Omega 3 Rich Diet Modulates Energy Metabolism via GPR120-Nrf2 crosstalk in a Novel Antioxidant Mouse Model
| Autor: | Carla Cook, Deborah Amos, Nalini Santanam |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Antioxidant NF-E2-Related Factor 2 medicine.medical_treatment Saturated fat Adipose tissue 030209 endocrinology & metabolism Type 2 diabetes Diet High-Fat Article Receptors G-Protein-Coupled 03 medical and health sciences Mice 0302 clinical medicine Insulin resistance Internal medicine Fatty Acids Omega-3 medicine Animals Molecular Biology medicine.diagnostic_test Chemistry Body Weight GPR120 Cell Biology medicine.disease Catalase Dietary Fats Disease Models Animal 030104 developmental biology Endocrinology Body Composition Metabolic syndrome Insulin Resistance Lipid profile Energy Metabolism Oxidation-Reduction |
| Popis: | With obesity rates reaching epidemic proportions, more studies concentrated on reducing the risk and treating this epidemic are vital. Redox stress is an important metabolic regulator involved in the pathophysiology of cardiovascular disease, Type 2 diabetes, and obesity. Oxygen and nitrogen-derived free radicals alter glucose and lipid homeostasis in key metabolic tissues, leading to increases in risk of developing metabolic syndrome. Oxidants derived from dietary fat differ in their metabolic regulation, with numerous studies showing benefits from a high omega 3 rich diet compared to the frequently consumed "western diet" rich in saturated fat. Omega 3 (OM3) fatty acids improve lipid profile, lower inflammation, and ameliorate insulin resistance, possibly through maintaining redox homeostasis. This study is based on the hypothesis that altering endogenous antioxidant production and/or increasing OM3 rich diet consumption will improve energy metabolism and maintain insulin sensitivity. We tested the comparative metabolic effects of a diet rich in saturated fat (HFD) and an omega 3-enriched diet (OM3) in the newly developed 'stress-less' mice model that overexpresses the endogenous antioxidant catalase. Eight weeks of dietary intervention showed that mice overexpressing endogenous catalase compared to their wild-type controls when fed an OM3 enriched diet, in contrast to HFD, activated GPR120-Nrf2 cross-talk to maintain balanced energy metabolism, normal circadian rhythm, and insulin sensitivity. These findings suggest that redox regulation of GPR120/FFAR4 might be an important target in reducing risk of metabolic syndrome and associated diseases. |
| Databáze: | OpenAIRE |
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