The effect of weight loss magnitude on pro-/anti-inflammatory adipokines and carotid intima-media thickness in obese adolescents engaged in interdisciplinary weight loss therapy.
BACKGROUND
Obesity is a chronic disease defined by an excess amount of adipose tissue and presents a low-grade inflammatory state, increasing cardiovascular risk.


OBJECTIVE
To assess the effect of weight loss magnitude on the inflammatory profile and carotid intima-media thickness (cIMT) in obese adolescents engaged in interdisciplinary therapy.


METHODS
Seventy-seven postpubertal obese adolescents with a BMI greater than the 95th percentile (37·18 ± 5·14), of both genders and between the ages of 14 and 19 years (16·74 ± 1·59) were subjected to a 1-year period of interdisciplinary intervention (nutrition, psychology, physical exercise and clinical support).


METHODS
Blood samples were collected to analyse glucose, lipid and adipokine concentrations. Body composition, anthropometric profiles and cIMT were measured. The results are presented according to quartiles of weight loss: 1st (≤5·80 kg) = low; 2nd (5·80-10·90 kg) = low to moderate; 3rd (10·90-15·90 kg) = moderate; and 4th (>15·90 kg) = massive.


RESULTS
Leptin, the leptin/adiponectin ratio and plasminogen activator inhibitor 1 (PAI-1) were decreased significantly in the low-to-moderate weight loss. The cIMT was reduced in the moderate weight loss. Moreover, adiponectin was increased only in the massive weight loss. Additionally, weight loss was an independent predictor of changes in leptin level, the adiponectin/leptin ratio (A/L ratio) and PAI-1 when the data were adjusted for age and gender. BMI changes were predictors of changes in leptin and PAI-1 levels. A/L ratio was associated with lean body mass (%), independent of gender and age. In addition, changes in A/L ratio were independent predictors of cIMT alterations.


CONCLUSIONS
Interdisciplinary therapy may reduce cardiovascular risk factors among adolescents depending on their degree of weight loss (moderate to massive) and when correlated with their inflammatory profile, metabolic state and cIMT.
Post-Graduate Program of Nutrition, Universidade Federal de São Paulo, SP, Brazil. deborahmasquio@yahoo.com.br
Deborah C L
DC
Masquio
Aline
A
de Piano
Priscila L
PL
Sanches
Flávia C
FC
Corgosinho
Raquel M S
RM
Campos
June
J
Carnier
Patrícia L
PL
da Silva
Danielle A
DA
Caranti
Lian
L
Tock
Lila M
LM
Oyama
Claudia M
CM
Oller do Nascimento
Marco T
MT
de Mello
Sergio
S
Tufik
Ana R
AR
Dâmaso
D054392:Adipokines / Q000097:blood*; D052242:Adiponectin / Q000097:blood; D000273:Adipose Tissue / Q000378:metabolism; D000293:Adolescent; D001786:Blood Glucose / Q000378:metabolism; D001823:Body Composition / Q000502:physiology; D002318:Cardiovascular Diseases / Q000097:blood / Q000503:physiopathology / Q000517:prevention & control; D059168:Carotid Intima-Media Thickness; D015243:Cholesterol, VLDL / Q000097:blood; D015444:Exercise / Q000502:physiology; D005260:Female; D006801:Humans; D020738:Leptin / Q000097:blood; D008297:Male; D009765:Obesity / Q000097:blood / Q000503:physiopathology / Q000628:therapy*; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D012044:Regression Analysis; D012307:Risk Factors; D013997:Time Factors; D016896:Treatment Outcome; D014280:Triglycerides / Q000097:blood; D015431:Weight Loss / Q000502:physiology*
D054392:Adipokines; D052242:Adiponectin; D001786:Blood Glucose; D015243:Cholesterol, VLDL; D020738:Leptin; D017395:Plasminogen Activator Inhibitor 1; D014280:Triglycerides