The role of gustatory and postingestive signals in the termination of delayed glucoprivic feeding and hypothalamic norepinephrine turnover

Abstract

If food is withheld for 6 hr after insulin injection, enhanced feeding in response to glucoprivation can still be demonstrated even though blood glucose has returned spontaneously to normal. Moreover, the magnitude of the glucoprivic feeding is unattenuated by the delay. Like feeding, glucoprivation-induced increases in hypothalamic norepinephrine (NE) turnover also persist after the spontaneous return to normoglycemia, fostering the notion that these neurons may mediate the feeding. Rats were allowed restricted access to saccharin (0.1% solution) or isocaloric quantities of D-glucose of D-fructose (18% solutions), fat (lard), or pelleted rat food during a 30 min period 1.5 to 2 hr after insulin (2.5 units/kg, s.c.) or saline injection in order to specify the conditions responsible for the termination of the glucoprivic stimulus to feed and to determine whether these same conditions would be associated with normalization of NE turnover. Delayed feeding was measured in a 2 hr test 4 to 6 hr later. Nutrients were selected for their differences as substrates for brain energy metabolism and their caloric values were equated with the number of calories (7.9 kcal) which abolishes delayed glucoprivic feeding (DGF) when ingested as pelleted food. Norepinephrine turnover (the decline of NE concentrations after synthesis inhibition with α methyl-p-tyrosine) was normalized after glucoprivation by ingestion of pelleted food and glucose but was unaltered by ingestion of fructose or fat by non-nutritive orogastric stimulation. Similarly, DGF was totally abolished only by ingestion of glucose or pelleted food and was unaffected by non-nutritive substances. However, fructose and lard significantly attenuated the feeding response. Thus, the activity of NE neurons may be controlled by substrate availability to the brain, whereas the termination of glucoprivic feeding may require the cooperative action of both central and peripheral signals.