title: Dietary supplementation of herring roe and milt enhances hepatic fatty acid catabolism in female mice transgenic for hTNFα.
abstract: OBJECTIVE
  The beneficial effects of a seafood-rich diet are highly documented and can be attributed to both n-3 polyunsaturated fatty acids and other less studied nutritional components including protein and antioxidants. The aim of the work was to investigate whether an under-utilized seafood source, eggs (roe) and sperm (milt) from herring (Clupea harengus), can affect lipid metabolism and inflammation in a mouse model transgenic for human tumor necrosis factor alpha (hTNFα).
  
  
  METHODS
  A high-fat control diet (25% total fats, 20% protein, w/w) or high-fat diets supplemented with herring roe (3.7% fat, 15% protein, w/w), or milt (1.3% fat, 15% protein) were administered to female C57BL/6 hTNFα mice. After 2 weeks, hepatic enzyme activity, gene expression, lipid and fatty acid composition, fatty acid composition of epididymal adipose tissue, and plasma lipid and cytokine levels were determined.
  
  
  RESULTS
  Animals fed herring roe and milt displayed an increased hepatic fatty acid β-oxidation and reduced fatty acid synthase activity. However, while plasma TAG was reduced, hepatic TAG and plasma and hepatic cholesterol levels were increased by the herring diets. Both herring diets led to a substantial shift in the n-6:n-3 ratio in both liver and ovarian white adipose tissue. The herring diets also increased plasma carnitine and reduced the carnitine precursor trimethyllysine. Plasma short-chained acylcarnitine esters were significantly increased, which may reflect an increased β-oxidation of long-chained fatty acids. In addition, the diets tended to reduce the plasma levels of pro-inflammatory cytokines.
  
  
  CONCLUSIONS
  Herring roe or milt diets enhanced lipid catabolism and influenced the chronic inflammatory state in hTNFα-transgenic mice.
authors: Institute of Medicine, University of Bergen, Bergen, Norway. bodil.bjorndal@med.uib.no
authors: Bodil
authors: B
authors: Bjørndal
authors: Lena
authors: L
authors: Burri
authors: Hege
authors: H
authors: Wergedahl
authors: Asbjørn
authors: A
authors: Svardal
authors: Pavol
authors: P
authors: Bohov
authors: Rolf K
authors: RK
authors: Berge
mesh_terms: D052436:Adipose Tissue, White / Q000276:immunology / Q000378:metabolism; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000737:chemistry / Q000627:therapeutic use; D002331:Carnitine / Q000097:blood; D016207:Cytokines / Q000097:blood; D059305:Diet, High-Fat / Q000009:adverse effects; D019587:Dietary Supplements / Q000032:analysis; D004531:Eggs / Q000032:analysis; D015525:Fatty Acids, Omega-3 / Q000378:metabolism; D043371:Fatty Acids, Omega-6 / Q000378:metabolism; D005234:Fatty Liver / Q000097:blood / Q000178:diet therapy* / Q000276:immunology / Q000378:metabolism; D005260:Female; D005399:Fishes; D006801:Humans; D050356:Lipid Metabolism; D008099:Liver / Q000276:immunology / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D065626:Non-alcoholic Fatty Liver Disease; D011994:Recombinant Proteins / Q000378:metabolism; D013094:Spermatozoa / Q000737:chemistry; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D015525:Fatty Acids, Omega-3; D043371:Fatty Acids, Omega-6; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D002331:Carnitine