Serum leptin and loss of control eating in children and adolescents.

BACKGROUND: Both insufficiency and resistance to the actions of the adipocyte-derived hormone leptin promote hunger, increased food intake and greater body weight. Some studies suggest that adults reporting binge eating have increased serum leptin compared with those without binge eating, even after adjusting for the greater adiposity that characterizes binge eaters. Pediatric binge or loss of control (LOC) eating are prospective risk factors for excessive weight gain and may predict development of metabolic abnormalities, but whether LOC eating is associated with higher leptin among children is unknown. We therefore examined leptin and LOC eating in a pediatric cohort. METHODS: A convenience sample of 506 lean and obese youth (7-18 years) was recruited from Washington, DC and its suburbs. Serum leptin was collected after an overnight fast. Adiposity was measured by dual-energy X-ray absorptiometry or air displacement plethysmography. LOC eating was assessed by interview methodology. RESULTS: Leptin was strongly associated with fat mass (r=0.79, P<0.001). However, even after adjusting for adiposity and other relevant covariates, youth with LOC eating had higher serum leptin compared with those without LOC episodes (15.42±1.05 vs 12.36±1.04 ng ml(-1), P<0.001). Neither reported amount of food consumed during a recent LOC episode nor number of LOC episodes in the previous month accounted for differences in leptin (P>0.05). The relationship between LOC eating and leptin appeared to be significant for females only (P=0.002). CONCLUSIONS: Reports of LOC eating were associated with higher fasting leptin in youth, beyond the contributions of body weight. Prospective studies are required to elucidate whether LOC eating promotes greater leptin or whether greater leptin resistance may promote LOC eating.

Maternal hen calls modulate memory formation in the day-old chick: the role of noradrenaline.

Facilitation of memory for discriminative learning in young chicks is enhanced following exposure to a synthesized rhythmic auditory stimulus. Increased arousal, mediated by noradrenergic activation, is believed to underlie this effect. In this report we examine whether ethologically relevant rhythmic auditory stimuli produce the same noradrenaline-mediated memory enhancement in neonate chicks (Gallus gallus domesticus). Maternal hen attraction calls which contained a rhythmic pattern were found to facilitate retention. Intracerebral injection of noradrenaline or the beta(2)-adrenergic antagonist propranolol demonstrated that this enhancement is likely to be mediated by noradrenergic activation of central beta(2)-noradrenergic receptors. In contrast, a rhythmic alarm call inhibited retention. Subcutaneous injection of the alpha(1)-adrenergic antagonist prazosin revealed that this impairment may be due to higher arousal levels resulting in activation of alpha(1)-noradrenergic receptors. It is concluded that the maternal hen calls of domestic chickens can influence the memory ability of the offspring via noradrenaline release in the brain. The current data suggest that call meaning and rhythmicity interact to yield the appropriate levels of beta(2)-adrenergic activation required to facilitate retention for a discriminative task.