obesity | VOLUME 20 NUMBER 4 | apRiL 2012 715
nature publishing group
Chronic subclinical inflammation may contribute to the patho-
genesis of metabolic diseases such as type 2 diabetes, cancer,
and atherosclerosis, the prevalence of which may differ with
ethnicity (1–4). For example, it has been shown that white (W)
men and women have a higher prevalence of atherosclerosis
when compared to African Americans (AA) (5,6); however,
it has been extensively documented that AA are more insulin
resistant and are more likely to develop type 2 diabetes and
hypertension (7–9). Whether potential differences in inflam-
mation are associated with ethnic differences in chronic meta-
bolic disease is not clear.
Adipose tissue is a source of proinflammatory cytokines, and
many cross-sectional studies have shown a relationship between
adiposity and circulating markers of inflammation (MOI; refs.
10–12). This characteristic of adipose tissue explains in part
the well-established association between obesity and chronic
metabolic disease. Intra-abdominal adipose tissue (IAAT) and
resident macrophages within this tissue are thought to be the
primary source of cytokines relevant to metabolic disease, such
as interleukin-6 (IL-6) or tumor necrosis factor-α (TNF-α). The
relationship between MOI and subcutaneous adipose tissue is
less clear. Liposuction studies have shown either an improve-
ment (13) or no effect (14) on MOI with removal of subcuta-
neous adipose tissue. Therefore, questions still exist over the
associations between MOI and abdominal fat depots.
Ethnic differences exist in body fat distribution, with W hav-
ing relatively more IAAT compared to AA (5,12). The poten-
tial role of these differences in fat distribution to inflammation
and chronic metabolic disease is not entirely clear. We have
previously shown that greater IAAT in W women explained
their greater concentrations of circulating TNF-α and soluble
cell-surface receptors (12). Several studies have shown higher
concentrations of CRP (15–17) and IL-6 (18) in AA compared
Markers of inflammation and Fat Distribution
Following Weight Loss in african-american
and White Women
Gordon Fisher1, Tanya C. Hyatt1, Gary R. Hunter2, Robert A. Oster3, Renee A. Desmond3
and Barbara A. Gower1
Changes in markers of inflammation (MOI) and fat distribution with weight loss between African-American (AA) and
white (W) women have yet to be characterized. The purpose of this study was to examine potential ethnic differences
in MOI and regional fat distribution with weight loss, and identify the associations between these markers and changes
in regional fat distribution with weight loss among AA and W women. Subjects were 126 healthy, premenopausal
women, BMI 27–30 kg/m2. They were placed on a weight-loss intervention consisting of diet and/or exercise until
a BMI <25 was achieved. Fat distribution was measured with computed tomography, and body composition with
dual-energy X-ray absorptiometry. Serum concentrations of tumor necrosis factor-α (TNF-α), soluble TNF receptor-I
(sTNFR-I), sTNFR-II, C-reactive protein (CRP), and interleukin-6 (IL-6) were assessed. All MOI and adiposity measures
significantly decreased with weight loss. Significant ethnic differences with weight loss were observed for fat mass,
body fat, intra-abdominal adipose tissue (IAAT), sTNFR-I, and sTNFR-II. Mixed-model analysis indicated that adjusting
for change in IAAT explained ethnic differences in change in TNF-α and the decrease in TNF-α with weight loss, while
total fat mass only explained the decrease in sTNFR-I and sTNFR-II with weight loss. In conclusion, all MOI decreased
following weight loss among W, whereas only IL-6 and CRP decreased following weight loss in AA. The most distinct
phenotypic difference observed was a greater impact of weight loss on TNF-α in W compared to AA, which was
directly associated with IAAT in W.
Obesity (2012) 20, 715–720. doi:10.1038/oby.2011.85
1Department of Nutrition Sciences, University of Alabama-Birmingham, Birmingham, Alabama, USA; 2Department of Human Studies,
University of Alabama-Birmingham, Birmingham, Alabama, USA; 3Department of Medicine, University of Alabama-Birmingham, Birmingham, Alabama, USA.
Correspondence: Gordon Fisher (firstname.lastname@example.org)
Received 21 October 2010; accepted 8 March 2011; published online 28 April 2011. doi:10.1038/oby.2011.85
VOLUME 20 NUMBER 4 | apRiL 2012 | www.obesityjournal.org
to W, while others have shown no difference (12,19). However,
these studies did not necessarily assess fat distribution (15,16);
thus, it is difficult to conclude whether ethnic differences in fat
distribution contributed to the observed differences in MOI.
Weight loss may be an effective means for reducing chronic
subclinical inflammation. Intervention studies have shown
that reductions in adiposity are associated with reductions in
MOI (20–22). However, whether AA and W respond similarly
to weight loss regarding inflammation is not known. Given
ethnic differences in fat distribution, it is possible that dif-
ferential loss of IAAT vs other adipose compartments could
affect AA and W differently. Therefore, the purpose of this
study was to examine potential ethnic differences in changes
in MOI with weight loss, and to identify the associations
between these changes and changes in total body fat and fat
distribution (IAAT, superficial subcutaneous adipose tissue
(SSAAT), deep subcutaneous adipose tissue (DSAAT)). We
hypothesized that MOI would decrease to a greater extent
with weight loss in W vs. AA due to greater IAAT, and loss of
IAAT, among W.
Methods and Procedures
Subjects were derived from a parent study involving 213 healthy, over-
weight, premenopausal women who volunteered for, and enrolled in a
study designed to examine metabolic factors that predispose women
to weight gain. The sample size included in this study was 126 women
comprised of subject who both adhered to the diet requirements of
the parent study and had serum samples available for analysis. A total
of 83 subjects dropped out of the study during the intervention, and
plasma samples were not available for four subjects. Inclusion criteria
for the parent study were BMI 27–30 kg/m2, premenopausal, age 20–41
years, sedentary (no more than one time per week regular exercise),
normal glucose tolerance (2-h glucose ≤140 mg/dl following 75 g oral
dose), family history of overweight/obesity in at least one first-degree
relative, and no use of medications that affect body composition or
metabolism. All women were nonsmokers and reported experiencing
menses at regular intervals. The study was approved by the institu-
tional review board for human use at the University of Alabama at
Birmingham. All women provided informed consent before partici-
pating in the study.
Subjects were evaluated in the overweight state (before any interven-
tion). Weight was stabilized for 4 weeks before testing through dietary
control. During the weight stabilization period, body weights were
measured 3–5 times per week at the General Clinical Research Center
(GCRC) at University of Alabama at Birmingham. During the weight
maintenance period, a macronutrient-controlled diet was provided by
the GCRC. The energy content was appropriately adjusted to ensure a
stable body weight (~1% variation from initial body weight). All diets
consisted of approximately ~22% of energy from fat, 23% from protein,
and 55% from carbohydrate. After discharge from the initial GCRC in-
patient visit, the GCRC kitchen provided all meals for the period of
weight reduction. Subjects were provided a 3,350 kJ (800 kcal) diet con-
sisting of the same dietary ratios as above, which was designed to meet
all nutrient requirements excluding energy requirements. Stouffer’s Lean
Cuisine entrées (Nestlé Food, Solon, OH) were provided for lunch and
dinner, and alcohol intake was not permitted during the study. Subjects
were maintained on the diet and/or exercise until ≥10 kg in body weight
was lost and a BMI <25 was achieved. Having attained a normal body
weight, subjects then repeated the 4-week protocol of energy balance
before testing. All testing was conducted in the follicular phase of the
menstrual cycle during a 4-day GCRC in-patient stay.
Body composition and fat distribution
Total and regional body composition, including total fat mass, percent
body fat, leg fat mass, and lean body mass were measured by dual-
energy X-ray absorptiometry (Prodigy; Lunar Radiation, Madison,
WI). The scans were analyzed with the use of ADULT software, ver-
sion 1.33 (Lunar Radiation). Intra-abdominal adipose tissue (IAAT)
and subcutaneous abdominal adipose tissue (SAAT) were analyzed
by computed tomography scanning (23,24) with a HiLight/Advantage
Scanner (General Electric, Milwaukee, WI) located in the University of
Alabama at Birmingham, Department of Radiology. SAAT was further
subdivided into superficial and deep compartments (25). Subjects were
scanned in the supine position with arms stretched above their heads.
A 5-mm scan at the level of the umbilicus (approximately the L4–L5
intervertebral space) was taken. Scans were analyzed for cross-sectional
area (cm2) of adipose tissue using the density contour program with
Hounsfield units for adipose tissue set at −190 to −30. All scans were
analyzed by the same individual. The coefficient of variation (CV) for
repeat cross-section analysis of scans among 40 subjects in our labora-
tory is <2% (ref. 24).
All analyses were conducted in the Core Laboratory of University of
Alabama at Birmingham’s GCRC, Diabetes Research Training Center,
and Nutrition and Obesity Research Center. Glucose was measured
using an Ektachem DT II System (Johnson and Johnson Clinical
Diagnostics, Rochester, NY). In the Core Laboratory, this analysis has
a mean intra-assay CV of 0.61%, and a mean interassay CV of 2.56%.
Insulin was assayed in duplicates of 100 μl aliquots using double-
antibody radioimmunoassay (Linco Research, St Charles, MO). In the
Core laboratory, this assay has a sensitivity of 3.35 μIU/ml, a mean
intra-assay CV of 3.49%, and a mean interassay CV of 5.57%. MOI
were assessed using enzyme-linked immunosorbent assays (ELISAs).
All samples were analyzed in duplicate. TNF-α was analyzed using
the high-sensitivity ELISA kit (Quantikine HSTA00C; R&D Systems,
Minneapolis, MN). Four TNF-α values were below the minimum
detectable concentration (0.50 pg/ml); these samples were assigned
the value of the minimum detectable concentration. sTNFR-I was
measured with the EASIA ELISA kit (KAC1761; Invitrogen, Carlsbad,
CA). sTNFR-II was measured with the EASIA ELISA kit (KAC1771;
Invitrogen). IL-6 was assayed using the high-sensitivity ELISA kit
(Quantikine HS600B; R&D Systems). CRP was assayed with the high-
sensitivity ELISA kit (030–9710s; ALPCO, Windham, NH).
Descriptive statistics were computed for each ethnic group (AA and W)
at baseline and following weight loss. All values are reported as means ±
SD. All statistical models were evaluated for residual normality and log-
arithmic transformations were performed when appropriate. All data
were analyzed using SAS (version 9.1; SAS Institute, Cary, NC).
Comparisons between baseline and the weight-reduced state were per-
formed using the two-group t-test. Overall comparisons of the change
in fat depots and MOI by ethnicity were performed using repeated-
measures ANOVA. Repeated-measures mixed-models analyses were
used to evaluate changes in MOI after weight loss. Independent variables
included in these models were ethnicity, time, total fat mass, and IAAT.
For all analyses, a P value <0.05 was deemed statistically significant.
There were no significant differences in any of the models after adjust-
ing for SSAAT and DSAAT; therefore these variables were not included
in the final analysis.
Baseline descriptive statistics by ethnicity are shown in Table 1.
At baseline, W had significantly greater IAAT than AA. Serum
obesity | VOLUME 20 NUMBER 4 | apRiL 2012 717
concentrations of TNF-α and its receptors were higher in W
than AA (Figure 1).
The effects of ethnicity, time, and the ethnicity × time inter-
action on all outcome variables are shown in Table 1. All MOI
and adiposity decreased with weight loss. Significant ethnic
differences with weight loss were observed for fat mass, body
fat, IAAT, sTNFR-I, and sTNFR-II. The significant ethnicity ×
time interactions seen in Table 1 indicated that body weight,
IAAT, and TNF-α decreased more in W than in AA.
In mixed modeling for TNF-α, there was a significant time
term and a significant ethnicity × time interaction (Table 2).
Adjusting for the change in IAAT not only explained the eth-
nic difference in change in TNF-α, but also explained the
decrease in TNF-α with weight loss. Including the change in
fat mass instead of IAAT explained the decrease in TNF-α
with weight loss, but it did not remove ethnicity as a signifi-
In mixed modeling for sTNFR-I, there was a significant eth-
nicity term and a significant time term (Table 3). Adjusting for
either IAAT or total fat mass explained the change in sTNFR-I
with weight loss. However, there was still an ethnic difference
in all models.
Similarly, mixed modeling for sTNFR-II revealed a signifi-
cant ethnicity term and a significant time term (Table 4). After
adjusting for IAAT, the ethnic difference, as well as the change
with weight loss, persisted. However, adjusting for total fat
mass explained the change in sTNFR-II with weight loss, even
though there was still an ethnic difference.
There were no significant effects of ethnicity or ethnicity ×
time on IL-6 or CRP, therefore these variables were not con-
sidered for further analysis.
table 1 Body composition and markers of inflammation with weight loss by ethnicity
W (n = 61)AA (n = 65)
ETE × T
Body weight (kg)79 ± 9a
66 ± 8b
77 ± 6a
65 ± 5b
BMI (kg/m2)28 ± 1a
24 ± 1b
28 ± 1a
24 ± 1b
Fat mass (kg) 34 ± 6a
23 ± 5b
32 ± 4a
21 ± 4b
Body fat (%)46 ± 4a
36 ± 5b
44 ± 4a
34 ± 5b
Lean mass (kg) 41 ± 440± 441 ± 441± 40.5250.7310.089
IAAT (cm2)96 ± 29a
64 ± 28b
66 ± 29b
40 ± 19c
SSAAT (cm2)196 ± 51a
133 ± 53b
190 ± 49a
141 ± 43b
DSAAT (cm2)141 ± 50a
90 ± 38b
140 ± 55a
82 ± 354b
TNF-α (pg/ml) 1.25 ± 1.40a
1.01 ± 0.84b
0.86 ± 0.62b
0.83 ± 0.54b
sTNFR-I (ng/ml)1.91 ± 0.37a
1.83 ± 0.34b
1.71 ± 0.36b
1.68 ± 0.35b
sTNFR-II (ng/ml)4.32 ± 1.19a
3.97 ± 0.89b
3.69 ± 0.86b
3.60 ± 0.93b
IL-6 (pg/ml) 1.96 ± 1.57a
1.33 ± 0.77b
1.65 ± 0.99a
1.35 ± 0.68b
CRP (mg/l)1.92 ± 1.67a
1.32 ± 1.58b
2.19 ± 2.19a
1.68 ± 1.82b
Far-right columns indicate results of repeated-measures two-way ANOVA for main effects of ethnicity (E), time (T), and the ethnicity × time interaction (E × T), values in
boldface indicate significant differences (P < 0.05). Within a row, results of post hoc analyses among the four groups are provided with superscripts; means with different
superscripts are significantly different (P < 0.05). All data are presented as means ± SD.
CRP, C-reactive protein; DSAAT, deep subcutaneous abdominal adipose tissue; IAAT, intra-abdominal adipose tissue; SI, insulin sensitivity; SSAAT, superficial sub-
cutaneous abdominal adipose tissue; sTNFR-I, tumor necrosis factor receptor-I; sTNFR-II, tumor necrosis factor receptor-II; TNF-α, tumor necrosis factor-α; IL-6,
W (n = 65)
AA (n = 61)
Figure 1 The TNF system decreased with weight loss in W but
not AA. All elements of the TNF system were greater in W vs.
AA at baseline. *Significantly different from baseline (P < 0.05).
**Significantly different from W (P < 0.05). AA, African American;
W, white; TNFR-I, tumor necrosis factor receptor-I; TNFR-II, tumor
necrosis factor receptor-II.
VOLUME 20 NUMBER 4 | apRiL 2012 | www.obesityjournal.org
The purpose of this study in healthy overweight premenopausal
AA and W women was to examine potential ethnic differences
in MOI and regional fat distribution with weight loss, and to
identify the associations between changes in these markers
and changes in regional fat distribution. We found that MOI
decreased following weight loss; however, responses differed
between AA and W women. Specifically, all MOI decreased
following weight loss in W women, whereas only IL-6 and CRP
decreased following weight loss in AA women. The ethnic dif-
ferences observed for TNF-α between W and AA women were
due in part to the greater loss of IAAT in W women. These
observations suggest that there are ethnic differences among
premenopausal AA and W women in the association between
changes in regional fat distribution and MOI with weight loss.
We initially speculated that greater baseline IAAT and greater
baseline TNF system markers among W women would result
in greater changes in these measures with weight loss. We
observed that W women had a greater loss of both IAAT and
TNF-α with weight loss compared to AA. In fact, in W women
circulating concentrations of the TNF system decreased with
weight loss to levels comparable to those of their AA counter-
parts (Table 1). Furthermore, statistically adjusting for change
in IAAT attenuated the ethnic difference in change in TNF-α
(P = 0.135 for ethnicity; P = 0.056 for ethnicity × time interac-
tion; Table 2). Both of these findings suggested that the change
in TNF-α in W women was in part due to the loss of IAAT in
We also observed an ethnic difference in the change in
sTNFR-I and sTNFR-II with weight loss. W women showed
decreases in both sTNFR-I and sTNFR-II, whereas AA women
showed no changes in these measures. Although it is tempting
to speculate that this ethnic difference was likewise attribut-
able to greater IAAT in the W, we did not observe a significant
association between the change in IAAT and the changes in
the receptors. Further, inclusion of measures of body fat in the
multiple regression models did not eliminate the significant
effect of ethnicity.
To further probe the mechanism for the differential change
in receptors between AA and W with weight loss, we examined
the possibility that lean body mass played a role. Lower levels of
sTNFR-I and sTNFR-II have been reported in lean compared
to obese individuals (26). In our cohort, AA tended to show a
preservation of lean mass with weight loss, whereas W tended
to show a decrease (P = 0.089 for ethnicity × time interaction;
Table 1). However, when change in lean mass was included
in the models for sTNFR-I and sTNFR-II, ethnicity was still a
significant determinant. Thus, the mechanism through which
weight loss alters the TNF receptors in W women cannot be
determined from our results.
Whether a decrease in TNF receptors indicates an improve-
ment in metabolic health is not entirely clear. TNF-α is thought
to exert its biological effects on cell function by binding to cell-
surface receptors sTNFR-I and sTNFR-II (27). The extracellular
portions of these receptors are present in serum as sTNFR-I and
sTNFR-II, and are thought to reflect TNF-α activity. sTNFR-I is
thought to mediate the metabolic actions of TNF-α, such as its
effects on insulin signaling (28), while the role of sTNFR-II is
less clear. These receptors are usually elevated in obese individ-
uals compared to lean controls (26,29,30). However, weight loss
studies have yielded equivocal results; Zahorska-Markiewicz
et al. found a significant increase in both sTNF receptors fol-
lowing weight loss (31), while Bastard et al. found a significant
decrease in sTNFR-I and no change in sTNFR-II (32). In our
table 2 Mixed models for tnF-α with weight loss (n = 124)
Ethnicity × time
Ethnicity × time 0.056
Ethnicity × time
Values in boldface indicate significant differences (P < 0.05).
table 3 Mixed models for tnFr-I with weight loss (n = 124)
Ethnicity × time0.244
Fat mass 0.104
Values in boldface indicate significant differences (P < 0.05).
table 4 Mixed models for tnFr-II with weight loss (n = 124)
Ethnicity × time 0.147
Values in boldface indicate significant differences (P < 0.05).
obesity | VOLUME 20 NUMBER 4 | apRiL 2012 719
study, the receptors either decreased (W women) or remained
unchanged (AA women). Differences among studies may be
due to the energy balance status of the subjects.
In this study, we found no significant differences in IL-6 or
CRP between ethnic groups at baseline or following weight
loss. The parallel responses of IL-6 and CRP were not unex-
pected as secretion of CRP by the liver is primarily regulated
by circulating IL-6 (ref. 33). The current literature examining
ethnic differences in circulating IL-6 and CRP is discrepant.
Cross-sectional studies have reported both significant (15–
18), and nonsignificant (12,19) differences in IL-6 and CPR
between AA and W women. Visceral fat is often mentioned
as the primary site of IL-6 secretion (34). However, in our
sample, greater IAAT in C did not correspond to greater IL-6,
suggesting that IL-6 may be released from other fat depots.
This hypothesis is reinforced by the observation that adjust-
ment for total fat but not IAAT eliminated the “time” effect
in the mixed model for IL-6 (data not shown). Further, we
found no significant associations of IAAT with IL-6 and CRP.
Although no significant associations between IAAT and IL-6
were observed, the possibility that the feedback loop involving
IL-6 may not simply be related to the amount of adipose tissue
but rather other stimuli can not be disregarded.
This study revealed several areas for further evaluation.
Ethnic differences have been reported for many variables,
including fat distribution, insulin sensitivity, disease risk, and
the TNF system. This study also showed ethnic differences
in the relationships between MOI and fat distribution. An
unexamined possibility is that MOI have a different effect on
adipose tissue in W vs. AA women. For example, TNF-α has
autocrine functions in tissues where it is expressed, as well as
more systemic paracrine functions in tissues that express the
receptors for it. Because W had greater circulating TNF-α and
its receptors than AA, it is possible the TNF system may be
of greater physiological relevance among obese/overweight W
women relative to AA.
Strengths of this study included robust measures of body
composition and body fat distribution. Additional strengths
included closely matching the number of AA (n = 65) and W
(n = 61) women and taking post-weight-loss measures after 4
weeks of weight maintenance. To our knowledge, this is the first
sufficiently powered longitudinal study to examine changes in
regional fat distribution and MOI following weight loss among
AA and W women. A limitation in this study was not exam-
ining all relevant lipid depots, such as intermuscular adipose
tissue and intramyocellular lipid. Furthermore, our results are
limited to a population of healthy, overweight, premenopausal
women. Similar studies on men, obese individuals, children,
and postmenopausal women should be performed.
In conclusion, we demonstrated that weight loss reduces MOI
in overweight premenopausal AA and W women. However, the
changes in these markers following weight loss differed between
ethnic groups. We found that all MOI decreased following
weight loss among W, whereas only IL-6 and CRP decreased
following weight loss in AA. The most distinct phenotypic dif-
ference observed in this study was a greater impact of weight
loss on TNF-α in W women compared to AA women, which
was directly associated with IAAT in W women. Therefore,
despite the higher prevalence of some metabolic diseases in
AA vs. W (e.g., hypertension, type 2 diabetes), our data suggest
that, regarding inflammation, weight loss may have stronger
health benefit among W when compared to AA women, in part
due to the greater loss of visceral fat in W women. Thus, health-
care providers should continue to emphasize the importance
of weight loss, even among demographic groups such as young
W women often assumed to be at relatively low risk for chronic
metabolic disease. Further study is needed to examine the pro-
gression of low-grade inflammation on the pathogenesis of
chronic diseases, and how these processes differ with ethnicity
This work was supported by RO1DK51684, RO1DK49779, UL 1RR025777,
p60DK079626, MO1-RR-00032, p30-DK56336, and 2T32DK062710-07.
Stouffer’s Lean Cuisine and Weight Watchers Smart Ones kindly provided
food used during the weight-maintenance periods. We acknowledge David
Bryan and Robert petri for technical assistance; Maryellen Williams and
Cindy Zeng conducted laboratory analyses; paul Zuckerman for project
The authors declared no conflict of interest.
© 2011 The Obesity Society
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