scholarly journals Effect of reduced maternal protein intake in pregnancy in the rat on the fatty acid composition of brain, liver, plasma, heart and lung phospholipids of the offspring after weaning

2003 ◽  
Vol 90 (2) ◽  
pp. 345-352 ◽  
Author(s):  
Graham C. Burdge ◽  
Emmanuelle Delange ◽  
Ludivine Dubois ◽  
Rebecca L. Dunn ◽  
Mark A. Hanson ◽  
...  

Reduced protein intake during pregnancy decreased maternal hepatic and plasma docosahexaenoic acid concentrations and impaired docosahexaenoic acid accumulation into fetal brain in the rat. The present study investigated whether restriction of maternal protein intake during pregnancy in the rat alters membrane phospholipid fatty acid composition in the offspring after weaning. Female rats (six per group) were mated and fed diets containing either 180 or 90 g protein/kg throughout pregnancy. Mothers were transferred to standard chow after delivery and the litters reduced to eight pups. Weaning was at 28 d and pups were killed 5 to 6 d later. Tissue weights or membrane total phosphatidylcholine (PC) and phosphatidylethanolamine (PE) concentrations in the offspring did not differ between dietary groups. There were significant differences between the 180 and 90 g/kg groups in liver, brain, lung and heart fatty acid composition that differed between tissues and phospholipid classes. For example, docosahexaenoic and arachidonic acid concentrations were 23 and 10 % lower respectively in hepatic PC, but not PE, in the 90 g/kg group. In brain, docosahexaenoic acid concentration was 17 % lower in PC, but not PE, while arachidonic acid content was 21 % greater in PE but unchanged in PC. The greatest differences were in unsaturated fatty acids, which suggests alterations to desaturase activities and/or the specificity of phospholipid biosynthesis. These results suggest that restricted maternal protein intake during pregnancy results in persistent alterations to membrane fatty acid content.

1992 ◽  
Vol 262 (3) ◽  
pp. R464-R471 ◽  
Author(s):  
T. Ohkubo ◽  
R. Jacob ◽  
H. Rupp

To define the effects of physical activity on vascular fatty acid composition and prostanoid generation, spontaneously hypertensive and normotensive rats were made to swim at 34-35 degrees C for 5-7 wk. Fatty acids were determined by gas chromatography and prostanoids by high-performance liquid chromatography and electrochemical detection. A characteristic feature of swimming rats was a markedly reduced linoleic acid content in the iliac artery and the aorta; in normotensive swimming rats stearic acid and arachidonic acid contents were increased. These changes could not be attributed to a heat loss during swimming or to depressed growth characteristics. A chemical sympathectomy using guanethidine (60 mg/kg body wt daily) did not prevent the alterations in fatty acid composition. A higher arachidonic acid content was correlated with an increased generation of 6-ketoprostaglandin F1 alpha in the aorta of untreated rats and sympathectomized rats. It is concluded that swimming can alter the vascular fatty acid composition in a manner which results in an increased potential for prostacyclin production.


1988 ◽  
Vol 60 (2) ◽  
pp. 217-224 ◽  
Author(s):  
M. J. Jackson ◽  
J. Roberts ◽  
R. H. T. Edwards

1. Giving diets containing 100 g fully-refined, non-hydrogenated fish oil/kg to rats caused substantial modification of skeletal-muscle-membrane fatty acid composition compared with control animals fed on an equivalent diet containing 100 g maize oil/kg.2. Total muscle arachidonic acid (20:4ω6) was reduced from 138 (sd 25) mg/g total fatty acids to 15 (sd 2) mg/ g and phospholipid arachidonic acid content showed equivalent changes.3. Reduction in muscle arachidonic acid content had no influence on the growth of individual muscles.4. Variation in muscle fatty acid composition exacerbated the response of muscle to calcium-induced damage assessed by efflux of intracellular creatine kinase (EC 2.7.3.2).5. It is concluded that metabolites of arachidonic acid are unlikely to be primary controlling factors of muscle growth or specific mediators of muscle sarcolemmal damage leading to enzyme efflux.


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