Introduction:

Obesity, especially visceral, is a major risk factor for several diseases such as Type 2 diabetes mellitus, cardiovascular diseases, atherosclerosis, dyslipidemia, non-alcoholic fatty liver disease, and cancer. Oxidative stress may be a unifying mechanism for the development of major obesity-related comorbidities.

Objective:

To evaluate the prooxidant-antioxidant balance in monosodium glutamate-induced obesity in Wistar rats (MSG- obese rats).

Material and Methods:

Female Wistar rats received subcutaneous (sc) injections of monosodium glutamate solution (4 mg/g of body weight) or vehicle (NaCl 0,9 %; control) to induce obesity during the neonatal period. At 90 days of life, obesity was determined. At 180 days of life, rats were anesthetized and killed to obtain blood and liver samples for the determination of biochemical markers.

Results:

MSG obese rats presented significantly higher triglycerides, uric acid and insulin levels, as well as elevated HOMA and TyG indexes. Increased concentrations of nitrate and nitrite, 2-deoxyribose oxidation products and advanced oxidation protein products levels were observed in obese rats.

Conclusions:

Obesity induced by monosodium glutamate reproduces the main metabolic alterations associated with human visceral obesity, among which oxidative stress is included. This model may be useful for the evaluation of therapeutic strategies to prevent or decrease complications associated with obesity.

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