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Acute Effects of Oral or Parenteral Aspartame on Catecholamine Metabolism in Various Regions of Rat Brain¹

Laboratory of Neuroendocrine Regulation, Department of Nutrition and Food Science, Massachusetts Institute of Technology, Cambridge, MA 02139

Hypertensive (SHR) and nonhypertensive [Wistar-Kyoto (WKY); Sprague-Dawley (SD)] strains of rats received the dipeptide sweetener aspartame (200 mg/kg) or, as a positive control, tyrosine (200 mg/kg) by gavage or parenterally, after a brief (2-h) fast. Two hours later, compared with those of saline controls brain levels of the norepinephrine metabolite 3-methoxy-4-hydroxyphenylethylethyleneglycol (MHPG) sulfate were significantly higher in the hypothalamus (WKY), locus coeruleus (SD and SHR) and brain stem (SHR) in tyrosine-treated animals, and in the locus coeruleus (SD) of those given aspartame. Brain norepinephrine levels were also higher, compared with those of saline-treated control rats, in the cerebral cortex (SD and SHR), amygdala (SD) and locus coeruleus (WKY) after tyrosine administration, and in the amygdala (SD) and cerebral cortex (SHR) after aspartame administration. In another study, oral aspartame was found to be at least as effective as the parenterally administered sweetener in raising regional brain levels of tyrosine or MHPG sulfate (i.e., compared with corresponding levels in saline-treated rats). Animals receiving oral aspartame also exhibited higher plasma tyrosine and phenylalanine ratios (i.e., the ratios of their plasma concentrations to the summed concentrations of other large neutral amino acids that compete with them for uptake into the brain), than animals receiving saline.

KEY WORDS: • aspartame • tyrosine • catecholamine • MHPG sulfate • sweetener • hypertension • rat

¹ Supported by a grant from the National Institutes of Health (NS-21231). Dr. Yokogoshi was a fellow of the Center for Brain Sciences and Metabolism Charitable Trust.

² Present address: Laboratory of Nutritional Biochemistry, Department of Agricultural Chemistry, Nagoya University, Nagoya, Japan 464.

³ Address for correspondence: Room E25-604, Massachusetts Institute of Technology, Cambridge, MA 02139.

Manuscript received 31 January 1985. Revision accepted 20 November 1986.