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

Abstract

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.

Body Adiposity of Young Male Rats Fed a Diet Containing Flaxseed Flour during Lactation or in Post-Weaning Period

“…Adiposity can also be associated with insulin concentration [12] and previous report that ALA prevents high insulin release [13]. Martin, et al [14] observed that ALA during pregnancy and lactation improving glucose tolerance, insulin sensitivity and reducing the fat mass stores in induced obese mice. However, Heskey, et al [15] related that higher adipose tissue ALA was inversely associated with insulin resistance.…”

Metabolic syndrome agravates cardiovascular, oxidative and inflammatory dysfunction during the acute phase of Trypanosoma cruzi infection in mice

“…To induce obesity, new-born Swiss mice underwent subcutaneous injection of MSG (Sigma, St. Louis, USA; 4 mg/g body weight) from day 1 to day 6 after control mice received an equimolar solution of saline injected in animals of the obese group 24 . The mice were separated after weaning by sex and weighed every 10 days; only male mice were used.…”

Obesity and endocrine-disrupting chemicals

“…The flavor enhancer monosodium glutamate (MSG) is well-known for its action to induce obesity and metabolic abnormalities in mice by its toxic effects on the arcuate nucleus, a critical hypothalamic nucleus involved in body mass and energy metabolism regulation (121)(122)(123)(124).…”

“…In addition to surfactants and emulsifiers, the widely used food preservative 3-tert-butyl-4-hydroxyanisole (3-BHA) induced adipocyte differentiation in 3T3-L1 preadipocytes ( 118 ); moreover, 3-BHA exposure increased adiposity and lipid plasma levels in exposed mice ( 119 ). The flavor enhancer monosodium glutamate (MSG) is well-known for its action to induce obesity and metabolic abnormalities in mice by its toxic effects on the arcuate nucleus, a critical hypothalamic nucleus involved in body mass and energy metabolism regulation ( 120 , 121 , 122 , 123 ). Notably, the central effects of MSG to promote obesity depend upon its entrance in the brain, which, in turn, is observed when it is administered centrally to adult mice or peripherally to neonate mice since the latter exhibit an immature blood-brain barrier allowing the passage of MSG ( 123 , 124 ).…”