Figure 8.

Leptin augments the inhibitory action of CCK on food intake. Cumulative food intake (in grams) is shown. A and B, Rats fasted for 13 h received a priming dose of leptin (80 μg/kg, ip), or saline, followed 2 h later by CCK8s (10 nmol, ip) or saline and refeeding; food intake was then recorded for 80 min. A, CCK8s alone inhibited food intake compared with saline over 0–40 min, and previous administration of leptin had no effect on this. B, There was increased food intake compared with control over 40–80 min after CCK8s (which is a compensatory response for inhibition over 0–40 min); leptin alone had no effect but significantly enhanced inhibition of food intake by CCK, thereby prolonging its satiety effects. C and D, Rats fasted for 13 h received leptin (80 μg/kg, ip) or CCK8s (10 nmol/kg) alone or in combination immediately before refeeding. Leptin alone did not significantly change food intake compared with saline. C, CCK8s inhibited food intake over 0–40 min, and leptin had no effect on this. D, Leptin alone had no effect on food intake over 40–80 min but significantly increased the effect of CCK in reducing food intake, thereby prolonging its satiety effects. E and F, Rats fasted for 13 h received leptin (80 μg/kg, ip) or lorglumide (8 mg/kg, ip) alone or in combination and were allowed to eat 3 g of food in 40 min; thereafter, ad libitum food intake was allowed and recorded. E, After 40 min, rats receiving leptin alone ate significantly less than those receiving leptin and lorglumide or saline. F, At 40–80 min, lorglumide significantly increased food intake compared with saline, leptin inhibited food intake compared with saline, and lorglumide inhibited the effect of leptin. Results are shown as means ± se (n = 6); letters denote significant differences between groups at that time point, i.e. a vs. b; c vs. a or b; ab not significantly different from a or b; *, P < 0.05; **, P < 0.01; ***, P < 0.001 (repeated ANOVA).