Neuropeptide Y (NPY) is one of several neuropeptides involved in body energy homeostasis through actions within the hypothalamus. It could contribute to the development of obesity and insulin resistance when hypothalamic concentrations remain high. High hypothalamic NPY-ergic activity has been reported in rodent genetic obesity syndromes [1±4], in which the leptin or leptin receptor gene is not functional [5,6]. In these rodents, the lack of leptin-mediated inhibition of NPY expression and secretion [1] is thought to be responsible for the associated increase in brain NPY expression. Although other peptides could be involved, further evidence suggests that NPY has a causative role in the aetiology of obesity Diabetologia (2000) Abstract Aims/hypothesis. Hypothalamic neuropeptide Y is implicated in the aetiology of obesity and insulin resistance because of its hyperinsulinaemic, hyperphagic effects. We investigated the interaction of adrenal glucocorticoids and the parasympathetic nervous system in the hyperinsulinaemia caused by neuropeptide Y infusion in rats. Methods. Neuropeptide Y was intracerebroventricularly given to normal or adrenalectomised rats for 3±6 days with pair-feeding, with or without subcutaneous dexamethasone infusion. We measured basal and intravenous glucose-induced insulinaemia and the effect of prior atropine injection. Results. Neuropeptide Y increased basal plasma insulin and C-peptide concentrations (380 90 and 1000 60 pmol/l, vs 190 20 and 590 50 pmol/l in controls, p < 0.05). Neuropeptide Y also increased the plasma concentrations of these hormones as early as 60 s after glucose injection (1630 170 and 3200 170 pmol/l for insulin and C peptide, respectively, vs 1080 80 and 1860 130 pmol/l in controls, p < 0.05). Atropine reversed the effect of neuropeptide Y on basal plasma insulin and C-peptide concentrations but had no effect on post-glucose plasma concentrations. The hyperinsulinaemic effects of neuropeptide Y were prevented by adrenalectomy, but were restored by dexamethasone infusion. Dexamethasone in itself did not statistically significantly increase insulinaemia in adrenalectomised rats. As in intact rats, atropine attenuated the basal hyperinsulinaemia of adrenalectomised rats that had been infused with neuropeptide Y and dexamethasone but had no effect on post-glucose hyperinsulinaemia. Conclusion/interpretation. These data suggest firstly that neuropeptide Y infused centrally induces basal hyperinsulinaemia in rats through glucocorticoid-dependant parasympathetic activation to the pancreas. Secondly, neuropeptide Y potentiates glucose-induced insulinaemia through a pathway dependant on adrenal glucocorticoids that cannot be reversed by short-term blockade of the increased parasympathetic tonus. [Diabetologia (2000) 43: 859±865]
Purpose: Many epidemiological studies have reported that sleep problems are frequent in children. A common sleep disturbance, sleep disordered breathing, is also known to vary by ethnicity, but little is known about other sleep problems that may be affected by racial background. The objective of this study was to assess the prevalence of sleep disturbances in community children and determine if racial differences exist. Methods: A detailed questionnaire related to sleep habits and sleep quality was mailed to parents of children enrolled in the community public school system. Children, aged 5 to 6 years of age, and who self-identified as Caucasian (C) or African American (AA) were eligible to participate. Results: 2000 questionnaires were eligible for analysis. Demographic data were as follows: 6 year olds, 1119 (56%); males, 1059 (53%); C, 1582 (79%). The average hours of nighttime sleep was 9.2 Ϯ 1.4 hours. The parents of C children reported more sleep hours than their AA counterparts (C, 9.4 Ϯ 1.3 hours vs. AA, 8.5 Ϯ 1.6 hours). Only 180 (9%) of parents reported no concerns with sleep issues, but of the remaining parents, racial differences did exist. More C parents reported that their children willingly went to bed (C, 60% vs. AA, 48%, p < .001) and were easy to arouse in the morning (C, 59% vs. AA, 52%, p = .007) than parents of AA children. Parents of AA children felt their children talked more during sleep (C, 12% vs. AA 29%, p < .001), had a higher frequency of sleepwalking (C, 1.9% vs. AA, 3.8%, p = .03), more nightmares (C, 1.9% vs. AA, 7.0%, p < .001), snored more frequently (C, 25% vs. AA, 45%, p < .001), and exhibited daytime somnolence more often (C, 8.9% vs. AA 13.2%, p < .001). Conclusion: Racial differences do exist in sleep habits and sleep quality. This study suggests AA children are more at risk for sleep disturbances than their C counterparts.
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