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Postprandial plasma adiponectin response is reduced in prepubertal premature pubarche girls

Elvira Larquéa, Mercedes Gil-Camposb, Isabel Villadac, MCarmen Ramírez-Tortosac, Ramón Cañeteb, Ángel GilcCorresponding Author Informationemail address

Received 17 June 2009; accepted 10 December 2009. published online 22 January 2010.
Corrected Proof

Abstract 

The association between premature pubarche (PP) and metabolic syndrome is controversial and not supported by some authors. The aim of this study was to determine insulin resistance syndrome, plasma adiponectin, and fatty acid profile in PP girls to discern potential confounder variables and markers of metabolic disturbances. We studied 22 prepubertal girls with a diagnosis of PP and 20 healthy controls who differed in body mass index (BMI) (19.33 ± 0.71 vs 17.30 ± 0.60). We evaluated insulin resistance syndrome components and postprandial response of adiponectin, nonesterified fatty acids, and fatty acid profile after consumption of a standardized breakfast. No lipid disturbances were detected in the PP group. High-density lipoprotein to low-density lipoprotein cholesterol ratio tended to be lower in PP girls (P = .052), but this effect disappeared when data were adjusted for both BMI and age (P = .480). Insulin levels tended to be higher at 2 hours in PP girls, who showed significantly higher C-peptide area under the curve. In contrast, adiponectin at 3 hours after the meal and postprandial adiponectin area under the curve were significantly lower. The PP girls showed significantly higher percentages of eicosapentaenoic acid in total plasma and plasma phospholipids. No differences were found in the postprandial fatty acid clearance rate. In conclusion, PP girls and controls differed in postprandial plasma adiponectin response and in postprandial plasma C-peptide response after both BMI and age adjustment. Cholesterol plasma disturbances were mainly attributable to their higher BMI, although n-3 polyunsaturated fatty acids were higher because of the PP.

a Department of Physiology, Faculty of Biology, University of Murcia, Murcia 30100, Spain

b Unit of Pediatric Endocrinology, Reina Sofia University Hospital, Córdoba 14004, Spain

c Institute of Nutrition and Food Technology, Department of Biochemistry and Molecular Biology, University of Granada, Granada 18071, Spain

Corresponding Author InformationCorresponding author. Department of Biochemistry and Molecular Biology, Faculty of Pharmacy, University of Granada, Campus Cartuja, 18071 Granada, Spain. Tel.: +34 958 246139; fax: +34 958 248960.

PII: S0026-0495(09)00521-6

doi:10.1016/j.metabol.2009.12.009

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