Serum Resistin and Inflammatory and Endothelial Activation Markers in Obese Adolescents

Article (PDF Available)inThe Journal of pediatrics 161(6) · August 2012with49 Reads
DOI: 10.1016/j.jpeds.2012.05.063 · Source: PubMed
Objectives: To assess the level of serum resistin in obese and lean children and to establish a relationship with circulating inflammatory and vascular markers. Study design: This is a cross-sectional study including 67 obese and 62 lean children (mean age 10.9 ± 2.8 years, age range 5.4-16.6 years). We assessed circulating hormones (insulin, leptin, insulin-like growth factor 1), markers of inflammation (resistin, high sensitivity C-reactive protein, interleukin-6, chemokine ligand 2), and endothelial cell activation (vascular and intercellular adhesion molecules: vascular cell adhesion molecule 1 and intercellular adhesion molecule; E-selectin; P-selectin; endothelin 1). Results: Body weight, body mass index (BMI), insulin, leptin, high-sensitivity C-reactive protein, vascular adhesion molecule 1, and E-selectin levels were significantly higher in obese than in lean subjects. Resistin was similar among the groups in the prepubertal period, but increased significantly in the obese adolescents (18.6 ± 24.9) compared with lean subjects (7.9 ± 10.7 ng/mL; P = .038). Resistin was not associated with BMI z score (P > .05). Subjects with resistin levels above 9 (ng/mL) had higher concentration of interleukin-6, chemokine ligand 2, endothelin-1, and insulin-like growth factor 1 but not of leptin, insulin, or BMI. Conclusion: Resistin was increased in obese adolescents independently of the quantity of the adipose tissue. In this population, increased resistin levels were related to inflammation and endothelial activation. We may hypothesize that interventions aiming to diminish resistin expression may slow down atherogenesis in adolescents.
Serum Resistin and Inammatory and Endothelial Activation Markers
in Obese Adolescents
Albane B. R. Maggio, MD
, Julie Wacker, MD
, Fabrizio Montecucco, MD, PhD
, Katia Galan
, Graziano Pelli
ois Mach, MD
, Maurice Beghetti, MD
, and Nathalie J. Farpour-Lambert, MD
Objectives To assess the level of serum resistin in obese and lean children and to establish a relationship with
circulating inflammatory and vascular markers.
Study design This is a cross- sectional study including 67 obese and 62 lean children (mean age 10.9 2.8 years,
age range 5.4-16.6 years). We assessed circulating hormones (insulin, lep tin, insulin-like growth factor 1), markers
of inflammation (resistin, high sensitivity C-reactive protein, interleukin-6, chem okine ligand 2), and endothelial cell
activation (vascular and intercellular adhesion molecules: vascular cell adhesion molecule 1 and intercellular adhe-
sion molecule; E-selectin; P-selectin; endothelin 1).
Results Body weight, body mass index (BMI), insulin, leptin, high-sensitivity C-reactive protein, v ascular adhesion
molecule 1, and E-selectin levels were significantly higher in obese than in lean subjects. Resistin was similar among
the groups in the prepubertal period, but increased significantly in the obese adoles cents (18.6 24.9) compared
with lean subjects (7.9 10.7 ng/mL; P = .038). Resistin was not ass ociated with BMI z score (P > .05). Subjects with
resistin levels above 9 (ng/mL) had higher concentration of interleukin-6, chemokine ligand 2, endothelin-1, and
insulin-like growth factor 1 but not of leptin, insulin, or BMI.
Conclusion Resistin was increased in obese adolescents independently of the quantity of the adipose tissue.
In this population, increased resistin levels were related to inflammation and endothelial activation. We may hy-
pothesize that interventions aiming to diminish resistin expression may slow down atherogenesis in adolescents.
(J Pediatr 2012;-:---).
ardiovascular diseases (CVDs) are increasing worldwide and are associated with premature death. The rising rate of
obesity and type 2 diabetes in the young population contributes to the development of CVD. It is well recognized
that the early signs of atherosclerosis are already present during childhood, especially in the obese population.
On one hand, in rodents, resistin is an adipocytokine selectively expressed and secreted by adipocytes.
On the other hand, in
humans, resistin is also expressed by macrophages
in response to inflammatory stimuli.
In adults, resistin has been shown to
be a potential determinant of glucose metabolism, activation of inflammatory markers,
and expression of cellular adhesion
molecules (CAMs) on endothelial cells surface.
Resistin has also been related to CVD.
Inflammation plays an important role in atherosclerotic plaque maturation until final rupture. Intraplaque macrophages
engulf lipids accumulated in the fatty streak, forming foam cells. In turn, these cells secrete proinflammatory mediators, which
upregulate the CAMs present on endothelial cells surface. The CAMs are composed of the immunoglobulin family, vascular cell
adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (IC AM-1), as well as the selectin family (P-, L-, and
E-selectin). The y promote the recruitment of T cells and macrophages, sustaining inflammation by cytokine production or
smooth muscle cell stimulation.
The elevation of cytokine levels is associated with hi gher morbidity,
and CAMs are con-
sidered as reliable biomarkers of endothelial activation and inflammation, leading to cardiovascular morbidities in different
age groups.
Obesity leads to adipocyte dysfunction and thereby is an independent contributor of the inflammation process. Indeed,
adipose tissue also secretes cytokines such as tumor necrosis factor-alpha (TNFa) and interleukin (IL)-6,
playing a direct
role in the development of CVD.
From the
Pediatric Sport Medicine and Obesity Care
Program and
Pediatric Cardiology Unit, Service of
Pediatric Specialties, Department of Child and
Adolescent, University Hospitals of Geneva and
University of Geneva, Switzerland; and
Division, Foundation for Medical Research, University
Hospitals of Geneva, Switzerland
Supported by the Swiss National Science Foundation,
the Geneva University Hospital Research and Develop-
ment Fund, and the Sir Jules Charitable Overseas Trust,
Geneva. The authors declare no conflicts of interest.
0022-3476/$ - see front matter. Copyright ª 2012 Mosby Inc.
All rights reserved.
BMI Body mass index
CAM Cellular adhesion molecule
CCL2 Chemokine ligand 2
CVD Cardiovascular disease
ET-1 Endothelin-1
ICAM-1 Intercellular adhesion molecule 1
IGF-1 Insulin-like growth factor 1
IL Interleukin
TNFa Tumor necrosis factor-alpha
VCAM-1 Vascular cell adhesion molecule 1
In the literature, studies comparing resistin levels in lean
and obese children or adolescents are scarce.
To date,
the relationship between resistin and markers of endothelial
activation and inflammation has not been studied in lean
and obese children.
Therefore, in this study, we aimed to compare serum resis-
tin concentrations between lean and obese childr en and ado-
lescents, as well as to investigate the relationships with age,
puberty, and visceral adipose tissue. The second aim of this
research was to assess associations between high resistin levels
and concentrations of inflammatory and endothelial cell
This cross-sectional study included children and adoles-
cents from 2 different studies aiming at measuring cardio-
vascular risk factors in prepubertal and adolescent obese
subjects compared with healthy controls. The present stud-
ied population was composed of 129 subjects, aged 5-16
years: 67 in the obese group and 62 in the lean group.
The obese subjects were recruited from the obesity clinic
at our institution. Obesity was defined as body mass index
(BMI) above the 97th age and sex-specific percentiles
(World Health Organization standards). Lean children
were recruited through peers of obese subjects and through
advertising. Their height and weight were within normal
range (2 SDs) and their BMI was <90th percentile for
age and sex.
Exclusion criteria were similar in both studies: (1) a history
of familial dyslipidemia or hype rtension; (2) a history of re-
cent illness, bone fracture, or viral syndrome within 2 weeks
of the blood draw; (3) the intake of medications or hor-
mones, which might influence cardiovascular function,
body composition, and lipid or glucose metabolism in the
preceding 6 months; (4) a genetic disorder or a chronic dis-
ease; and (5) participation in competition sport.
Informed written consent was obtained from both pare nts
and child. The Mother and Child Ethics Committee of the
University Hospitals of Geneva approved the study.
Anthropometrics Measures
We assessed body weight (in kilograms) and height (in cen-
timeters). BMI was calculated as weight/height squared
), and z scores were derived using the World Health
Organization references.
Pubertal development (Tanner
stage) was assessed using a validated self-assessment ques-
and children were classified into 2 categories:
no signs of puberty (Tanner stage I) or signs of puberty (Tan-
ner stage $II). Data were complete for all obese and 82% (51
of 62) of lean children. Eleven lean children had incomplete
data but were not in the prepubertal stage. Total body fat
mass (in kilograms), fat-free mass (in kilograms), percentage
of total body fat, and percentage of trunk fat were measured
using dual-energy x-ray absorptiometry (GE Lunar Prodigy;
GE Lunar Corp, Madison, Wisconsin). The percentage
of trunk fat is considered a marker of visceral fat.
intraclass correlation for repeated measurements of body
fat mass was 0.998 in our laboratory.
Biomarkers and Inflamm atory Markers
Blood samples were collected by phlebotomy following
a 10-hour overnight fast. Fasting plasma insulin (mU/mL)
concentration was measured using radioimmunoassay
(Access ultrasensitive insulin; Beckman Coulter Ireland
Inc, Mervue, Galway, Ireland). High-sensitivity CRP levels
were measured using laser nephelometry. Serum resistin,
leptin, chemokine ligand 2 (CCL2), IL-6, insulin-like
growth factor 1 (IGF-1), VCAM-1, ICAM-1, P-selectin, E-
selectin, and endothelin-1 (ET-1) levels were measured by
colorimetric enzyme-linked immunosorbent assay (R&D
Systems, Minneapolis, Minnesota). The limits of detection
were the following: resistin, 31.25 pg/mL; leptin, 31.25 pg/
mL; CCL2, 15.625 pg/mL; IL-6, 0.156 pg/mL; IGF-1, 31.25
pg/mL; VCAM-1, 15.60 pg/mL; ICAM-1, 15.60 pg/mL ; P-
selectin, 125 pg/mL; E-selectin, 93.75 pg/mL; and ET-1,
0 pg/mL. Mean intra-assay and interassay coefficients of
variation were <7% for all markers. All subjects were tested
for serum resistin levels (the primary outcome) as well as
high-sensitivity CRP, insulin, leptin, VCAM-1, ICAM-1,
and P- and E-selectins. Twenty-five (40%) lean and 24
(36%) obese adolescents had additional assessment of
ET-1, IL-6, IGF-1, and CCL2 concentrations. These analyses
could not be performed for all the subjects due to a lack of
Physical Activity
Objective measures of physical activity level were obtained
using a uniaxial acceler ometer (Actigraph MT 6471; MTI,
Pensacola, Florida). The method has been previously de-
Data were expressed as total activity counts per reg-
istered time (counts per minute). Data were available for 47
of 67 obese and 44 of 62 lean adolescents.
Statistical Analyses
Statistical analyses were performed using SPSS software
18.0 (SPSS Inc, Chicago, Illinois). Data were screened ini-
tially for a normal distribution, using skewness and kurto-
sis tests. Several variables were transformed and
successfully normalized in log10: resistin, leptin, P-selectin,
E-selectin, VCAM-1, ICAM-1, IGF-1, and CCL2. Data are
presented as mean and SDS or median and IQR (25th to
75th percentile) when indicated. We used nonparametric
tests (Mann-Whitney) to compare IL-6 among groups, be-
cause normalization was not possible. Statistical differences
between groups were analyzed using independent Student t
test and c
or Fisher test for normally distributed variables.
We used a 1-way ANOVA with Bonferroni post-hoc test to
compare the resistin levels among age categories. The rela-
tionships between dependent and independent variables
using univariate and standard multivariate regression anal-
yses were evaluated. We excluded cases only if data were
missing for the specific analysis. Differences were consid-
ered significant if P < .05.
2 Maggio et al
The mean age of subjects was 10.9 2.8 years (age range 5.4-
16.6). Our sample included 42% boys (n = 54) and 58% girls
(n = 75) with similar distribution by sex between groups (P =
.987). There was no difference in pubertal development or
physical activity between sexes (P > .05).
The subjects characteristics and blood biomarkers results
are presented in Table I. No subjects had type 2 diabetes.
Resistin levels were similar among groups and sex (P =
.324) and were highly dependent of age (t = 4.3, P < .001).
After adjustment for this variable, resistin concentrations be-
came significantly different between lean and obese children
(F = 18.6, P < .001).
As age may have an influence on resistin concentration, we
divided our population by age categories accordi ng to per-
centiles ( <33th, 33th to 66th, >66th percentiles) in order
to obtain 3 homogeneous groups: category I, <9 years (N =
43; obese: n = 23; lean: n = 20); category II, 9-12 years (N
= 42; obese: n = 22; lean: n = 21), and category III, >12 years
(N = 43; obese: n = 22; lean: n = 21). One-way ANOVA anal-
ysis with post-hoc test showed that resistin was significantly
higher in the oldest subjects compare d with others (mean re-
sistin: category I, 2.51 1.85; category II, 3.46 4.44; cate-
gory III, 14.52 20.87 ng/mL; F = 12.5, P < .001). When
analyzing the obese and lean separately, we found that resis-
tin increased significantly with age in both groups (lean: F =
3.6, P = .034; obese: F = 10.0, P < .001) (Figure 1). The
increase was larger in female subjects (P = .001) even if the
difference between boys and girls, in this age category, was
not significant (resistin concentration in >12 years: girls,
28.5 28.8, and boys, 9.5 17.3, P = .071).
As pubertal development may explain the increase of resis-
tin level with age, we compared prepubertal (n = 70) and cir-
cumpubertal (n = 59) subjects for resistin levels. We found
that its level was significantly different between the 2 puberty
groups (P < .001), even when analyzing the sexes separately
(female: P = .002; male: P = .022). The difference in resistin
levels during pubertal development in lean and obese subjects
is presented in Figure 2 (available at
Another explanation for this increase of resistin through
age categories may be a change in adiposity. However,
mean BMI z score or the percentage of total body fat did
not differ among age categories (for BMI z score: category
I, 1.47 1.96; category II, 1.41 1.63; category III, 1.26
1.57 kg/m
; P = .847; for percentage of total body fat: P =
.405). In fact, resistin was independent of BMI z score
(t = 0.5, P = .587), percentage of total body fat (t = 1.2,
P = .220), or percentage of trunk fat (t = 1.2, P = .238).
Figure 3 shows the relationship between resistin levels and
the percentage of trunk fat by puber tal development. The
resistin level was not related to the percentage of trunk fat
in prepubertal subjects (t = 1.05; P = .297) but tends to be
in circumpubertal adolescents (t = 2.0; P = .05).
Table I. Physical characteristics and biochemical
markers comparison between obese and lean subjects
Lean subjects,
Obese subjects,
Age, y 11.1 2.9 10.8 2.7
Female sex, no. 36 39
Pubertal stage I, no. 27 43*
Physical activity, counts/min 605.0 245.8 467.7 184.3*
Height, cm 147.9 16.9 146.9 15.1
Weight, kg 39.6 13.4 59.9 21.8
BMI, kg/m
17.5 2.5 26.8 5.5
BMI z score 0.11 0.84 2.78 0.98
Body composition
Percentage of total body fat, % 20.4 8.0 42.8 7.0
Percentage of trunk fat, % 21.4 10.9 49.7 7.9
Total body fat mass, kg 4.1 4.8 14.1 10.4
Fat-free mass, kg 15.2 13.7 18.6 11.5
Insulin, mU/L 6.5 4.0 12.5 6.5
Leptin, ng/mL 11.3 11.2 51.3 41.3
IGF-1, ng/mL (n = 25/24) 58.1 39.4 43.5 23.7
Inflammatory markers
Resistin, ng/mL 5.2 8.6 8.4 16.6
hs-CRP, mg/L 1.63 1.6 3.1 2.5
CCL2, pg/mL (n = 25/24) 25.6 11.0 40.4 43.6
IL-6, pg/mL (n = 25/24) 1.10 (0.33-3.04) 1.81 (0.77-9.47)
Endothelial markers
VCAM-1, ng/mL 369.2 198.2 835.6 1842.5*
ICAM-1, ng/mL 187.6 131.7 199.9 147.2
E-selectin, ng/mL 22.7 14.0 33.8 19.9
P-selectin, ng/mL 93.0 62.8 111.0 105.7
ET-1, pg/mL (n = 25/24) 2.38 0.67 2.50 0.74
hs-CRP, high-sensitivity C-reactive protein.
Results are expressed as mean and SDS. IL-6 is expressed as median and IQR.
*P < .05.
P < .001.
Figure 1. Resistin levels by age categories and groups. Filled
circles, outliers.
Serum Resistin and Inflammatory and Endothelial Activation Markers in Obese Adolescents
Furthermore, the resistin level was negatively corre-
lated with physi cal activ ity ( r = 0.329, P = .001) in
all subjects, as well as when separating lean (r =
0.537, P < .001) and o bese (r = 0.402, P = .005)
children. This relationship was not dependent on puber-
tal development (prepubertal: r = 0.251, P = .082; cir-
cumpubertal: r = 0.065, P = .685) but disappeared
when adju sting the age.
To understand which factors may influence resistin con-
centration, we divided the subjects according to the 90th
percentiles of resistin level (90th percentile: >9 ng/mL)
and compared subjects’ characteristi cs and biomarker con-
centrations according to this cut-off. Results are presented
in Table II. With this cut-off, all subjects with an increased
level (n = 12) were in the circumpubertal group. IL-6,
CCL2, ET-1, and IGF-1 were higher and physica l activity
was lower in the high resistin group, even after adjusting
the percentage of total body fat, percentage of trunk fat,
or BMI z score (results not shown). Adjusting the age
did not influence the results except for IGF-1 and
physical activity, because IGF-1 concentration and the
level of physical activity level decreased through age in
the high resistin group. Standard multiple regression
analysis, includi ng all the positively associated variables
mentioned abov e, showed that only IL-6 ( t = 2.7, P =
.009) remained significantly associated with res istin, and
CCL2 was close to significance (t = 2.0, P = .052).
Physical activity was not associated with resistin level.
Our study demonstrates that resistin leve ls are increased sig-
nificantly in obese adolescents independently of the quantity
of adipose tissue. This increase of resistin level is associated
with an activation of inflammatory (IL-6, CCL2) and endo-
thelial biomarker (ET-1), suggesting a potential role in the
development of atherosclerosis.
We demonstrated through a wide age range that after ad-
justing the age, resistin leve l is increased in obese children.
In fact, this difference in resistin concentration was only pres-
ent in adolescent subjects. Alth ough similar resistin concen-
trations (ranging from 3 to 10 ng/mL) were reported,
conflicting results have been shown in the literature.
Furthermore, we confirmed that puberty seems to play
a role in resistin secretion. Our results suggested that obese
adolescents, especially female subjects, show a sudden in-
crease of resistin concentrations, and it was more gradual
in lean controls, suggesting a triggering” factor in this pop-
ulation. This “triggering” factor could be due to the decrease
of physical activity observed in adolescent girls because phys-
ical activity is associated with decreased resistin levels.
However, there was no difference of physical activity between
boys and girls in our study. Furthermore, due to the difficulty
in adequately assessing pubertal development with our ques-
tionnaire, we could not analyze pubertal stages independently
to be more specific in our conclus ions. Gerber et al confirmed
the potential relationship between resistin concentration
and pubertal development, but they also found similar
resistin concentration between lean and obese children.
Figure 3. Relationship between resistin levels and percent-
age of trunk fat by pubertal categories.
Table II. Relationship between low and high resistin
level and biochemical markers
Resistin cut-off, ng/mL
P<9 >9
Total number (%) 117 (91) 12 (9)
Resistin, ng/mL 3.1 2.0 43.2 21.5 <.001
Gender female, no. (%) 68 (58) 7 (58) .989
Lean/obese, no. 56/61 6/6 .888
Total body fat, % 32.1 13.5 31.6 13.7 .915
Trunk fat, % 36.0 17.2 35.6 16.9 .937
Physical activity,
556.1 225.8 370.1 150.5 .009*
Hormones, no. (#9/>9)
Insulin, mU/L 110/11 9.5 6 12.7 8 .657
Leptin, ng/mL 117/12 31.1 36.2 42.4 41.1 .306
IGF-1, pg/mL 38/11 43.4 25.9 77.0 42.7 .003*
Endothelial markers
VCAM-1, ng/mL 117/12 628.4 1417.2 445.8 97.9 .462
ICAM-1, ng/mL 117/12 194.3 145.7 191.3 52.8 .393
E-selectin, ng/mL 117/12 28.6 18.8 27.3 10.0 .662
P-selectin, ng/mL 117/12 101.5 91.7 110.3 32.5 .179
ET-1, pg/mL 38/11 2.3 0.6 3.0 0.8 .002*
Inflammatory markers
hs-CRP, mg/L 110/11 2.4 2.2 2.4 2.6 .963
CCL2, pg/mL 38/11 25.3 9.7 59.1 60.0 .001*
IL-6, pg/mL 38/11 0.96 (0.40-2.40) 9.54 (3.13-87.82) <.001
Results are expressed as mean and SDS. IL-6 is expressed as median and IQR.
*P < .05.
P < .001.
4 Maggio et al
Some authors found that resistin is secreted by adipocytes
cells and its concentr ation increases with total body fat
Other studies suggest that mononuclear cells may
be the principal source of resistin production.
In our
study, resistin was not related to total body fat mass, even
during puberty, confirming the presence of other influences.
This lack of association has been also found in hypertensive
and diabetic adults.
As we found that the degree of adiposity was not related to
the production of resistin, we investigated the raw resistin
values and factors asso ciated with increased resistin levels.
As no normative references exist, we chose a cut-off value
of 9 ng/mL, which was the 90th per centile of resistin levels
in our population. Mean resistin levels found in other pedi-
atric studies have been quite wide, ranging from 4 to 16
ng/mL, probably due to the different methods of measure-
In our study, we found the same number of
lean and obese children with a high resistin level. Further-
more, high resistin levels (>9 ng/mL) w ere not related to total
body fat or trunk fat masses but to biomarkers of inflamma-
tion and endothelial activation (IL-6, CCL2, ET-1, and
IGF-1). Multiple regression showed that IL-6 was the main
cytokine related to resistin level. This interdependency be-
tween IL-6 and resistin is not well understood, but an
in vitro study showed that the production of IL-6 and other
cytokines such as IL-1 and TNF a increases the expression
of resistin in mononuclear cells,
and others co nfirm this
role for TNFa but not for IL-6 or IL-1. However, more re-
cently, authors showed that the increase of resistin stimulates
the secretion of the 3 cytokines, suggesting that resistin exerts
control of the cytokine inflammatory cascade.
A positive re-
lationship between resistin and TNFa and IL-6 has been con-
firmed in serum of healthy normal-weight adults.
Very few
studies have measured ET-1 and results are contradicting.
Shetty et al di d not find any correlation between resistin
and ET-1 in diabetic adults,
and 2 in vitro studies show op-
posite results. The first one suggests an inhibitory role of ET-1
for the secretion of resistin,
and the second study demon-
strates an increase in ET-1 after the administration of resis-
In addition, IGF-1 has been shown to be positively
related with resistin in subjects with rheumatoid arthritis.
Leptin and insulin were not different between subjects with
low and high resistin concentrations, ruling out the contribu-
tion of these factors to resistin levels during puberty. Kaser
et al also found similar results for leptin.
The role of resistin
in glucose homeostasis is controversial in humans,
an increase in resistin may lead to impaired glucose tolerance
in mice.
The cross-sectional des ign of this study does not allow us
to establish a link in the sequence of cascade activation. How-
ever, we hypothesize that adipocyte dysfunction seen in obe-
sity activates local inflammatory cytokines such as IL-6.
IL-6 plays a role in stimulating the expression of resistin in
mononuclear cells. Then, resistin, secreted by macrophages,
might further activate the production of inflammatory
markers, such as CCL2 and IL-6, as well as some endothelial
markers, such as ET-1. In addition, IGF-1 takes part in the
cascade of inflammation, through its production by fibro-
blasts and macrophages, after stimulation by proinflamm a-
tory cytokines, such as TNFa and IL-1.
According to our
data, this process seems to be independent of the quantity
of visceral adipose tissue.
This study has some weaknesses and strengths. First, not all
markers were tested with all subjects, so we cannot extrapo-
late the relationship between resistin and some markers
found in adolescence in all children. Second, we did not mea-
sure sexual hormones; therefore, we cannot evaluate their in-
fluence on resistin and other biomarkers. However, we
performed an analysis of resistin in a large number of chil-
dren and adolescents with a wide age range.
Interventions aiming at reducing resistin expression may
slow down the first phase of atherogenesis in adolescents.
Further studies will be needed to evaluate this concept.
We thank the subjects for volunteering for the study and the Pediatric
Policlinic staff and the staff of the Pediatric Research Platform for their
Submitted for publication Mar 20, 2012; last revision received May 7, 2012;
accepted May 31, 2012.
Reprint requests: Albane B.R. Maggio, MD, Pediatric Sport Medicine and
Obesity Care Program, Service of Pediatric Specialties, Department of Child
and Adolescent, University Hospitals of Geneva, 6, rue Willy-Donz
e, 1211
Geneva 14, Switzerland. E-mail: albane
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6 Maggio et al
Figure 2. Resistin levels by pubertal categories in lean and
obese subjects. C, Outliers.
Serum Resistin and Inflammatory and Endothelial Activation Markers in Obese Adolescents
    • "In addition to examining the relationship of resistin levels with anthropometric variables, an additional strength of our study is that we analyzed the association between these levels and percentage of fat mass, an aspect seldom addressed in Caucasian children. Contrary to results previously reported in some child populations [8,15,22] but in agreement with results from other studies [7,21], we not only failed to find significant correlations of resistin with weight or BMI, but also did not find significant differences between mean resistin levels in normal-weight and overweight/obese children. Conventionally, waist circumference is used in both clinical practice and biomedical research as a marker of abdominal obesity. "
    [Show abstract] [Hide abstract] ABSTRACT: The relationship of resistin levels with obesity remains unclear. The aim of this study was to determine resistin levels in prepubertal children and adolescents and evaluate their association with anthropometric parameters and body composition. The study population included 420 randomly selected 6- to 8-year-old children and 712 children aged 12 to 16 years. Anthropometric data were measured and body mass index (BMI) and waist-to-hip and waist-to-height ratios were calculated. Body composition was assessed using an impedance body composition analyzer. Serum resistin levels were determined using a multiplexed bead immunoassay. Resistin levels were not significantly different between sexes. No significant differences in serum resistin concentrations were found between obese, overweight, and normal weight children at any age, and no significant correlations were observed between resistin concentrations and weight or BMI. However, resistin levels showed a significant positive correlation with fat mass in 12- to 16-year-old children, particularly in girls. In addition to describing serum resistin levels in prepubertal children and adolescents, our study suggests that resistin is related to body fat rather than to BMI in adolescents.
    Full-text · Article · Sep 2013
  • [Show abstract] [Hide abstract] ABSTRACT: Resistin is a recently described adipokine which is expressed in low levels in human adipose tissue, pulmonary tissue and resting endothelial cells, and in high levels in mononuclear leukocytes, macrophages, and spleen and bone marrow cells. Serum levels of resistin have been found to be elevated in obese subjects and in subjects with insulin resistance and diabetes mellitus (DM). There is evidence that resistin is related to a variety of diseases, including rheumatoid arthritis, systemic lupus erythematous, sepsis, asthma and allergic rhinitis. A possible role of resistin has been documented in pathological metabolic conditions observed in children and adolescents, but the data are conflicting. This review summarizes the currently available data concerning the role of resistin in metabolic abnormalities and diseases in children and adolescents.
    Article ·
  • [Show abstract] [Hide abstract] ABSTRACT: Objective: Previous few studies have shown that resistin is significantly elevated in breast cancer (BC) patients. Therefore, we investigated whether serum resistin could be used as a potential diagnostic and prognostic tool for postmenopausal BC (PBC), taking into account clinicopathological features, serum tumor markers, anthropometric, metabolic, and, for the first time, inflammatory parameters. Methods: Serum resistin, tumor markers (CA 15-3 and CEA), metabolic, anthropometric and inflammatory parameters (TNF-α, IL-6, hsCRP) were determined in 103 postmenopausal women with incident, pathologically confirmed, invasive BC, 103 controls matched on age and time of diagnosis, and 51 patients with benign breast lesions (BBL). Results: Mean serum resistin was significantly higher in cases than in controls and patients with BBL (p<0.001). In patients, resistin was significantly associated with tumor and inflammatory markers, cancer stage, tumor size, grade and lymph node invasion but not with anthropometric, metabolic parameters and hormone receptor status. Multivariable regression analysis revealed that serum IL-6 (p=0.02) and cancer stage (p=0.048) were the strongest determinants of serum resistin in cases adjusting for demographic, metabolic and clinicopathological features. Although resistin's diagnostic performance was low based on ROC curve analysis [0.72, 95% CI: 0.64-0.79], it could, however, represent a BC biomarker reflecting advanced disease stage and inflammatory state. Conclusion: Further prospective and longitudinal studies are needed to evaluate whether serum resistin could be used as a prognostic tool in BC monitoring and management. More research is essential to elucidate resistin's ontological role in the association between obesity, representing a chronic low-grade subclinical inflammation, and PBC.
    Article · Jan 2013
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