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Diets Containing α-Linolenic (ω3) or Oleic (ω9) Fatty Acids Rescues Obese Mice From Insulin Resistance
V Oliveira1, R Marinho1, D Vitorino1
1Laboratories of Nutritional Genomics (V.O., D.E.C.), Limeira 13484-350, Cell Signaling (V.O., D.V., J.C.M., N.D., L.A.V., D.E.C.), and Molecular Biology of Exercise (R.M., L.P., A.S.R.d.S., E.R.R., J.R.P.); Innovare (G.A.S., R.R.C.); and Nutrigenomics and Lipids Center (A.S.-C., D.E.C.) and Biotechnology Center (E.R.R., J.R.P., D.E.C.), School of Applied Sciences, State University of Campinas, Campinas, Brazil 13083-887; and Laboratory of Exercise Biochemistry and Physiology (C.T.D.S.), Health Sciences Unit, Universidade do Extremo Sul Catarinense Criciúma, Brazil 88806-000.
Dietary unsaturated fatty acids, specifically omega-3 and omega-9, combat obesity-related inflammation and insulin resistance by activating G protein-coupled receptors (GPR)120 and GPR40. This activation improves metabolic health in obese mice.
Area of Science:
- Metabolic disease research
- Inflammation and immunology
- Nutritional science
Background:
- Subclinical systemic inflammation is a key feature of obesity and insulin resistance.
- Targeting inflammatory pathways may improve metabolic health.
- Unsaturated fatty acids possess anti-inflammatory properties via multiple mechanisms.
Purpose of the Study:
- To investigate the anti-inflammatory and insulin-sensitizing effects of omega-3 and omega-9 fatty acids via G protein-coupled receptor (GPR)120 and GPR40 pathways.
- To elucidate the role of these receptors in mediating the benefits of dietary unsaturated fatty acids in obesity-induced insulin resistance.
Main Methods:
- Administration of diets enriched with omega-3 and omega-9 fatty acids to obese mice.
- Assessment of GPR120 and GPR40 activation in key metabolic tissues (liver, skeletal muscle, adipose tissue).
- Evaluation of inflammatory markers, macrophage infiltration, insulin sensitivity, glucose homeostasis, and gluconeogenic enzyme expression.
Main Results:
- GPR120 activation in liver, muscle, and adipose tissue reduced inflammation and insulin resistance in obese mice.
- GPR40 activation in muscle partially mediated these beneficial effects.
- Pair-feeding and immunoneutralization studies confirmed GPR120's central role.
- Improved insulin sensitivity correlated with reduced tissue inflammation, decreased macrophage infiltration, and increased IL-10.
- Enhanced glucose homeostasis was linked to reduced hepatic gluconeogenic enzyme expression and body mass reduction.
Conclusions:
- GPR120 and GPR40 are critical mediators of the beneficial effects of dietary unsaturated fatty acids on obesity-induced insulin resistance.
- Targeting these G protein-coupled receptors presents a potential therapeutic strategy for metabolic disorders associated with inflammation.
