Treatments of human and rodent
obesity frequently involve administration of
amphetamine derivatives, much like
phenylpropanolamine, which suppress food intake. The Zucker rat is a commonly employed model of youth-onset
obesity in which the homozygous genotype manifests
hyperphagia as well as other characteristics that parallel human
obesity. Using a macronutrient selection procedure, we examined
phenylpropanolamine's differential actions in controlling dietary intake, spontaneous open-field activity, and regional hypothalamic
neurotransmitter levels in obese female Zucker rats of varying fat food preference. We hypothesized that
phenylpropanolamine would alter hypothalamic monoamine levels differently in low-fat preferring and high-fat preferring Zucker rats, and hence affect feeding behavior and activity differently in these two groups. It was found that in high-fat preferring animals,
phenylpropanolamine significantly decreased spontaneous open-field activity, decreased only
carbohydrate caloric intake, and increased
serotonin and
5-HIAA levels in the paraventricular nucleus (PVN). In low-fat preferring animals,
phenylpropanolamine decreased
carbohydrate,
protein, and total caloric intake, had no significant effect of spontaneous activity, and increased
serotonin and
5-hydroxyindole acetic acid levels in the PVN. Inherent and induced physiological differences of low-fat and high-fat preferring animals are discussed as well as
phenylpropanolamine's potential in
combination drug therapy for the treatment of human hyperphagic
obesity.