Low grade inflammation in juvenile obesity and type 1 diabetes associated with early signs of atherosclerosis.
BACKGROUND
Subclinical inflammation has been implicated in the initiation and/or progression of atherosclerosis. Diabetes mellitus and obesity are risk factors for atherosclerosis, and asymptomatic low grade inflammation occurs prior to overt vascular lesions in these patients. In contrast to adults, little information exists concerning low grade inflammation in young type 1 diabetes and juvenile obesity.


OBJECTIVE
To investigate low grade inflammation and immune activation in juvenile diabetes mellitus and obesity.


METHODS
hs-CRP, soluble interleukin-2 receptor (sIL-2R), C-peptide, insulin, cortisol, vitamin B12, folic acid, leptin, and homocysteine were determined in 148 patients with juvenile type 1 diabetes, 86 obese children and 142 normal weighted age-matched healthy controls. Intima-media thickness (IMT) and lumen diameter of both common carotid arteries (CCA) was measured by ultrasonography in 52 healthy pediatric controls, 10 diabetics, and 34 obese juveniles.


RESULTS
Serum hs-CRP was significantly elevated in patients with type 1 diabetes (p < 0.0001), and obese children (p < 0.0001) as compared to the control group. The obese juveniles (p < 0.0001) and the diabetics (p < 0.0001) showed significantly increased values for IMT of CAAs. Levels of homocysteine, sIL-2R, insulin, cortisol, vitamin B12, and folic acid did not differ from the controls. The elevation of hs-CRP was more pronounced in obesity as compared to type 1 diabetes (p < 0.0001), and the hs-CRP values correlated significantly with body mass index standard deviation score (BMI-SDS) values. Furthermore, the IMT and the luminal diameter of CCAs showed significant correlations with BMI-SDS values.


CONCLUSIONS
A low grade inflammation as determined by serum hs-CRP is significantly increased in children with type 1 diabetes, and even more pronounced in apparently healthy juveniles with obesity. The increased IMT of CCAs strongly argues for an association between this low grade inflammation and early atherosclerotic vessel injury.
Mangge
H
H
Clinical Institute of Medical and Chemical Laboratory Diagnosis, Medical University of Graz, Austria. harald.mangge@uni-graz.at
Schauenstein
K
K
Stroedter
L
L
Griesl
A
A
Maerz
W
W
Borkenstein
M
M
D000293:Adolescent; D001161:Arteriosclerosis / Q000209:etiology*; D015992:Body Mass Index; D002096:C-Peptide / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D017536:Carotid Artery, Common / Q000473:pathology; D002648:Child; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000150:complications* / Q000473:pathology; D005260:Female; D005492:Folic Acid / Q000097:blood; D006710:Homocysteine / Q000097:blood; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000150:complications* / Q000473:pathology; D020738:Leptin / Q000097:blood; D008297:Male; D009765:Obesity / Q000097:blood / Q000150:complications* / Q000473:pathology; D015375:Receptors, Interleukin-2 / Q000097:blood; D017539:Tunica Intima / Q000473:pathology; D014805:Vitamin B 12 / Q000097:blood
D002096:C-Peptide; D020738:Leptin; D015375:Receptors, Interleukin-2; D006710:Homocysteine; D002097:C-Reactive Protein; D005492:Folic Acid; D014805:Vitamin B 12