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Monosodium glutamate neonatal treatment induces cardiovascular autonomic function changes in rodents
Signorá Peres Konrad1, Vera Farah, Bruno Rodrigues
1Basic Health Sciences Institute, Physiology Department, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre/RS, Brazil.
Insights
Neonatal monosodium glutamate (MSG) treatment in rodents causes obesity, leading to impaired cardiovascular autonomic function, increased arterial pressure, and insulin resistance in adulthood.
Area of Science:
- Cardiovascular Physiology
- Neuroendocrinology
- Metabolic Disorders
Background:
- Neonatal exposure to certain substances can have long-term health consequences.
- Obesity is associated with significant cardiovascular and metabolic dysregulation.
Purpose of the Study:
- To investigate the impact of monosodium glutamate (MSG)-induced obesity on cardiovascular autonomic function in a rodent model.
- To assess baroreflex sensitivity and autonomic nerve activity in MSG-treated rats.
Main Methods:
- Rodents were treated with MSG during the first week of life to induce obesity.
- Cardiovascular autonomic function was evaluated at 33 weeks, including arterial pressure, heart rate variability, and responses to autonomic blockade.
- Insulin resistance was assessed using glucose and insulin measurements.
Main Results:
- MSG-treated rats exhibited higher body weight, Lee index, and adipose tissue compared to controls.
- These rats developed insulin resistance, characterized by a reduced glucose/insulin index and hyperinsulinemia.
- MSG-induced obesity was associated with elevated mean arterial pressure and significantly reduced heart rate variability, bradycardic responses, vagal, and sympathetic effects.
Conclusions:
- Obesity induced by neonatal MSG treatment significantly impairs cardiac autonomic function in rodents.
- This impairment likely contributes to the observed increases in arterial pressure and insulin resistance.
Objectives:
The aim of this study was to evaluate cardiovascular autonomic function in a rodent obesity model induced by monosodium glutamate injections during the first seven days of life.
Method:
The animals were assigned to control (control, n = 10) and monosodium glutamate (monosodium glutamate, n = 13) groups. Thirty-three weeks after birth, arterial and venous catheters were implanted for arterial pressure measurements, drug administration, and blood sampling. Baroreflex sensitivity was evaluated according to the tachycardic and bradycardic responses induced by sodium nitroprusside and phenylephrine infusion, respectively. Sympathetic and vagal effects were determined by administering methylatropine and propranolol.
Results:
Body weight, Lee index, and epididymal white adipose tissue values were higher in the monosodium glutamate group in comparison to the control group. The monosodium glutamate-treated rats displayed insulin resistance, as shown by a reduced glucose/insulin index (-62.5%), an increased area under the curve of total insulin secretion during glucose overload (39.3%), and basal hyperinsulinemia. The mean arterial pressure values were higher in the monosodium glutamate rats, whereas heart rate variability (>7 times), bradycardic responses (>4 times), and vagal (~38%) and sympathetic effects (~36%) were reduced as compared to the control group.
Conclusion:
Our results suggest that obesity induced by neonatal monosodium glutamate treatment impairs cardiac autonomic function and most likely contributes to increased arterial pressure and insulin resistance.
