S. Amaro

Kalèdo, a new educational board-game, gives nutritional rudiments and encourages healthy eating in children: a pilot cluster randomized trial

IntroductionPrevention of obesity and overweight is an important target for health promotion. Early prevention requires an intervention during childhood and adolescence. At these stages, the game could be an appropriate means to teach nutrition knowledge and to influence dietary behaviour. To this end, the authors developed Kalèdo, a new board-game.ObjectiveThe aim of the present study was to test the efficacy of Kalèdo on changes in nutrition knowledge and dietary behaviour in a pilot study conducted in three middle schools in Naples, Italy.Materials and MethodsA simple two-group design (treatment and control) with pre- and post-assessment was employed. The classroom was the unit of recruitment and random assignment to groups. All students (307) in the participating schools were invited to participate. Data analysis was performed on 241 subjects. During 24 weeks, a group of 153 children from 8 classrooms (11–14 year old Caucasian subjects; 78 male, 75 female) was involved in 15–30 minute-long play sessions once a week. A questionnaire was given to the participants at the beginning and at the end of the study to evaluate nutrition knowledge (31 questions), physical activity (8 questions) and food intake (34 questions). Anthropometric measurements were also carried out. A second group of 88 children from 5 classrooms (same age and ethnicity; 55 male, 33 female) was investigated at the same times with the same questionnaire and anthropometric measures but they did not receive any play sessions with Kalèdo.ObservationChildren playing Kalèdo showed a significant increase in nutrition knowledge (p<0.05) and in weekly vegetable intake (p<0.01) with respect to the control.ConclusionThe results suggest that Kalèdo could be an effective instrument to teach children about healthy diet. More research is needed to study the long term effect of this intervention.

Posterior hypothalamic activity and cortical control during the PGE1 hyperthermia.

THE firing rate of the posterior hypothalamic neurones, and interscapular brown adipose tissue, and colonic temperatures (TIBAT, and TC) were monitored in 36 urethane-anaesthetized male Sprague-Dawley rats before, and after an intracerebroventricular (i.c.v.) injection of 400 ng prostaglandin E1 (PGE1) or saline. The i.c.v. injection was preceded by functional decortication in half of each group. The results show an increase of firing rate, TIBAT, and TC after PGE, injection in the rats without decortication. Functional decortication significantly reduced these enhancements. These findings demonstrate that the posterior hypothalamus plays a significant role in the hyperthermia induced by PGE, and that the cerebral cortex is involved in the control of posterior hypothalamic activity.

Injection of muscimol in the posterior hypothalamus reduces the PGE1-hyperthermia in the rat.

The firing rate of the nerves innervating interscapular brown adipose tissue (IBAT), IBAT and colonic temperatures (TIBAT and Tc), heart rate, and oxygen (O2) consumption were monitored in urethane-anesthetized male Sprague-Dawley rats. These variables were measured for 40 min before (baseline values) and 40 min after a 56 ng muscimol injection in the posterior hypothalamus and an intracerebroventricular administration of 500 ng prostaglandin E1 (PGE1). The same variables were monitored in other rats with muscimol injection or PGE1 administration alone. No drug was injected in control rats. The results show that muscimol injection reduces the increases in firing rate, TIBAT, Tc, heart rate, O2 consumption induced by PGE1. These findings suggest that GABAergic tone in the posterior hypothalamus is important in the control of thermogenic changes induced by PGE1.

Nitric oxide reduces body temperature and sympathetic input to brown adipose tissue during PGE1-hyperthermia

The firing rate of the nerves innervating interscapular brown adipose tissue (IBAT) and IBAT and colonic temperatures (TIBAT and TC were monitored in urethane-anaesthetized male Sprague-Dawley rats. These variables were measured for 40 min before (baseline values) and 40 min after a 4 micromoles L-arginine (L-arg) or 400 nmoles nitroprusside (NP) injection in a lateral cerebral ventricle and an intracerebroventricular administration of 500 ng prostaglandin E1 (PGE1). The same variables were monitored in other rats with L-arg or NP or PGE1 administration alone. No drug was injected in control rats. The results show that L-arg or NP injection reduces the increases in firing rate, TIBAT, Tc induced by PGE1. These findings suggest that nitric oxide is important in the control of thermogenic changes during the PGE1 hyperthermia.

Non-shivering thermogenesis during prostaglandin E1 fever in rats: role of the cerebral cortex

We have tested the hypothesis that there is a role for the cerebral cortex in the control of non-shivering thermogenesis during fever induced by prostaglandin E1 (PGE1). While under urethan anesthesia, the firing rate of nerves innervating interscapular brown adipose tissue (IBAT), IBAT and colonic temperatures (TIBAT and Tc) and oxygen (O2) consumption were monitored during the fever from PGE1 injection (400 and 800 ng) in a lateral cerebral ventricle in controls and in functionally decorticated Sprague-Dawley rats. Rats were functionally decorticated by applying 3.3 M KCl solution on the frontal cortex which causes cortical spreading depression (CSD). Pyrogen injections caused dose-related increases in firing rate, TIBAT, Tc and O2 consumption and CSD reduced these enhancements. Our findings indicate that the cerebral cortex could be involved in the control of non-shivering thermogenesis during PGE1-induced febrile response.

LATERAL HYPOTHALAMIC LESION INDUCES SYMPATHETIC STIMULATION AND HYPERTHERMIA BY ACTIVATING SYNTHESIS OF CEREBRAL PROSTAGLANDINS

This experiment tests the effect of intracerebroventricular (icv) injection of lysine acetylsalicylate on the sympathetic and thermogenic changes induced by lesion of the lateral hypothalamus (LH). The firing rate of the nerves innervating interscapular brown adipose tissue (IBAT), along with IBAT and colonic temperatures (TIBAT and Tc) were monitored in urethane-anaesthetized male Sprague-Dawley rats lesioned in the LH. These variables were measured before and after an icv injection of 1mg lysine acetylsalicylate. The same variables were also monitored in: a) lesioned rats with icv administration of saline; b) sham-lesioned animals with icv injection of lysine acetylsalicylate; c) sham-lesioned rats with icv injection of saline. In an additional experiment, the same variables were monitored after an icv injection of lysine acetylsalicylate or saline in rats with LH lesion performed 48 h before the icv injection. The results show that lysine acetylsalicylate injection reduces the increases in firing rate, TIBAT and Tc induced by LH lesion. These findings suggest that cerebral prostaglandin synthesis plays a key role in the sympathetic and thermogenic changes following LH lesion.

Nitric oxide reduces the thermogenic changes induced by lateral hypothalamic lesion

The experiment described here tests the effect of intracerebroventricular (icv) injection of nitric oxide (NO) precursors, such as L-arginine (L-arg) and nitroprusside (NP), on the thermogenic changes induced by lesion of the lateral hypothalamus (LH). The firing rate of the nerves innervating interscapular brown adipose tissue (IBAT), along with IBAT and colonic temperatures (TIBAT and TC) were monitored in urethane-anaesthetized male Sprague-Dawley rats lesioned in the LH. These variables were measured before and after an icv injection of 4 mumol L-arg or 400 nmol NP. The same variables were also monitored in: a) lesioned rats with icv administration of saline; b) sham-lesioned animals with icv injection of L-arg or NP; c) sham-lesioned rats with icv injection of saline. The results show that L-arg or NP injection reduces the increases in firing rate. TIBAT and TC induced by LH lesion. These findings suggest that NO plays a key role in the thermogenic changes following LH lesion.

Postprandial thermogenesis and conditioned taste aversion or preference

Postprandial thermogenesis is under the control of the autonomic nervous system and alimentary conditioned stimuli change sympathetic and parasympathetic activity. Here we studied the effect of conditioned taste aversion on postprandial thermogenesis in rats. Two groups of animals were used, rats of the first group were controls, these were placed on a standard diet and, for some days, on two other different diets: one thiamine-free and the other thiamine-rich. Each diet had a different taste. The treated animals belonged to the second group, these were fed with the same three diets but for different lengths of times: thiamine-free diet for the first 5 wk afterwards, with thiamine-rich diet for 3 wk, and finally with laboratory standard diet for a few days. After a preference test with the three familiar diets, oxygen consumption rate and brown adipose tissue temperature were evaluated three times in both groups after ingestion of a test meal, each time with one of the three different diets. The preference test was unvaried for the three different familiar foods in controls, while the treated animals showed a lower preference for thiamine-free food than for the other two. Treated rats had a significantly higher increase in O2 consumption rate than controls. In this group intake of thiamine-free food induced a significantly lower increase in O2 consumption than the other two. The increase in brown adipose tissue temperature was also higher in treated than in control animals but in treated rats this was lower after intake of thiamine-free food than after the intake of the other two.(ABSTRACT TRUNCATED AT 250 WORDS)

EEG Arousal, Sympathetic Activity, and Brown Adipose Tissue Thermogenesis after Conditioned Taste Aversion

Conditioned taste aversion was induced in rats by pairing saccharin with intraperitoneal LiCl injection. Animals injected with NaCl served as controls. After evaluating the preference levels for saccharin in rats of both groups, the animals were anesthetized with urethane and the duration of EEG desynchronization, firing rate of sympathetic nerves innervating interscapular brown adipose tissue (BAT), and temperature of the same tissues were recorded, before and after oral stimulation with saccharin or water. The EEG desynchronization was longer in conditioned rats after stimulation with saccharin. Firing rate of sympathetic nerves was higher in conditioned rats after presentation of saccharin. BAT temperature, decreased in conditioned rats after saccharin stimulus, was unchanged in the three other conditions. In a second experiment temperature and firing rate of sympathetic nerves of BAT were recorded after oral presentation of water or saccharin in rats treated as in the first experiment and injected with the alpha 1-adrenergic blocker prazosin. As in the first experiment, saccharin presentation in conditioned animals enhanced the neural sympathetic activity, whereas differently from the first experiment it increased BAT temperature. No changes were found in the same measurements in the three other conditions. The drop in interscapular BAT temperature found in the first experiment, an unexpected finding, probably depends on the use of lithium as unconditioned stimulus, because LiCl interacting with adrenergic receptors changes the two-phase response, normally seen in interscapular BAT after increased sympathetic activity, in a single-phase response.

Role of seizure activity in the decreased pineal response to isoproterenol in rats chronically treated with electroconvulsive shock

Chronic electroconvulsive shock (ECS) has been previously reported to blunt the melatonin response to acute isoproterenol administration in rats. To assess whether electrically induced seizures are indeed required for the appearance of the blunted pineal response to isoproterenol, pineal and serum melatonin levels were measured after isoproterenol stimulation in rats treated with ECS (80 mA, 0.5 sec), subconvulsive shock (15 mA, 0.5 sec), or sham-ECS once per day at 11:30-12:00 h for 8 days. In ECS-treated rats, both pineal and serum melatonin levels after isoproterenol administration were significantly lower than those in sham-treated animals and in rats receiving subconvulsive shock. Moreover, as compared with sham treatment, chronic subconvulsive shock did not affect the melatonin response to isoproterenol. These data show that seizure activity is indeed required for the ECS-induced decrease in the pineal response to acute beta-adrenergic stimulation.