Blood metabolites and feeding during postinsulin hypophagia.

Physiological changes accompanying a period of voluntary hypophagia in male Sprague-Dawley rats after insulin-induced hyperphagia and body weight gain were investigated. Postinsulin hypophagia was manifested as a reduction in meal duration diurnally and nocturnally (Geary et al., Behav. Neural Biol. 31: 435-442, 1981). Gastrointestinal transit of 14C-labeled nutrients was unchanged in hypophagic rats, suggesting a postabsorptive mechanism controlled the hypophagia. Basal blood glucose and plasma nonesterified fatty acids, 3-hydroxybutyrate, glycerol, and some amino acids were elevated during hypophagia, while liver glycogen content was reduced. Hypophagic rats' arteriovenous blood glucose differences and glucose oxidation rates, however, were not different from controls. After nutrient repletion blood glucose and plasma glycerol remained elevated in hypophagic rats in comparison to controls, while differences in other plasma metabolites were reduced. Liver glycogen accumulated faster in hypophagic rats. These data were related to the lipostatic and other hypotheses how energy balance status affects hunger and satiety.