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  • Cambridge University Press (CUP)  (3)
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  • Cambridge University Press (CUP)  (3)
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  • 1
    Online-Ressource
    Online-Ressource
    Cambridge University Press (CUP) ; 2008
    In:  British Journal of Nutrition Vol. 100, No. 4 ( 2008-10), p. 776-785
    In: British Journal of Nutrition, Cambridge University Press (CUP), Vol. 100, No. 4 ( 2008-10), p. 776-785
    Kurzfassung: There is growing evidence that dietary proteins may interfere with lipid metabolism. We therefore examined the effects of feeding obese Zucker rats a single cell protein (SCP) with low ratios of methionine:glycine and lysine:arginine for 6 weeks. SCP feeding reduced the hepatic steatosis and lowered the plasma transaminase levels when compared with casein-fed rats (controls). The fatty acid oxidation was increased in liver mitochondria and peroxisomes, whereas the activities of enzymes involved in lipogenesis and TAG biosynthesis were unaffected. SCP feeding affected the fatty acid composition of liver lipids and plasma, and reduced the mRNA levels of the fatty acid desaturases. The decreased gene expression of stearoyl-CoA desaturase suggested that the fatty acids were directed towards oxidation rather than esterification as TAG. The decreased mRNA levels of VLDL-receptor and lipoprotein lipase in the liver after SCP feeding suggested that the uptake of TAG-rich lipoprotein to the liver was decreased. To conclude, the reduced fatty liver by SCP feeding may be caused by the increased capacity for fatty acid β-oxidation in the liver, combined with changed fatty acid composition and possibly a reduced hepatic clearance of circulating VLDL. An increased awareness of the effect of dietary proteins on lipid metabolism could be of relevance in future dietary treatment of non-alcoholic fatty liver disease.
    Materialart: Online-Ressource
    ISSN: 0007-1145 , 1475-2662
    Sprache: Englisch
    Verlag: Cambridge University Press (CUP)
    Publikationsdatum: 2008
    ZDB Id: 2016047-1
    SSG: 12
    SSG: 21
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
    In: British Journal of Nutrition, Cambridge University Press (CUP), Vol. 102, No. 6 ( 2009-09-28), p. 803-815
    Kurzfassung: Conjugated linoleic acid (CLA) isomers have been reported to reduce body weight and beneficially affect glucose metabolism in animals, but the results are inconsistent and seem to depend on animal model and type of CLA isomer. In the present study, feeding male Zucker fa/fa rats diets supplemented with 1 % trans -10, cis -12-CLA for 10 d reduced the liver TAG content without improving the overall adiposity, and enhanced hepatic mitochondrial and peroxisomal β-oxidation. The increased carnitine palmitoyltransferase (CPT)-I activity and mRNA level as well as the increased n -3: n -6 PUFA ratio in liver suggest that trans -10, cis -12-CLA increased the hepatic β-oxidation by stimulation of PPARα. The reduced hepatic TAG content may be partly due to lower activity of stearoyl-CoA desaturase, as the ratios of 18 : 1 n -9:18 : 0 and 16 : 1 n -7:16 : 0 were reduced in liver. Trans -10, cis -12-CLA increased the CPT-I mRNA in retroperitoneal white adipose tissue (WAT), and increased uncoupling protein-2 mRNA in epididymal and inguinal WAT depots. Leptin mRNA level was decreased in all examined WAT depots, implying reduced insulin sensitivity. The resistin mRNA level was increased in all WAT depots, whereas adiponectin mRNA was reduced in inguinal and retroperitoneal WAT. The present results suggest that dietary supplementation with trans -10, cis -12-CLA may increase the catabolism of lipids in liver and adipose tissue. Moreover, we provide new data suggesting that trans -10, cis -12-CLA modulates the expression of resistin and adiponectin inversely in adipose tissue. Hence, the present results suggest that trans -10, cis -12-CLA may have some beneficial effects on lipid metabolism and adiposity but possibly reduces insulin sensitivity.
    Materialart: Online-Ressource
    ISSN: 0007-1145 , 1475-2662
    Sprache: Englisch
    Verlag: Cambridge University Press (CUP)
    Publikationsdatum: 2009
    ZDB Id: 2016047-1
    SSG: 12
    SSG: 21
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
    In: British Journal of Nutrition, Cambridge University Press (CUP), Vol. 96, No. 2 ( 2006-08), p. 249-257
    Kurzfassung: Casein-based diets containing a low (LDI) or high (HDI) dose of soya protein concentrate enriched with isoflavones were fed to obese Zucker rats for 6 weeks. HDI feeding, but not LDI feeding, reduced the fatty liver and decreased the plasma levels of alanine transaminase and aspartate transaminase. This was accompanied by increased activities of mitochondrial and peroxisomal β-oxidation, acetyl-CoA carboxylase, fatty acid synthase and glycerol-3-phosphate acyltransferase in liver and increased triacylglycerol level in plasma. The decreased fatty liver and the increased plasma triacylglycerol level appeared not to be caused by an increased secretion of VLDL, as HDI decreased the hepatic mRNA levels of apo B and arylacetamide deacetylase. However, the gene expression of VLDL receptor was markedly decreased in liver, but unchanged in epididymal white adipose tissue and skeletal muscle of rats fed HDI, indicating that the liver may be the key organ for the reduced clearance of triacylglycerol-rich lipoproteins from plasma after HDI feeding. The n −3/ n −6, 20:4 n -/8:2 n −6 and (20:5 n −3+22:6 n −3)/18:3 n −3 ratios were increased in liver triacylglycerol by HDI. The phospholipids in liver of rats fed HDI contained a low level of 20:4 n −6 and a high level of 20:5 n −3, favouring the production of anti-inflammatory eicosanoids. When obese Zucker rats were fed soya protein, this also resulted in reduced fatty liver, possibly through reduced clearance of VLDL by the liver. We conclude that the isoflavone-enriched soya concentrate as well as soya protein may be promising dietary supplements for treatment of non-alcoholic fatty liver.
    Materialart: Online-Ressource
    ISSN: 0007-1145 , 1475-2662
    Sprache: Englisch
    Verlag: Cambridge University Press (CUP)
    Publikationsdatum: 2006
    ZDB Id: 2016047-1
    SSG: 12
    SSG: 21
    Standort Signatur Einschränkungen Verfügbarkeit
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