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N-3 long-chain PUFA supplementation prevents high fat diet induced mouse liver steatosis and inflammation in relation to PPAR-a upregulation and NF-kB DNA binding abrogation
Artículo de publicación ISIScope: Dietary n-3 long-chain PUFAs (n-3 LCPUFAs) supplementation was studied in an
HFD-induced (HFD is high-fat diet) steatosis and inflammation in relation to peroxisome
proliferator-activated receptor alpha (PPAR- ) and nuclear factor B (NF- B) signaling.
Methods and results: Male C57BL/6J mice received (i) control diet (10% fat, 20% protein, 70%
carbohydrate), (ii) control diet plus n-3 LCPUFAs (daily doses of 108 mg/kg body weight of
eicosapentaenoic acid plus 92mg/kg body weight of docosahexaenoic acid), (iii) HFD (60% fat,
20% protein, 20% carbohydrate), or (iv) HFD plus n-3 LCPUFAs for 12 wk. PPAR- , tumor
necrosis factor alpha (TNF- ), and IL-1 mRNA expression, acyl-CoA oxidase 1 (ACOX1), and
carnitine-acyl-CoA transferase 1 (CAT-I) protein contents, and NF- B DNA binding activity
weremeasured. HFD significantly decreased liver PPAR- , ACOX1, and CAT-I levels with NF-
B activation, higher TNF- and IL-1 expression, and steatosis development. These changes
were either reduced or normalized to control values in animals subjected to HFD plus n-3
LCPUFAs, with establishment of an inverse association between NF- B activation and PPAR-
mRNA expression (r=−0.66, p < 0.0001).
Conclusion: Data presented indicate that n-3 LCPUFAs supplementation prevents liver steatosis
and inflammation induced by HFD, with underlying mechanisms involving enhanced PPAR-
signaling and diminished NF- B activation.This work was supported by grant 1110043 from FONDECYT
(National Fund for Scientific and Technological Development) to
G. T., Chile