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Indian Pediatr 2011;48:
815-816 |
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Adiponectin and Pro-inflammatory Cytokines in
Obese Diabetic Boys |
Hala O El-Mesallamy, Nadia M Hamdy,
and *Sherine M Ibrahim
Biochemistry Department, Faculty of Pharmacy,
Ain Shams University and
*Modern Sciences and Arts University, Cairo, Egypt.
Email: nadia_ [email protected]
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Adiponectin serum levels were significantly lower in obese diabetic
than in non-obese healthy boys (P<0.001). Circulating soluble
E-selectin levels was significantly higher in obese diabetic boys than
the healthy non-obese (P<0.01). There were significant inverse
correlations between adiponectin and sE-selectin, hsCRP, IL-1 b,
and MCP-1 and positively with NOx. We conclude that sE-selectin
and MCP-1 may represent a link between obesity and related
co-morbidities in children and adults.
Key words: Adiponectin, Children, Egypt,
Inflammation, Obesity, sE-selectin, Type 2 Diabetes.
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We conducted this study to investigate circulating levels of
pro-inflammatory cytokines (hsCRP, IL-1 b,
and MCP-1) in children and the influence of obesity in early life on
adulthood as well as the correlation to markers of glucose metabolism (adiponectin)
and endothelial damage (NO and sE-selectin).
Twenty boys (age 10-13 years) were included in this
study, 10 of which were healthy non-obese controls (Group I). The other 10
were obese boys with newly diagnosed type 2 diabetes mellitus (T2DM)
(Group II) and not receiving insulin. They were compared to 20 male adults
with normal glucose metabolism with mean age 38.5 ア 3.7 years and BMI 31 ア
1.2 kg/m2. Fifty male obese
adults with impaired glucose metabolism were also recruited for comparison
(mean age 42.2 ア 2.8 years). Table I compares the recruited
boys and adults for various biochemical markers. Fasting blood sugar,
lipids, insulin, insulin resistance (IR) as HOMA-IR, HDL-C, NO x,
and adiponectin differed significantly between cases and controls, both
for the boys and adults.
TABLE I Clinical and Hemodynamic Characteristics of Subjects
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Adults |
Boys |
P value |
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Group I (n=20)
Normal glucose
metabolism |
Group II (n=50)
Impaired glucose
metabolism |
Group III (n=10)
Control |
Group IV (n=10)
Diabetic |
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Age (years) |
38.5 ア 3.7 |
42.2 ア 2.8a |
11.4 ア 1 |
11 ア 1 |
NS |
BMI (kg/m2) |
31 ア 1.2 |
32.1 ア 1.4 |
24 ア 1 |
28.5 ア 1 |
NS |
DM Duration (years) |
末 |
3.3 ア 1 |
末 |
2.7 ア 1 |
末 |
CVD (MI/-) |
末 |
25/- |
末 |
末 |
末 |
FBG (mg/dL) |
102.6 ア 3.1 |
208.2 ア 89a |
106 ア 5.1 |
256 ア 7b |
-0.05 |
HbA1c% |
4.5 ア 0.6 |
9.6 ア 4.3a |
4.2 ア 0.7 |
12.6 ア 0.7b |
0.05 |
TAG (mg/dL) |
115.7 ア 25 |
280 ア 21a |
97.4 ア 7.45 |
222 ア 10b |
0.05 |
TC (mg/dL) |
176 ア 16 |
305.4 ア 44.45a |
136.4 ア 11.2 |
250 ア 4.5b |
0.05 |
HDL-C (mg/dL) |
39 ア 1.6 |
26 ア 2.3a |
40.3 ア 1.3 |
39 ア 1.8b |
0.05 |
LDL-C (mg/dL) |
115.5 ア 20 |
266 ア 22.3a |
108 ア 14.3 |
227.2 ア 9b |
0.05 |
MDA (nmol/mL) |
2.9 ア 0.7 |
5 ア 1.8a |
2.6 ア 0.45 |
4.8 ア 0.4b |
0.05 |
hsCRP (mg/L) |
1.7 ア 0.4 |
34.8 ア 12.7a |
0.21 ア 0.12 |
3.8 ア 1.9b |
0.05 |
Insulin (uIU/mL) |
8 ア 1.3 |
105.2 ア 13.7a |
12 ア 1 |
58 ア 8.2b |
0.05 |
HOMA-IR |
2 ア 1.47 |
73 ア 11.6a |
3 ア 0.3 |
36.6 ア 5.6b |
0.05 |
NOx (Umol/L) |
39.9 ア 7.9 |
5.9 ア 1.3a |
37.6 ア 6.3 |
8.7 ア 1.2b |
0.05 |
IL-1β (pg/mL) |
20 ア 1.7 |
28.4 ア 2.3a |
21 ア 1.3 |
28 ア 1.4b |
NS |
sE-selectin (ng/mL) |
22.3 ア 5 |
37.8 ア 5a |
30 ア 2.5 |
31 ア 2.9 |
0.05 |
Adiponectin(pg/mL) |
732.4 ア 142.4 |
266 ア 47.2a |
597 ア 75.4 |
282.5 ア 61b |
0.05 |
MCP-1 (ng/mL) |
110.5 ア 7.4 |
137.2 ア 16a |
104.5 ア 3.6 |
218 ア 32b |
0.05 |
Data is given as mean ア S.D; BMI: body mass index; FBG: Fasting blood glucose, HbA1c %: glycated hemoglobin,
TAG: triacylglyceriol, TC: total cholesterol, HDL: high density lipoprotein, LDL: low density lipoprotein,
MDA: malondialdehyde, hsCRP: high sensitivity C-reative protein, HOMA-IR: homeostasis model of
assessment-insulin resistance, NOx: nitric oxide metabolites, NS: not significant a,b significant difference
from control adult and control boys, respectively; P values are for the comparison between the control
and the study groups at significance level ≥0.05.
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Correlation of either adiponetin or sE-selectin with
selected anthropometric, biochemical, and clinical parameters in the
studied groups was negative and positive, respectively, for boys in the
case as well as in the control groups. Negative correlation between
adiponectin and BMI demonstrated in our study, has been observed
previously [1]. Since, NO inhibits leukocyte adhesion and rolling as well
as cytokine-induced expression of MCP-1, its level correlated negatively
with hyperglycemia, dyslipidemia, and inflammation. The abundance of
MCP-1 in blood is increased in obese subjects, suggesting that MCP-1 might
be an adipokine whose expression is increased in obesity [2].
Our results demonstrated an elevated level of MCP-1 and
sE-selectin in newly diagnosed T2DM obese boys, where both are considered
as amplifiers of the inflammatory cascade, and moreover, both showed an
inverse correlation with adiponectin. Winer, et al. [3] reported
that adiponectin may function as a biomarker of the metabolic syndrome (MetS)
in childhood obesity because of its strong correlation with several
indices of IR. Similarly, Gilardini, et al. [4] reported that
hypoadiponectinemia may be associated with a high risk for the MetS.
Another explanation was provided by Rosa, et al. [5] who reported
that infiltration of inflammatory cells may represent the critical step in
adipose tissue-associated inflammation, although the initial trigger(s)
for accumulation of these cells remains elusive. The present study extends
the existing knowledge about alterations in the pro-inflammatory cytokines
family in obese adults to obese children. It also supports the widely
accepted theory that low adiponectin
levels promote the production of adhesion molecule(s)
(namely sE-selectin) in ECs [6].
References
1. Yudkin JS. Adipose tissue, insulin action and
vascular disease: inflammatory signals. Int J Obes. 2003;27:S25-S28.
2. Sartipy P, Loskutoff DJ. Monocyte chemoattractant
protein 1 in obesity and insulin resistance. Proc Natl Acad Sci USA.
2003;100:7265-70.
3. Winer JC, Zern TL, Taksali SE, Dziura J, Cali AM,
Wollschlager M, et al. Adiponectin in childhood and adolescent
obesity and its association with inflammatory markers and components of
the metabolic syndrome. J Clin Endocrinol Metab. 2006;91:4415-23.
4. Gilardini L, McTernan PG, Girola A, da Silva NF,
Alberti L, Kumar S, et al. Adiponectin is a candidate marker of
metabolic syndrome in obese children and adolescents. Atherosclerosis.
2006;189:401-7.
5. Rosa JS, Flores RL, Oliver SR, Pontello AM, Zaldivar
FP, Galassetti PR. Sustained IL-1 b,
IL-4, and IL-6 elevations following correction of hyperglycemia in
children with type 1 diabetes mellitus. Pediatric Diabetes. 2008; 9:9-16.
6. Desideri G, De Simone M, Iughetti L, Rosato T, Iezzi
ML, Marinucci MC, et al. Early activation of vascular endothelial
cells and platelets in obese children. J Clin Endocrinol Metab.
2005;90:3145-52.
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