A thermally oxidized dietary oil does not lower the activities of lipogenic enzymes in mammary glands of lactating rats but reduces the milk triglyceride concentration.
It was shown that dietary thermoxidized oils suppress gene expression of lipogenic enzymes in the liver. This study was performed to investigate whether oxidized oils also influence the activities of lipogenic enzymes in the mammary gland of lactating rats. Female rats (n = 24) were divided into two groups at 4 wk of age. They were fed for 14 wk diets with either fresh oil (a mixture of sunflower oil, linseed oil, and palm oil, 73:15:12) or oxidized oil (a mixture of sunflower oil and linseed oil, 80:20) prepared by heating at a temperature of 50 degrees C for 16 d. At the age of 12 wk, the rats were mated. At birth, litters were adjusted to 7 pups/dam. Milk was sampled at d 14 of lactation; mammary glands were taken at d 19 of lactation. Rats fed the oxidized oil had a lower activity of glucose-6-phosphate dehydrogenase (G6PDH) in their mammary glands than those fed the fresh oil (P < 0.05); the activities of fatty acid synthase (FAS) and acetyl-CoA-carboxylase in mammary glands did not differ. Relative mRNA concentrations of G6PDH, FAS, and sterol-regulatory element binding protein-1, a regulator of lipogenesis, in the mammary gland did not differ between groups. The concentrations in the milk of medium-chain fatty acids (C8-C14), the major products of fatty acid synthesis in mammary glands, also did not differ. The concentrations of triglycerides and long-chain fatty acids (C18-C22), however, were lower in the milk of rats fed the oxidized oil than in the milk of rats fed the fresh oil (P < 0.05). In conclusion, this study shows that feeding oxidized oils to lactating rats does not affect lipogenic enzymes in mammary glands but reduces the triglyceride concentrations in their milk.
Institute of Nutritional Sciences, Martin-Luther-University of Halle-Wittenberg, D-06108 Halle/Saale, Germany.
Corinna
C
Brandsch
Norbert
N
Nass
Klaus
K
Eder
D000199:Actins / Q000235:genetics; D000818:Animals; D001483:Base Sequence; D022762:CCAAT-Enhancer-Binding Proteins / Q000235:genetics; D017931:DNA Primers; D004268:DNA-Binding Proteins / Q000235:genetics; D004041:Dietary Fats / Q000494:pharmacology*; D064429:Fatty Acid Synthases / Q000235:genetics; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D007774:Lactation / Q000187:drug effects / Q000502:physiology*; D008321:Mammary Glands, Animal / Q000187:drug effects / Q000201:enzymology / Q000502:physiology*; D008892:Milk / Q000187:drug effects / Q000502:physiology*; D009821:Oils / Q000008:administration & dosage / Q000494:pharmacology*; D010084:Oxidation-Reduction; D016133:Polymerase Chain Reaction; D051381:Rats; D051780:Sterol Regulatory Element Binding Protein 1; D014157:Transcription Factors; D014280:Triglycerides / Q000378:metabolism*
D000199:Actins; D022762:CCAAT-Enhancer-Binding Proteins; D017931:DNA Primers; D004268:DNA-Binding Proteins; D004041:Dietary Fats; D009821:Oils; C497389:Srebf1 protein, rat; D051780:Sterol Regulatory Element Binding Protein 1; D014157:Transcription Factors; D014280:Triglycerides; D064429:Fatty Acid Synthases