH7777 hepatomas.…”

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Hypercholesterolemia in rats with hepatomas: Increased oxysterols accelerate efflux but do not inhibit biosynthesis of cholesterol

et al. 2006

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Hypercholesterolemia is an important paraneoplastic syndrome in patients with hepatoma, but the nature of this defect has not yet been identified. We investigated the molecular mechanisms of hypercholesterolemia in a hepatoma-bearing rat model. Buffalo rats were implanted in both flanks with Morris hepatoma 7777 (McA-RH7777) cells. After 4 weeks, tumor weight was 5.5 ؎ 1.7 g, and serum cholesterol level increased from 60 ؎ 2 to 90 ؎ 2 mg/dL. Protein and mRNA expression of the ATP-binding cassette transporters A1 and G1 (ABCA1 and ABCG1) was markedly higher in tumors than in livers. These increases were associated with activation of liver X receptor ␣ (LXR␣) as a result of the increased tissue oxysterol concentrations. The accumulation of oxysterols in the hepatomas appeared to be caused mainly by the upregulation of cholesterol biosynthesis, despite the increased tissue sterol concentrations. Overexpression of the sterol regulatory element-binding protein (SREBP) processing system relative to sterol concentration contributed to the resistance to sterols in this tumor. In addition, bile acid biosynthesis was inhibited despite the reduced expression of the small heterodimer partner (SHP) and activated LXR␣, which also appeared to contribute to the accumulation of oxysterols followed by the acceleration of cholesterol efflux. In conclusion, hypercholesterolemia in McA-RH7777 hepatoma-bearing rats was caused by increased cholesterol efflux from tumors as a result of activation of LXR␣. Overexpression of the SREBP processing system contributed to the activation of LXR␣ by maintaining high oxysterol levels in tissue. (HEPATOLOGY 2006;44:602-611.) H ypercholesterolemia is one of the well-known paraneoplastic manifestations that may occur in patients with hepatomas. 1,2 It presents in 10%-25% of patients with hepatomas 2,3 and is an unfavorable prognostic factor for these patients. 4 Hypercholesterolemia associated with hepatoma has also been reported in rats implanted with some types of Morris hepatomas. 5-7 Although the exact mechanism remains to be identified, hypercholesterolemia in rats has been reported to be a result of the increased release of cholesterol from the tumor into the blood. 6,8 Many years ago, Siperstein et al. reported that cholesterol feedback control, which is characteristic of normal liver function, was consistently lost in all hepatomas regardless of animal species, degree of tumor differentiation, or method of induction of the hepatoma. 9 However, further studies demonstrated that dietary cholesterol slightly but significantly inhibited the activity of HMGCoA reductase, the rate-limiting enzyme in the cholesterol biosynthetic pathway, in rat hepatomas. 10 In addition, the injection of mevalonolactone, a precursor of cholesterol, into rats bearing hepatomas suppressed cholesterol biosynthesis in the tumors. 11 Therefore, defective cholesterol feedback regulation in hepatomas was considered to result from the secondary effects of altered cholesterol metabolism rather than from an inherent defe...

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Serum lipoproteins of rats bearing transplanted morris hepatoma 7777

Abstract: The serum lipoprotein patterns of Buffalo-strain

Cited by 10 publications

References 5 publications

Rat serum lipoproteins during carcinogenesis of the liver in the preneoplastic and the neoplastic state

Rat serum lipoproteins during carcinogenesis of the liver in the preneoplastic and the neoplastic state

Lipid composition of yoshida ascites hepatoma and of livers and blood plasma from host and normal rats

Hypercholesterolemia in rats with hepatomas: Increased oxysterols accelerate efflux but do not inhibit biosynthesis of cholesterol

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