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Fish Oil Protects Wild Type and Uncoupling Protein 1‐Deficient Mice from Obesity and Glucose Intolerance by Increasing Energy Expenditure
Author(s) -
Oliveira Tiago E.,
Castro Érique,
Belchior Thiago,
Andrade Maynara L.,
ChavesFilho Adriano B.,
Peixoto Albert S.,
Moreno Mayara F.,
OrtizSilva Milene,
Moreira Rafael J.,
Inague Alex,
Yoshinaga Marcos Y.,
Miyamoto Sayuri,
MoustaidMoussa Naima,
Festuccia William T.
Publication year - 2019
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201800813
Subject(s) - energy expenditure , fish oil , fish <actinopterygii> , medicine , obesity , endocrinology , type 2 diabetes , uncoupling protein , biology , fishery , food science , diabetes mellitus , brown adipose tissue
Scope The mechanisms and involvement of uncoupling protein 1 (UCP1) in the protection from obesity and insulin resistance induced by intake of a high‐fat diet rich in omega‐3 (n‐3) fatty acids are investigated. Methods and results C57BL/6J mice are fed either a low‐fat (control group) or one of two isocaloric high‐fat diets containing either lard (HFD) or fish oil (HFN3) as fat source and evaluated for body weight, adiposity, energy expenditure, glucose homeostasis, and inguinal white and interscapular brown adipose tissue (iWAT and iBAT, respectively) gene expression, lipidome, and mitochondrial bioenergetics. HFN3 intake protected from obesity, glucose and insulin intolerances, and hyperinsulinemia. This is associated with increased energy expenditure, iWAT UCP1 expression, and incorporation of n‐3 eicosapentaenoic and docosahexaenoic fatty acids in iWAT and iBAT triacylglycerol. Importantly, HFN3 is equally effective in reducing body weight gain, adiposity, and glucose intolerance and increasing energy expenditure in wild‐type and UCP1‐deficient mice without recruiting other thermogenic processes in iWAT and iBAT, such as mitochondrial uncoupling and SERCA‐mediated calcium and creatine‐driven substrate cyclings. Conclusion Intake of a high‐fat diet rich in omega‐3 fatty acids protects both wild‐type and UCP1‐deficient mice from obesity and insulin resistance by increasing energy expenditure through unknown mechanisms.