Abstract
From the pathophysiological viewpoint, feeding responses to various stimuli were examined in Zucker fatty rats and their lean littermates. Intraventricular administration of norepinephrine (NE, 10 micrograms/rat) stimulated food intake in both rats. Intraventricular administration of 2-deoxy-D-glucose (2DG, 3.8 mg/rat) induced hyperphagia and concomitant hyperglycemia in lean rats. However, in fatty rats, the blood glucose was elevated but food intake was unaltered after 2DG administration. Subcutaneous administration of insulin (2 or 8 U/kg) stimulated food intake of both rats. Streptozotocin (STZ)-induced hypoinsulinemia produced transient reduction of food intake followed by sustained diabetic hyperphagia in lean rats. In fatty rats, the experimental hypoinsulinemia caused transient aphagia but not sustained diabetic hyperphagia. Daily injection of insulin (5 U/rat) restored energy assimilation in both diabetic rats. An increase in food intake due to insulin injection was remarkable only in diabetic fatty rats. From these findings, the regulatory system of food intake in fatty rats appears to be sensitive to changes in the circulating insulin level but insensitive to either glucoprivation or changes in body storage of energy.
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