Advertisement
Journal Home
Search for

Volume 153, Issue 1, Pages 71-75 (July 2008)


View previous. 33 of 58 View next.

Serum Amyloid A Concentration is Increased in Obese Children and Adolescents

Javier Gómez-Ambrosi, PhDad, Cristina Azcona, MD, PhDb, Ana Patiño-García, PhDb, Gema Frühbeck, RNutr, MD, PhDacdCorresponding Author Informationemail address

Received 19 September 2007; received in revised form 26 November 2007; accepted 9 January 2008. published online 10 March 2008.

Objective

To compare the circulating concentrations of the acute-phase protein serum amyloid A (SAA) in lean, overweight, and obese children and adolescents and analyze the influence of body fat.

Study design

A total of 63 children and adolescents (65% girls) with an average age of 12.1 ± 2.7 years (range, 6 to 18 years) were included in the study. Each child was classified on the basis of age- and sex-specific body mass index (BMI) percentile as normal weight (BMI <85th percentile; n = 17), overweight (BMI ≥85th and <95th percentiles; n = 26), or obese (BMI ≥95th percentile; n = 20). Body fat was estimated by air-displacement plethysmography.

Results

Both overweight and obese children exhibited significantly increased circulating SAA concentrations (log SAA: lean, 0.66 ± 0.20; overweight, 0.83 ± 0.29; obese, 0.96 ± 0.21; P = .002) compared with the lean children. Significant correlations were found between log SAA and body fat (r = 0.48; P < .0001). In multiple linear regression analysis, log C-reactive protein (CRP) (P = .014) and body fat (P = .031) emerged as significant predictors of log SAA.

Conclusions

Plasma SAA concentrations are elevated in overweight and obese children, being strongly related to adiposity and log CRP. This finding suggests that increased body fat may contribute to the development of a low-grade chronic proinflammatory state at an early age, possibly contributing to the obesity-associated cardiovascular disease risk.

a From the Metabolic Research Laboratory, Clínica Universitaria de Navarra, University of Navarra, Pamplona, Spain

b Department of Pediatrics, Clínica Universitaria de Navarra, University of Navarra, Pamplona, Spain

c Department of Endocrinology, Clínica Universitaria de Navarra, University of Navarra, Pamplona, Spain

d CIBER (CB06/03) Fisiopatología de la Obesidad y Nutrición, Instituto de Salud Carlos III, Madrid, Spain.

Corresponding Author InformationReprint requests: Gema Frühbeck, RNutr, MD, PhD, Department of Endocrinology, Clínica Universitaria de Navarra, Avda. Pío XII 36, 31008-Pamplona, Spain.

 Supported by grants from the Instituto de Salud Carlos III, Ministerio de Sanidad y Consumo, Spain (FIS PI030381 and FIS PI061458) and the Department of Health of the Gobierno de Navarra, Spain (48/2003 and 20/2005).

 The authors have no conflicts of interest to report.

PII: S0022-3476(08)00009-7

doi:10.1016/j.jpeds.2008.01.006


View previous. 33 of 58 View next.

Advertisement