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A high-fish-oil diet prevents adiposity and modulates white adipose tissue inflammation pathways in mice
Thereza Cristina Lonzetti Bargut1, Carlos Alberto Mandarim-de-Lacerda1, Marcia Barbosa Aguila1
1Laboratory of Morphometry, Metabolism, and Cardiovascular Disease, Biomedical Center, State University of Rio de Janeiro, Av 28 de Setembro 87 fds, Rio de Janeiro 20551-030, Brazil.
Abstract:
Fish oil improves obesity and its comorbidities, but its mechanisms of action remain unknown. We evaluate the effects of a diet rich in fish oil in white adipose tissue (WAT) inflammation pathways, renin-angiotensin system (RAS) and mitogen-activated protein kinases (MAPKs). To achieve our aims, four groups of male C57BL/6 mice were fed different diets: standard chow diet (SC; 10% energy from fat), SC+fish oil diet (SC-FO; 10% energy from fat), high-fat lard diet (HF-L; 50% energy from lard) and HF fish oil diet (HF-FO; 50% energy from fish oil). We evaluated body mass, epididymal fat pad mass, food intake and glucose tolerance. In WAT, we assessed adipocyte hypertrophy, monocyte chemotactic protein-1 immunofluorescence, and gene and protein expression of insulin signaling, inflammation, MAPKs, RAS, peroxisome proliferator-activated receptors (PPARs) and AMP-activated protein kinase (AMPK). In relation to the results, the HF-L group, as expected, showed elevated body mass and adiposity, glucose intolerance and hypertrophied adipocytes. In WAT, we found a defect in insulin signaling, infiltration of macrophages and inflammatory markers with the associated activation of MAPKs and local RAS. On the contrary, the HF-FO group did not present increased body mass, adiposity or glucose intolerance. In this group, insulin signaling, macrophage infiltration and inflammation were reduced in WAT in comparison with the HF-L group. We also observed decreases of MAPKs and local RAS and elevation of PPAR and AMPK. In summary, fish oil activates PPAR (the three isoforms) and AMPK, decreases WAT insulin resistance and inflammation, and inhibits MAPK and RAS pathways activation.
Insights
Fish oil combats obesity by reducing white adipose tissue inflammation and improving insulin sensitivity. It activates PPARs and AMPK while inhibiting MAPK and RAS pathways, offering a potential therapeutic strategy.
Area of Science:
- Metabolism and Nutrition
- Molecular Biology
- Endocrinology
Background:
- Obesity is linked to white adipose tissue (WAT) inflammation, impacting metabolic health.
- The precise mechanisms by which fish oil exerts its beneficial effects on obesity and comorbidities are not fully understood.
- Key signaling pathways like renin-angiotensin system (RAS) and mitogen-activated protein kinases (MAPKs) are implicated in obesity-related inflammation.
Purpose of the Study:
- To investigate the effects of a fish oil-rich diet on WAT inflammation, RAS, and MAPKs in a mouse model of obesity.
- To elucidate the molecular mechanisms underlying fish oil's impact on metabolic dysfunction.
Main Methods:
- Male C57BL/6 mice were fed standard chow, standard chow with fish oil, high-fat lard, or high-fat fish oil diets.
- Evaluated body mass, fat pad mass, food intake, and glucose tolerance.
- Assessed WAT for adipocyte size, macrophage infiltration, and expression of genes/proteins related to insulin signaling, inflammation, MAPKs, RAS, PPARs, and AMPK.
Main Results:
- High-fat lard diet induced obesity, glucose intolerance, WAT inflammation, macrophage infiltration, and activation of MAPKs and RAS.
- Fish oil-supplemented high-fat diet prevented obesity, adiposity, and glucose intolerance.
- Fish oil reduced WAT inflammation, macrophage infiltration, and suppressed MAPK and RAS activation, while upregulating PPARs and AMPK.
Conclusions:
- Fish oil consumption, particularly in a high-fat context, ameliorates obesity-induced WAT inflammation and insulin resistance.
- Fish oil activates peroxisome proliferator-activated receptors (PPARs) and AMP-activated protein kinase (AMPK).
- Fish oil inhibits the activation of mitogen-activated protein kinase (MAPK) and renin-angiotensin system (RAS) pathways, contributing to its metabolic benefits.
