Maternal Metabolic Alterations in Monosodium Glutamate Fed Rats during Gestation and Lactation Period

Document Type : Original Article

Authors

1 Physiology department, Faculty of medicine, Ain shams university, Cairo, Egypte

2 Physiology department, Faculty of medicine, Ain shams university, Cairo, Egypt

Abstract

Background: Monosodium glutamate (MSG), an extensively used food additive, is claimed to cause many health problems, its use is still under debate.
Aim: to explore the metabolic and hypertensive effect of MSG dietary administration in pregnant and lactating female rats, and its possible underlying mechanism.
Methods: 16 adult female albino Wister rats were divided into 2 groups, control group; were fed standard rat chow, and MSG group; were fed 2% MSG supplemented rat chow throughout gestation and lactation period. Oral glucose tolerance test (OGTT) and arterial blood pressure (ABP) were measured at mid and late gestation, mid and late lactation periods. At mid lactation period, a retroorbital samples were analyzed for fasting glucose, lipid profile; triglycerides (TGs), total cholesterol (TC) and low density lipoprotein-cholesterol (LDL-C), hormonal assays; insulin, glucagon, prolactin, corticosterone and ACTH, as well as pancreatic lipase, amylase and malondialdehyde (MDA). By the end of lactation, adipose tissue was assessed for glucose transporter-4 (GLUT-4) and hormone sensitive lipase (HSL) relative expression.
Results: MSG rats showed elevated ABP during pregnancy and lactation, with impaired OGTT at mid and late lactation period. Fasting serum glucose, TGs, TC, LDL-C, glucagon, corticosterone, pancreatic lipase and amylase, MDA as well as adipose tissue HSL expression were significantly elevated, while, fasting serum insulin, ACTH and adipose tissue GLUT-4 expression were significantly declined in MSG fed rats as compared to control group.
Conclusion: MSG feeding during pregnancy and lactation induced hypertension and metabolic alterations that could be due to pancreatic and adrenal affection secondary oxidative stress.

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