A physiological role for pleasure has been suggested from observations that glucose loads reduced pleasantness ratings for sweet stimuli in normal weight but not in weight-reduced subjects. This hypothesis was reexamined in fasting and food-loaded, lean and obese subjects. Magnitude estimates of sweetness and pleasantness were obtained for seven sucrose concentrations. Indices of obesity including percent overweight, percent body fat, and body mass index were calculated. Pleasantness ratings of fasting subjects either increased up to a moderate concentration and then declined (type I hedonic response) or increased monotonically with concentration (type II hedonic response). Both types of response were found in lean and obese subjects. Within each weight group there appeared a negative correlation between pleasantness response and indices of obesity. Caloric loads reduced hedonic ratings of type II lean and obese subjects, but did not affect pleasantness response of type I lean and obese subjects. These findings indicate the presence of an hedonic monitor biased by body weight and caloric intake. The data suggest a physiological role for pleasure in regulating body weight at different set points in lean and obese subjects.

Intracellular glucopenia induced by 2-deoxy-D-glucose (2DG) administration in man produces increased hunger ratings and magnitude estimates of pleasantness for sucrose solutions. Augmented food intake substantiates these changes in affective behavior and relieves experimentally induced hunger. Intracellular glucopenia activates counterregulatory mechanisms to raise plasma glucose concentrations. Inducing hunger experimentally with 2DG provides a useful method for studying appetitive behavior in humans. The neurohumoral control of pituitary hormone release and other hypothalamic functions may be examined after 2DG infusion.

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To determine whether high-energy phosphate metabolism and mobile phosphoester indexes of membrane metabolism are altered in Alzheimer disease and to help resolve some inconsistencies in the literature, brain phosphate metabolite concentrations and ratios were measured in 11 patients with mild to severe dementia of the probable Alzheimer type and 14 healthy subjects. Fully relaxed, spatially localized, phosphorus-31 nuclear magnetic resonance (NMR) spectroscopy and proton (hydrogen-1) MR imaging were performed. No significant differences were found in the concentrations and relative ratios of phosphocreatine, nucleoside triphosphate, inorganic phosphate, phosphomonoester, and phosphodiesters in whole axial sections through the lateral cerebral ventricles of the brain that could not be accounted for by atrophy. There was no correlation between P-31 NMR indexes and the severity of dementia as assessed with neuropsychologic testing. High-energy phosphate and membrane metabolism, as detected in vivo with P-31 NMR spectroscopy in whole-brain sections, do not appear to play a major role in the disease process, except as a direct consequence of atrophy quantified with H-1 MR imaging.