Leptin and acute appetite control
Moderate physical activity and snack intake suppress the appetite of obese and lean women acutely. The associations between circulating leptin and appetite-satiety ratings suggest that there is some physiological involvement of leptin in short-term appetite regulation in response to physical activity-induced factors but only in obese women. The exercise-related factors considered in this thesis as possible mediators of leptin action were catecholamines, fatty acids, glucose and insulin. Adrenaline is unlikely to be the exercise factor responsible for the coupling between leptin and satiety since adrenaline infusion stimulated an increase in subsequent energy intake in obese women. Labetalol decreased circulating FFA and increased glucose concentrations, which confirms at least b-adrenoceptor blockade. Any conclusion with respect to the a- adrenoceptor blockade should be drawn with caution since labetalol, an a/b blocker, has greater affinity for b- than a-adrenoceptors. No differences in appetite/satiety sensations were found following exercise with adrenoceptor blockade compared to exercise alone. This indicates that the observed anorexic effect of exercise on appetite in obese women was not mediated by b-adrenoceptors. Noradrenaline is another possible exercise factor that could mediate the coupling between leptin and appetite in obese women since it is known that leptin and noradrenaline (NA) have common hypothalamic targets (e.g. NPY) and their effects are mediated by a-1 adrenoceptors. Labetalol probably was not a sufficiently strong a-adrenoceptor blocker to investigate such effects. A study of a more selective a1-adrenoceptor antagonist might be helpful in the investigation of the interaction between leptin and NA in the regulation of eating. Study 4: In endurance-trained athletes a short term detraining increases postprandial plasmin leptin, induces insulin resistance but has no effect on appetite/satiety ratings. The results of the present studies implicate leptin, insulin, insulin resistance and noradrenergic factors in the control of eating following exercise and detraining.