Diet-induced changes in plasma membrane fatty acid composition affect physical properties detected with a spin-label probe

King, Mary E.; Stavens, Bruce W.; Spector, Arthur A.

doi:10.1021/bi00643a018

Cited by 90 publications

(20 citation statements)

References 46 publications

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“…The surges in plasma thyroxine and corticosterone known to occur during the mid-suckling period are likely to effect clusters of enzymes including those involved in hepatic lipid metabolism and in the biosynthesis of membranes (16,17). The final steps of biochemical and structural differentiation in the liver may, in part, be related to the major change in diet associated with weaning (23). Since a Na+K+ ATPase and a proposed bile acid receptor have been localized to the liver plasma membrane, the organization of this membrane in particular should play a key role in the maturation of bile acid transport (1, 3; 10).…”

Section: Discussionmentioning

confidence: 99%

Uptake of Taurocholate by Hepatocytes Isolated from Developing Rats

Suchy

Balistreri

1982

Pediatr Res

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Summaryon Purina rat chow and water ad libitum. Male rats were utilizedTo further define developmental changes in bile acid metabolism, we determined the kinetics of taurocholate uptake by hepatocytes isolated from Sprague-Dawley rats at 7, 14,21,28, and 56 days of age. There was a progressive increase in taurocholate uptake with age. The uptake process exhibited saturable kinetics in every age group with a maximum uptake velocity attained above a taurocholate concentration of 200 pM. There were no differences in Km values but Vmax increased progressively between 7 and 56 days of age. These data suggest that the deficit in hepatic excretory function observed in immature mammals of several species may, in part, be related to decreased transport of bile acids. SpeculationImpaired transport of bile acids by the liver may limit bile flow during development and lead to inefficient fat digestion, altered hepatic excretion of drugs, and an increased susceptibility to cholestasis. Comparable Km values for the uptake process indicate that hepatocyte affinity for taurocholate remains constant during development; whereas the rise in Vmax with postnatal age may reflect an increase in the number of binding sites. Specific changes in the liver cell plasma membrane are likely to be important determinants of the ontogeny of bile acid transport and bile flow.Bile acids are major synthetic and excretory products of the liver and are of primary importance in the generation of bile flow (1 1, 15, 20). There is increasing evidence in humans and in experimental animals that the enterohepatic circulation of bile acids is not fully developed at birth and that the perinatal liver is normally subject to a period of "physiological cholestasis" (13,14,41). In the normal human infant and in the suckling rat, bile acid pool size is decreased (42, 44) and the concentration of bile acids in serum is elevated (5, 6, 41). As a consequence of decreased bile secretion, biliary elimination of many drugs and organic anions such as bilirubin may be impaired (30,43,46) and the concentrations of bile acids reaching the intestine may be inadequate for optimal fat digestion (45). This immaturity of liver function may also place the infant at increased risk for clinical cholestasis as is commonly observed during gram negative infection or during parenteral nutrition (2,8,18). It is our hypothesis that during development, efficient enterohepatic cycling of bile acids may, in part, be limited by immaturity of bile acid transport by the liver. We, therefore, sought maturational changes in the uptake of taurocholate by hepatocytes isolated from suckling and weanling rats.for hepatocyte isolation and all studies were conducted at midday.The chemicals used in this study were: tauro-[~arbonyl-'~C] cholic acid, (52.0 mCi/mmoles; greater than 98% pure by thin layer chromatography) and [3H]-inulin, (1 mCi/6.9 mg) both from New England Nuclear Corp. (Boston, MA); collagenase (type II), Sigma Chemical Corp. (St. Louis, MO); sodium taurocholate (greater than 98% pure ...

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Section: Discussionmentioning

confidence: 99%

Uptake of Taurocholate by Hepatocytes Isolated from Developing Rats

Suchy

Balistreri

1982

Pediatr Res

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“…Modification of cellular FA composition may affect physical properties such as membrane fluidity and permeability, and certain cellular functions including transport systems, receptor binding, and eicosanoid production (De Kruyff et al, 1973;King et al, 1977;King & Spector, 1978). These might change the responses of cells to hormones, and their susceptibility to immune attack (Burns et al, 1979;Fulton & Heppner, 1985;Guffy et al, 1984;Schlager & Ohanian, 1979, 1980a.…”

Section: Discussionmentioning

confidence: 99%

Changes in the Tissue Fatty Acid Composition in Murine Malignancy and Following Anticancer Therapy

Yazıcı¹,

Tavares²,

Stamford³

et al. 1993

Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation and Radiation Injury

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Summary We studied the mouse NC tumour, a subcutaneously transplanted adenocarcinoma originally of mammary origin. Measurements per g tissue were made of 17 fatty acids (FAs), the combined amounts of n-3, n-6, saturated, unsaturated, and total FAs, and of various FA ratios in the tumour, mammary tissue, spleen, liver and plasma. Compared with mammary tissue from normal mice, tumours of vehicle-treated controls had less of seven of the FAs and more of two FAs. Mice bearing the NC tumour often had changed (usually decreased) amounts of FAs in the 'normal' spleen, liver and plasma, but not in mammary tissue. Treatment with methotrexate (MTX) was studied alone and with indomethacin which can potentiate MTX cytotoxicity. Indomethacin 1.25 mg kg-' (INDO) increased the amounts of 3/17 tumour FAs and the unsaturated FAs, but reduced 9/17 FAs, the saturated and the unsaturated FAs in 'normal' mammary tissue, and usually had no effect on the FAs of other tissues. MTX 2 or 4 mg kg-' (MTX 2 or 4 mg) ± INDO in general partly restored (increased) the amounts of tumour FAs, and reduced the saturated/unsaturated FA ratio. In the 'normal' spleen and plasma also, but not in the liver, MTX 2 mg generally somewhat restored the FA composition. However, as in the liver, the spleen 20:4 and 22:6 (which form prostaglandins and lipid peroxides) did not increase in the presence of INDO. With MTX 4 mg, some of the plasma and liver FAs decreased, in contrast to the tumour. There was generally no evidence of MTX potentiation by INDO. These results are discussed in relation to carcinogenesis, cachexia, and the response to treatment.

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“…(3) Increase in arachidonic acid in membranes may change membrane fluidity and, therefore, alter cellular interactions and functions [26][27][28] and thereby possibly affect immunologic and inflammatory responses.…”

Section: Discussionmentioning

confidence: 99%

Effects of Dietary Linoleic Acid Enrichment on Induction of Immune Complex Nephritis in Mice

Kher¹,

Barcelli²,

Weiss³

et al. 1985

Nephron

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In pharmacologic doses E series prostaglandins attenuate the development of immune complex nephritis. We studied the effect of the dietary prostaglandin precursor linoleic acid on murine apoferritin-induced immune complex glomerulonephritis. High, normal, or low linoleic acid diets were fed to mice for 4 weeks prior to and during the intraperitoneal apoferritin administration. A high linoleic acid diet feeding was associated with less proteinuria, less renal histologic damage, and prevented a rise in serum creatinine. We conclude that linoleic acid has a protective effect on the development of murine apoferritin-induced immune complex nephritis.

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Diet-induced changes in plasma membrane fatty acid composition affect physical properties detected with a spin-label probe

Cited by 90 publications

References 46 publications

Uptake of Taurocholate by Hepatocytes Isolated from Developing Rats

Uptake of Taurocholate by Hepatocytes Isolated from Developing Rats

Changes in the Tissue Fatty Acid Composition in Murine Malignancy and Following Anticancer Therapy

Effects of Dietary Linoleic Acid Enrichment on Induction of Immune Complex Nephritis in Mice

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