Early atherogenesis and visceral fat in obese adolescents.
OBJECTIVE
Little information is available as to the cause of increased thickening of the intima-media of the carotid artery (cIMT) in the pediatric population. Therefore, cIMT was compared in obese adolescents and normal-weight controls, and associations between cIMT and lipid and non-lipid cardiovascular risk factors were assessed.


METHODS
Subjects included 61 obese non-diabetic male and female volunteers aged 12-18 years inclusive with a body mass index (BMI) >95th percentile for age and 2-h blood glucose <200 mg dl(-1) matched to 25 normal-weight control volunteers with normal glucose levels. Each subject underwent a 2-h glucose tolerance test and measurement of hemoglobin A1c, ultrasensitive C-reactive protein, fasting insulin, blood lipids, visceral, subcutaneous abdominal and hepatic fat, and cIMT.


RESULTS
Maximum cIMT was 0.647±0.075 mm in the obese subjects versus 0.579±0.027 mm in normal-weight controls (P<0.001). There was no difference in maximum cIMT between male and female subjects. There were significant correlations between maximum cIMT and BMI z-score, 2-h glucose, fasting insulin, homeostasis model assessment (HOMA), total low-density lipoprotein (LDL) cholesterol, very LDL cholesterol, high-density lipoprotein (HDL) cholesterol, HDL2 cholesterol, HDL3 cholesterol, triglycerides, remnant lipoprotein cholesterol, intermediate-density lipoprotein cholesterol, lipoprotein(a), apoprotein B100, abdominal subcutaneous fat volume, visceral fat volume and hepatic phase difference. On multiple regression analysis, visceral fat was the most significant predictor of maximum cIMT. Two-hour blood glucose, HOMA and systolic blood pressure were also significant predictors of maximum cIMT.


CONCLUSIONS
cIMT was increased in the obese adolescents compared with the normal-weight-matched controls. Visceral fat was a key predictor of arterial wall thickening in these subjects. The results suggest that the focus of cardiovascular disease prevention in the adolescent obese should be visceral obesity, and not blood lipids or lipid subclasses.
Department of Pediatrics, Lehigh Valley Health Network, Allentown, PA, USA.
A H
AH
Slyper
Department of Radiology, Lehigh Valley Health Network, Allentown, PA, USA.
H
H
Rosenberg
Scripps Clinic, Division of Cardiovascular Medicine, La Jolla, CA, USA.
A
A
Kabra
Network Office of Research and Innovation, Lehigh Valley Health Network, Allentown, PA, USA.
M J
MJ
Weiss
B
B
Blech
S
S
Gensler
Cardiovascular Research Institute, Lehigh Valley Health Network, Allentown, PA, USA.
M
M
Matsumura
D000293:Adolescent; D050197:Atherosclerosis / Q000209:etiology* / Q000473:pathology / Q000517:prevention & control; D001786:Blood Glucose / Q000378:metabolism; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000378:metabolism; D059168:Carotid Intima-Media Thickness / Q000009:adverse effects*; D002648:Child; D005260:Female; D005951:Glucose Tolerance Test; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D050152:Intra-Abdominal Fat / Q000473:pathology*; D008055:Lipids / Q000097:blood; D008297:Male; D063766:Pediatric Obesity / Q000150:complications* / Q000473:pathology / Q000517:prevention & control; D012307:Risk Factors
D001786:Blood Glucose; D002097:C-Reactive Protein; D006442:Glycated Hemoglobin; D007328:Insulin; D008055:Lipids; C517652:hemoglobin A1c protein, human