Differential inflammatory status in rats susceptible or resistant to diet-induced obesity: effects of EPA ethyl ester treatment.
BACKGROUND
Obesity has been associated with a chronic low degree inflammatory response, characterized by an increase of inflammatory adipocytokines like tumoral necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) as well as the synthesis of acute phase reactants such as haptoglobin.


OBJECTIVE
To evaluate if impairments in the inflammatory response at the white adipose tissue (WAT) level could be involved in the mechanisms conferring susceptibility or resistance to high-fat diet-induced obesity (DIO).


METHODS
The expression levels of WAT genes and systemic markers related to inflammation were evaluated in two groups of rats fed with a high-fat diet during 15 days that showed either an early susceptibility (DIO) or resistance (DR) to develop obesity. We also tested the efficacy of the eicosapentaenoic (EPA) omega-3 fatty acid treatment (35 days) to potentially counteract the obesity-associated inflammatory features in DIO rats.


RESULTS
This trial showed that high-fat diet induces an increase on mRNA levels on TNF-alpha and haptoglobin in DIO animals (P < 0.05), while no significant changes were observed on DR rats. Furthermore, a significant increase in IL-6 mRNA (P < 0.05) was found in both DR and DIO rats. EPA-treatment caused a significant decrease in IL-6 mRNA (P < 0.05), without significant changes in haptoglobin mRNA levels in adipose tissue. An unexpected decrease was observed in haptoglobin serum levels (P < 0.05) in DIO rats, which was reverted to control values in EPA-treated animals.


CONCLUSIONS
Our data suggest that obesity susceptibility or resistance may depend on the genetic make up related to inflammatory features, and support a role for omega-3 fatty acids in the prevention of obesity-associated inflammation in adipose tissue. In addition, our data do not support the hypothesis that serum haptoglobin is an acute phase protein expected to be positively related to increased adiposity in rats, at least in early and medium stages of DIO.
Pérez-Echarri
Nerea
N
Dept. of Nutrition and Food Sciences, Physiology and Toxicology, University of Navarra, 31008, Pamplona, Spain.
Pérez-Matute
Patricia
P
Marcos-Gómez
Beatriz
B
Baena
Maria J
MJ
Marti
Amelia
A
Martínez
J Alfredo
JA
Moreno-Aliaga
María Jesus
MJ
D052436:Adipose Tissue, White / Q000737:chemistry* / Q000378:metabolism; D000818:Animals; D004041:Dietary Fats / Q000008:administration & dosage*; D015118:Eicosapentaenoic Acid / Q000494:pharmacology*; D006242:Haptoglobins / Q000235:genetics / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000453:epidemiology* / Q000235:genetics; D015850:Interleukin-6 / Q000097:blood / Q000235:genetics; D008297:Male; D009765:Obesity / Q000097:blood / Q000235:genetics / Q000276:immunology*; D012333:RNA, Messenger / Q000378:metabolism*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
D004041:Dietary Fats; D006242:Haptoglobins; D015850:Interleukin-6; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D015118:Eicosapentaenoic Acid