Effects of Excess Amounts of Synthetic Amino Acid Preparations on Hypothalamus of Mice and Kittens

Abstract

The relationship between the neurotoxicity caused by excess amounts of synthetic amino acid preparations and serum levels of a certain amino acid was examined using suckling mice and kittens. Three preparations, two of which contained aspartic acid and glutamic acid, were injected intraperitoneally into neonatal mice. Almost all the animals which were treated with the preparations containing aspartic acid and glutamic acid at a dosage of more than 40 μl/g body weight (b.w.) showed hypothalamic lesions. The severity of these increased according to each dose increment. On the other hand, none of the animals treated with the preparation containing neither aspartic acid nor glutamic acid sustained hypothalamic lesions. All kittens injected intravenously with the preparation containing aspartic acid and glutamic acid at dosages of more than 20 μl/g b.w. also showed hypothalamic lesions, but none of the kittens treated with dosages of less than 10 μl/g b.w. did. Serum levels of each amino acid reached their highest values as early as 5 min after injection and then returned abruptly to the control value within 3 h.

Effect oftrans-fat, fructose and monosodium glutamate feeding on feline weight gain, adiposity, insulin sensitivity, adipokine and lipid profile

“…In common with dogs and rabbits, glutamate is rapidly absorbed from the feline intestine ( 40 ) . [ 3 H]Glutamate has been shown to bind specifically to the feline central nervous system under physiological conditions of pH and temperature ( 41 ) , and hypothalamic lesions were demonstrated to occur in kittens injected intravenously with glutamate ( 42 ) . Electrolytic destruction of the posterior commissure and the commissure of the inferior colliculus in cats was shown to result in hyperphagia and weight gain ( 43 ) .…”

Nutrigenomics of hepatic steatosis in a feline model: effect of monosodium glutamate, fructose, and Trans-fat feeding

“…Given the fact that maternal oral administration of MSG can result in detectable levels of glutamic acid accumulation in the fetal brain (Hermanussen and Tresguerres 2003;Nemeroff et al 1978), and that in rodents, the hepatotoxic effects of MSG may also be apparent even when administered orally (Yu et al 1997), it would be of interest to ascertain the effects of neonatal administration of dietary MSG in a higher animal model. It has previously been shown that intravenous injections of MSG promote the development of hypothalamic lesions in young cats (Tanaka et al 1983); and we have previously shown that whereas neonatal exposure to MSG promotes a phenotype of increased feline adiposity and reduced insulin sensitivity, Trans-fat and HFCS feeding results in an apparent elevation in cortisol and markers of liver dysfunction (Collison et al 2011). The present study seeks to further investigate the effect of Trans-fat, HFCS, and/or MSG on feline hepatic steatosis and gene expression.…”