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1.
J Clin Psychiatry ; 71(7): 949-54, 2010 Jul.
Article in English | MEDLINE | ID: mdl-20492839

ABSTRACT

OBJECTIVE: Pediatric obesity (body mass index [BMI] > or = 95th percentile for sex and age) and overweight (BMI > or = 85th percentile < 95% percentile) are priority public health targets for the prevention of diabetes and cardiovascular disease. We examined the prevalence and risk of overweight and obesity in adolescents with serious mental disorders. METHOD: Height, weight, demographic, diagnostic, and treatment data were reviewed for 114 adolescents attending a partial hospitalization program over 18 consecutive months between January 2003 and July 2004. Sample data were compared to normative National Health and Nutrition Examination Survey data and regional county data for BMI. Unadjusted odds ratios and their 95% CIs were calculated for each categorical risk factor using the chi-squared test. A logistic regression model was conducted to detect the effects of these risk factors on the occurrence of overweight and obesity. RESULTS: The combined prevalence of overweight and obesity was 55.4% (n = 63); the prevalence for obesity alone was 30% (n = 34), approximately double the rate in national and county norms. Lack of private insurance, smoking, and antidepressant and antipsychotic treatment were associated with overweight and obese status. CONCLUSIONS: Adolescents with severe mental illness are at increased risk for overweight and obesity. Identification of elevated BMI, associated risk factors, and efforts to prevent weight gain should begin at initiation of mental health treatment.


Subject(s)
Mental Disorders/drug therapy , Mental Disorders/epidemiology , Obesity/chemically induced , Obesity/epidemiology , Overweight/chemically induced , Overweight/epidemiology , Psychotropic Drugs/adverse effects , Adolescent , Anticonvulsants/adverse effects , Anticonvulsants/therapeutic use , Antidepressive Agents/adverse effects , Antidepressive Agents/therapeutic use , Antipsychotic Agents/adverse effects , Antipsychotic Agents/therapeutic use , Body Mass Index , Cross-Sectional Studies , Day Care, Medical/statistics & numerical data , Female , Humans , Insurance Coverage/statistics & numerical data , Male , Netherlands , Psychotropic Drugs/therapeutic use , Risk Factors , Smoking/epidemiology
2.
J Invest Dermatol ; 122(5): 1214-24, 2004 May.
Article in English | MEDLINE | ID: mdl-15140225

ABSTRACT

Prostaglandins (PG) are key mediators of diverse functions in the skin and several reports suggest that PG mediate post-inflammatory pigmentary changes through modulation of melanocyte dendricity and melanin synthesis. The proteinase-activated receptor 2 (PAR-2) is important for skin pigmentation because activation of keratinocyte PAR-2 stimulates uptake of melanosomes through phagocytosis in a Rho-dependent manner. In this report, we show that activation of keratinocyte PAR-2 stimulates release of PGE(2) and PGF(2alpha) and that PGE(2) and PGF(2alpha) act as paracrine factors that stimulate melanocyte dendricity. We characterized the expression of the EP and FP receptors in human melanocytes and show that human melanocytes express EP1 and EP3, and the FP receptor, but not EP2 and EP4. Treatment of melanocytes with EP1 and EP3 receptor agonists resulted in increased melanocyte dendricity, indicating that both EP1 and EP3 receptor signaling contribute to PGE(2)-mediated melanocyte dendricity. Certain EP3 receptor subtypes have been shown to increase adenosine 3',5'-cyclic monophosphate (cAMP) through coupling to Gs, whereas EP1 is known to couple to Gq to activate phospholipase C with elevation in Ca(2+). The cAMP/protein kinase A system is known to modulate melanocyte dendrite formation through modulation of Rac and Rho activity. Neither PGF(2alpha) or PGE(2) elevated cAMP in human melanocytes showing that dendricity observed in response to PGE(2) and PGF(2alpha) is cAMP-independent. Our data suggest that PAR-2 mediates cutaneous pigmentation both through increased uptake of melanosomes by keratinocytes, as well as by release of PGE(2) and PGF(2alpha) that stimulate melanocyte dendricity through EP1, EP3, and FP receptors.


Subject(s)
Dinoprost/metabolism , Dinoprostone/analogs & derivatives , Dinoprostone/metabolism , Keratinocytes/metabolism , Melanocytes/metabolism , Receptor, PAR-2/metabolism , Receptors, Prostaglandin E/metabolism , Cell Size/drug effects , Cell Size/physiology , Cells, Cultured , Cyclic AMP/metabolism , Dinoprost/pharmacology , Dinoprostone/pharmacology , Gene Expression , Humans , Keratinocytes/cytology , Keratinocytes/drug effects , Melanocytes/cytology , Melanocytes/drug effects , Misoprostol/pharmacology , Oxytocics/pharmacology , Paracrine Communication/physiology , Receptors, Prostaglandin/genetics , Receptors, Prostaglandin/metabolism , Receptors, Prostaglandin E/agonists , Receptors, Prostaglandin E/genetics , Receptors, Prostaglandin E, EP1 Subtype , Receptors, Prostaglandin E, EP2 Subtype , Receptors, Prostaglandin E, EP3 Subtype , Receptors, Prostaglandin E, EP4 Subtype
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