International Journal of Endocrinology (Jan 2016)

Maternal Diet Supplementation with n-6/n-3 Essential Fatty Acids in a 1.2 : 1.0 Ratio Attenuates Metabolic Dysfunction in MSG-Induced Obese Mice

  • Josiane Morais Martin,
  • Rosiane Aparecida Miranda,
  • Luiz Felipe Barella,
  • Kesia Palma-Rigo,
  • Vander Silva Alves,
  • Gabriel Sergio Fabricio,
  • Audrei Pavanello,
  • Claudinéia Conationi da Silva Franco,
  • Tatiane Aparecida Ribeiro,
  • Jesuí Vergílio Visentainer,
  • Elton Guntendeorfer Banafé,
  • Clayton Antunes Martin,
  • Paulo Cezar de Freitas Mathias,
  • Júlio Cezar de Oliveira

DOI
https://doi.org/10.1155/2016/9242319
Journal volume & issue
Vol. 2016

Abstract

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Essential polyunsaturated fatty acids (PUFAs) prevent cardiometabolic diseases. We aimed to study whether a diet supplemented with a mixture of n-6/n-3 PUFAs, during perinatal life, attenuates outcomes of long-term metabolic dysfunction in prediabetic and obese mice. Seventy-day-old virgin female mice were mated. From the conception day, dams were fed a diet supplemented with sunflower oil and flaxseed powder (containing an n-6/n-3 PUFAs ratio of 1.2 : 1.0) throughout pregnancy and lactation, while control dams received a commercial diet. Newborn mice were treated with monosodium L-glutamate (MSG, 4 mg g−1 body weight per day) for the first 5 days of age. A batch of weaned pups was sacrificed to quantify the brain and pancreas total lipids; another batch were fed a commercial diet until 90 days of age, where glucose homeostasis and glucose-induced insulin secretion (GIIS) as well as retroperitoneal fat and Lee index were assessed. MSG-treated mice developed obesity, glucose intolerance, insulin resistance, pancreatic islet dysfunction, and higher fat stores. Maternal flaxseed diet-supplementation decreased n-6/n-3 PUFAs ratio in the brain and pancreas and blocked glucose intolerance, insulin resistance, GIIS impairment, and obesity development. The n-6/n-3 essential PUFAs in a ratio of 1.2 : 1.0 supplemented in maternal diet during pregnancy and lactation prevent metabolic dysfunction in MSG-obesity model.