RESUMO
Objective: The objective of this study was to determine whether there is an association between under-reporting of body weight and social desirability as is found with self-reports of energy intake. Methods: Twenty-seven lean individuals (mean body mass index ± standard deviation = 21.6 ± 2.0 kg m-2) and 26 individuals with obesity (mean body mass index = 35.4 ± 4.8 kg m-2) were e-mailed a questionnaire on which they had to state their body weight and conduct a home food inventory. The next day, research team members went to their homes to weigh the participants, conduct their own food inventory and administer the Marlowe-Crowne scale for social desirability. Results: Among individuals with obesity, lower social desirability scores were associated with a greater degree of under-reporting body weight (r = +0.48, p < 0.02). Among lean individuals, the correlation was negative but statistically non-significant (p = -0.22, p > 0.10). Nine individuals with obesity were extreme under-reporters (2.27 kg or more), and eight of these had social desirability scores in the bottom half of the Marlowe-Crowne scale (p < 0.01). Six under-reported on the home food inventory by three or more items. Conclusions: Individuals with obesity and low social desirability scores are more likely than others to be extreme under-reporters of body weight, possibly due to a lack of awareness of their own weight.
RESUMO
Activation of group I metabotropic glutamate receptors (mGlu1 or -5 receptors) is known to either enhance or attenuate excitotoxic neuronal death depending on the experimental conditions. We have examined the possibility that these receptors may switch between two different functional modes in regulating excitotoxicity. In mixed cultures of cortical cells, the selective mGlu1/5 agonist, 3,5-dihydroxyphenylglycine (DHPG), amplified neurodegeneration induced by a toxic pulse of NMDA. This effect was observed when DHPG was either combined with NMDA or transiently applied to the cultures prior to the NMDA pulse. However, two consecutive applications of DHPG consistently produced neuroprotection. Similar effects were observed with DHPG or quisqualate (a potent agonist of mGlu1/5 receptors) in pure cultures of cortical neurons virtually devoid of astrocytes. In cultures of hippocampal pyramidal neurons, however, only protective effects of DHPG were seen suggesting that, in these particular cultures, group I mGlu receptors were endogenously switched into a "neuroprotective mode". The characteristics of the activity-dependent switch from facilitation to inhibition were examined in mixed cultures of cortical cells. The switch in the response to DHPG was observed when the two applications of the drug were separated by an interval ranging from 1-45 min, but was lost when the interval was extended to 90 min. In addition, this phenomenon required the initial activation of mGlu5 receptors (as indicated by the use of subtype-selective antagonists) and was mediated by the activation of protein kinase C. We conclude that group I mGlu receptors are subjected to an activity-dependent switch in regulating excitotoxic neuronal death and, therefore, the recent "history" of these receptors is critical for the response to agonists or antagonists.
