Overweight Latino children and adolescents have marked endothelial dysfunction and subclinical vascular inflammation in association with excess body fat and insulin resistance.
OBJECTIVE
We measured plasma markers of endothelial dysfunction, vascular inflammation, and pro-coagulation in obese Hispanic/Latino children and adolescents with normal glucose tolerance and determined their relationship to body composition and indexes of glucose and lipid metabolism.


METHODS
A total of 38 lean or obese Hispanic children and adolescents (10-18 years of age) were selected. The overweight group (n = 21) had a BMI >85th percentile for their age and sex, and the lean group (n = 17) had a BMI between the 25th and 50th percentiles. Studies included an oral glucose tolerance test, measurements of plasma glucose and lipids, several markers of endothelial function and inflammation, and determination of body composition by dual X-ray absorptiometry.


RESULTS
The obese group had higher systolic blood pressure and plasma triglycerides and was more insulin resistant than the lean group. The obese group also had higher plasma soluble intercellular adhesion molecule (259.5 +/- 60.0 vs. 223.2 +/- 47.5 ng/ml, P = 0.047), tumor necrosis factor-alpha (2.57 +/- 1.1 vs. 1.74 +/- 0.6 pg/ml, P = 0.008), high-sensitivity C-reactive protein (2.0 vs. 0.13 mg/l, P < 0.0001), plasminogen-activated inhibitor-1 (47.0 +/- 35.7 vs. 12.0 +/- 5.2 ng/ml, P < 0.0001), tissue plasminogen activator (6.1 +/- 1.9 vs. 4.1 +/- 0.8 ng/ml, P = 0.001), and white blood cell count (6.9 vs. 5.3 x 10(3), P = 0.031) and lower levels of adiponectin (8.7 +/- 3.3 vs. 12.6 +/- 5.2 microg/ml, P = 0.022). No significant differences were observed for soluble vascular cell adhesion molecule or interleukin-6.


CONCLUSIONS
Overweight Hispanic children and adolescents with normal glucose tolerance exhibit increased plasma markers of endothelial dysfunction and subclinical inflammation in association with obesity and insulin resistance. These abnormalities may predispose them to the development of type 2 diabetes and cardiovascular disease.
Caballero
A Enrique
AE
Joslin Diabetes Center, Clinical Research Center, Harvard Medical School, Boston, Massachusetts 02215, USA. enrique.caballero@joslin.harvard.edu
Bousquet-Santos
Kelb
K
Robles-Osorio
Ludivina
L
Montagnani
Valeria
V
Soodini
Geetha
G
Porramatikul
Sriurai
S
Hamdy
Osama
O
Nobrega
Antonio C L
AC
Horton
Edward S
ES
D015502:Absorptiometry, Photon; D052242:Adiponectin / Q000097:blood; D000273:Adipose Tissue / Q000503:physiopathology*; D000293:Adolescent; D001794:Blood Pressure; D002097:C-Reactive Protein / Q000378:metabolism; D002648:Child; D004730:Endothelium, Vascular / Q000473:pathology / Q000503:physiopathology*; D005260:Female; D005951:Glucose Tolerance Test; D006630:Hispanic or Latino / Q000706:statistics & numerical data*; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D007958:Leukocyte Count; D008297:Male; D009765:Obesity / Q000097:blood / Q000208:ethnology / Q000503:physiopathology; D050177:Overweight / Q000097:blood / Q000208:ethnology / Q000503:physiopathology*; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D010959:Tissue Plasminogen Activator / Q000097:blood; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D014657:Vasculitis / Q000097:blood / Q000503:physiopathology
D052242:Adiponectin; D017395:Plasminogen Activator Inhibitor 1; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D002097:C-Reactive Protein; D010959:Tissue Plasminogen Activator