The Relationship between Plasma Adiponectin Concentration and Insulin

Resistance Is Altered in Smokers

Fahim Abbasi, Helke M. F. Farin, Cindy Lamendola, Tracey McLaughlin, Eric A. Schwartz, Gerald M. Reaven and
Peter D. Reaven
J. Clin. Endocrinol. Metab. 2006 91:5002-5007 originally published online Sep 26, 2006; , doi: 10.1210/jc.2006-0419

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The Journal of Clinical Endocrinology & Metabolism 91(12):50025007

Copyright 2006 by The Endocrine Society
doi: 10.1210/jc.2006-0419

The Relationship between Plasma Adiponectin

Concentration and Insulin Resistance Is Altered
in Smokers
Fahim Abbasi, Helke M. F. Farin, Cindy Lamendola, Tracey McLaughlin, Eric A. Schwartz,
Gerald M. Reaven, and Peter D. Reaven
Department of Medicine (F.A., H.M.F.F., C.L., T.M., G.M.R.), Stanford University School of Medicine, Stanford, California
94305; and Medical Research Service (E.A.S., P.D.R.), Division of Endocrinology and Metabolism, Department of Medicine,
Carl T. Hayden Veterans Affairs Medical Center, Phoenix, Arizona 85012
Context: Low plasma adiponectin concentrations in smokers may
contribute to the adverse consequences that occur in these
individuals.

Main Outcome Measures: Measures included fasting plasma adiponectin and C-reactive protein (CRP) concentrations and changes in
adiponectin after pioglitazone treatment in IR and IS smokers.

Objective: The objective of the study was to define the relationship

among smoking, plasma adiponectin concentrations, insulin resistance, and inflammation.

Results: Being either a smoker or having insulin resistance was independently associated with lower adiponectin concentrations (P 0.046 and
0.001, respectively). The difference in mean adiponectin concentration between smokers and nonsmokers did not depend on the insulin resistance
status of the subjects. No difference was detected in average CRP concentrations between smokers and nonsmokers (P 0.18) and between IR and
IS subjects (P 0.13). CRP concentrations were unrelated to adiponectin
in smokers (r 0.05, P 0.78) and nonsmokers (r 0.03, P 0.86).
Finally, pioglitazone treatment increased adiponectin concentrations in
both IR (P 0.001) and IS smokers (P 0.001).

Design: This was a cross-sectional, observational study with a 2 2

factorial design and a prospective longitudinal arm.
Setting: The study was conducted at a general clinical research
center.
Participants: Apparently healthy smokers (n 30) and nonsmokers
(n 30), subdivided into insulin resistant (IR) (n 15) and insulin
sensitive (IS) (n 15) subgroups participated in the study.
Intervention: Intervention included pioglitazone administration for
3 months to 12 IR smokers and eight IS smokers.

DIPONECTIN, AN ADIPOCYTE gene product, is secreted in large amounts from adipose tissue and is
present in relatively high concentration in the blood. Low
circulating concentrations of adiponectin have been associated with obesity, dyslipidemia, essential hypertension, type
2 diabetes, and cardiovascular disease (15). It is apparent
that the clinical syndromes in which hypoadiponectinemia
occurs are all associated with peripheral resistance to insulinmediated glucose uptake (6). In addition, variations in
plasma adiponectin concentration and/or molecular forms
have been suggested to modulate insulin sensitivity (2, 79).
More recently, plasma adiponectin concentrations have
been reported to be low in smokers (10 13). Because results
of in vitro studies have indicated that addition of proinflammatory cytokines, such as TNF- and IL-6, to isolated adipocytes can reduce adiponectin expression (14 16), it is posFirst Published Online September 26, 2006
Abbreviations: ANCOVA, Analysis of covariance; BMI, body mass
index; CI, confidence interval; CRP, C-reactive protein; GFR, glomerular
filtration rate; IR, insulin resistant; IS, insulin sensitive; SSPG, steadystate plasma glucose.
JCEM is published monthly by The Endocrine Society (http://www.
endo-society.org), the foremost professional society serving the endocrine community.

Conclusions: Plasma adiponectin concentrations are lower in smokers

and IR subjects and are unrelated to CRP concentrations. These findings
suggest that low levels of adiponectin in smokers may be independent of
both insulin resistance and a generalized inflammatory response.
(J Clin Endocrinol Metab 91: 50025007, 2006)

sible that the association between smoking and lower

adiponectin concentrations results from inflammation-mediated down-regulation of adiponectin expression in adipose
tissue. In support of this notion is evidence of an inverse
relationship between markers of inflammation such as C-reactive protein (CRP) with adiponectin (17, 18). In addition,
smoking has been identified as a source of reactive oxygen
species (19, 20) and is associated with increased levels of
inflammatory markers (2123), further suggesting that smoking-induced inflammation may contribute to lower adiponectin levels in smokers.
On the other hand, because the prevalence of insulin resistance may also be increased in smokers (24, 25), it is not
clear whether hypoadiponectinemia in these individuals is
due to smoking, and possibly the associated inflammation,
or to the coexistence of insulin resistance. The possible contribution of insulin resistance, as estimated by a surrogate
indicator, to reduced adiponectin concentrations in smokers
was considered in one brief correspondence (12), and the
results of multivariate analysis suggested that the relationship between smoking and adiponectin was independent of
insulin action. However, we felt that the possible relationship
among smoking, hypoadiponectemia, and insulin resistance
was important enough to evaluate further, using a specific

5002

Abbasi et al. Smoking, Adiponectin, and Insulin Resistance

measure of insulin action, rather than a surrogate estimate.

To address these issues, we have in the present study measured adiponectin and CRP concentrations in smokers and
nonsmokers, with each group further stratified into insulinresistant (IR) and insulin-sensitive (IS) subgroups.
If adiponectin is lower in smokers, and this is not simply
related to the extent of insulin resistance, identification of
therapies that correct this abnormality may be clinically important. In this context, thiazolidinedione compounds have
been shown to increase plasma adiponectin concentrations
(9, 26), and there is evidence that they can exert a beneficial
antiinflammatory effect independent of their ability to enhance insulin sensitivity (27). The ability of such agents to
increase adiponectin may be particularly useful to prevent
cardiovascular disease in smokers in light of the observation
that smokers with low adiponectin concentrations are at
greater risk for coronary stenosis than smokers with high
concentrations of adiponectin (28). Thus, irrespective of the
reasons that adiponectin concentrations are lower in smokers, we thought it would be important to also evaluate the
ability of pioglitazone treatment to increase plasma adiponectin concentrations in the two smoking groups.
Subjects and Methods
The study population consisted of 30 smokers and 30 nonsmokers
who responded to print advertisements describing our research interest
in smoking-associated metabolic abnormalities. Screening inclusion criteria included: healthy individuals between ages 29 and 65 yr; body mass
indices (BMIs) between 20 and 35 kg/m2; and no medications known to
affect glucose, insulin, or lipoprotein metabolism. In addition, the smokers had to have a history of smoking a minimum of 10 cigarettes per day
for at least the past 5 yr. Potential participants were further evaluated
by medical history, physical examination, and routine clinical laboratory
measurement to exclude individuals with apparent disease, laboratory
evidence of type 2 diabetes, anemia, and abnormal liver or kidney
function. Renal function was also evaluated by calculating the estimated
glomerular filtration rate (GFR) using the Cockcroft-Gault formula (29).
Volunteers meeting these eligibility criteria were scheduled for admission to the General Clinical Research Center of the Stanford University
Medical Center. The Stanford Human Subjects Committee approved the
study, and each subject gave informed consent.
Insulin-mediated glucose disposal was quantified by a modified version (30) of the insulin suppression test as described and validated by
our research group (31, 32). After an overnight fast, an iv catheter was
placed in each arm of the subject. One arm was used for the simultaneous
infusion of octreotide (0.27 g/m2min), insulin (32 mU/m2min), and
glucose (267 mg/m2min) for 180 min, and the other arm was used for
collection of blood samples. During the last 30 min of the infusion, blood
was sampled at 10-min intervals to measure plasma glucose and insulin
concentrations, and the values obtained were averaged to determine the
steady-state plasma glucose (SSPG) and insulin concentrations. Because
the steady-state plasma insulin concentrations are comparable in all
individuals and glucose infusion is identical, the resultant SSPG concentrations provide a direct measure of the ability of insulin to mediate
the disposal of a given glucose load; i.e. the higher the SSPG concentration, the more insulin resistant the individual. For the purpose of this
study, individuals with a SSPG concentration more than 145 mg/dl were
considered IR, whereas those with a SSPG concentration less than 95
mg/dl were classified as IS; and both sets of individuals were included
in the study. The cut point for defining IR was based on a prospective
study showing that apparently healthy, nonobese individuals with SSPG
concentrations greater than 140 mg/dl had a significant increase in the
incidence of a number of age-related diseases (33). The cut point for the
IS stems from evidence that approximately one third of a large, apparently healthy population had values below this level (34).
Given evidence that administration of thiazolidinedione compounds
increased plasma adiponectin concentrations in IR nonsmokers (26), we

J Clin Endocrinol Metab, December 2006, 91(12):50025007

5003

evaluated the possibility that this intervention would be equally effective in both IR and IS smokers. To accomplish this goal, we enrolled 20
smokers, 12 classified as being IR and eight IS by the criteria outlined
above, and treated them for 3 months with pioglitazone. Treatment was
initiated with 15 mg/d for 2 wk, increased to 30 mg/d for the next 2 wk,
and followed by 45 mg/d for 8 wk. Plasma alanine aminotransferase
levels were checked at the end of each month, and the daily dose of
pioglitazone increased only in the presence of continued normal liver
function. Liver function did not deteriorate in the 20 volunteers studied,
and they all completed the treatment period on the full pioglitazone
dose.
Plasma glucose and insulin levels were measured as described previously (26). Plasma adiponectin levels were measured with a RIA
established by Linco Research, Inc. (St. Charles, MO). This assay has a
sensitivity of 0.01 mg/dl and intra- and interassay coefficient of variation
of less than 8%. Serum high-sensitivity CRP was measured with a chemiluminescent assay established for use on an Immulite automatic analyzer (Diagnostics Products Corp., Los Angeles, CA). This assay has a
sensitivity of 0.01 mg/dl and intra-and interassay coefficients of variation of less than 8%.
Summary statistics are expressed as mean sd or number of subjects.
Adiponectin and CRP values were log transformed for statistical analyses. Means and the 95% confidence intervals (CIs) of the log-transformed data were calculated, and these values were then back transformed to the original scale. The resultant adiponectin and CRP
averages, known as geometric means, are reported along with their 95%
CI. One-way ANOVA and Tukeys post hoc comparison test were used
to compare the mean clinical and metabolic variables among the IR
smokers, IS smokers, IR nonsmokers, and IS nonsmokers. A 2 test was
used to assess the differences in gender distribution among these four
subgroups. Two-factor ANOVA was performed to evaluate the main
effects of smoking (smoker vs. nonsmoker) and insulin resistance (IR vs.
IS) and their interaction on plasma adiponectin and CRP concentrations.
Because differences in gender and body fat have been shown to influence
adiponectin levels, an analysis of covariance (ANCOVA) was performed
to explore the effects of gender and BMI as covariates on plasma adiponectin concentrations in addition to the main effects of smoking and
insulin resistance and their interaction. Pearson correlation coefficients
were calculated to assess the strength of association between adiponectin and estimated GFR and between adiponectin and CRP concentrations. For the longitudinal pioglitazone treatment study in smokers,
differences in baseline characteristics of the IR and IS subjects were
compared with unpaired t test, and gender distribution was compared
with Fishers exact test. The effect of pioglitazone treatment in smokers
was evaluated using paired t test.

Results

The study participants were primarily of Caucasian ancestry (n 44) of whom four were of Hispanic ethnicity; the
rest of the volunteers were of Asian (n 11) and African (n
5) ancestries. Clinical and metabolic characteristics of the
smokers and nonsmokers further divided into IR and IS
groups are given in Table 1. All four groups were similar in
terms of age, gender distribution, and BMI. The creatinine
levels were normal and 1.2 mg/dl or less in all subjects. The
estimated GFR of the subjects was 107 19 ml/min per 1.73
m2, and there was no significant correlation between adiponectin and the estimated GFR (r 0.19; P 0.16). By
design, IR individuals, both smokers and nonsmokers, had
SSPG concentrations that were approximately three times
higher than the values in the two IS groups.
Figure 1A shows adiponectin concentrations in the 30
smokers and the 30 nonsmokers, with the IR and IS individuals in each group identified. The most obvious finding
is that the variability of plasma adiponectin concentrations
was much greater in the nonsmokers. For example, adiponectin concentrations were 20.9 g/ml or less in all smokers, whereas that value was exceeded in 20% of nonsmokers.

5004

J Clin Endocrinol Metab, December 2006, 91(12):50025007

Abbasi et al. Smoking, Adiponectin, and Insulin Resistance

TABLE 1. Clinical and metabolic characteristics of the 60 study subjects classified by smoking status and insulin resistance
Characteristic

Age (yr)
Gender (female/male)
BMI (kg/m2)
SSPG (mg/dl)

Smokers

Nonsmokers

IR (n 15)

IS (n 15)

IR (n 15)

IS (n 15)

52 9
5/10
28.2 2.9
189 39

49 6
8/7
26.7 3.1
77 15c

51 10
6/9
28.0 2.0
212 28

52 7
8/7
27.3 2.1
72 10c

P value

0.54a
0.61b
0.42a
0.001a

Data are expressed as mean SD or number of subjects.

a
P value denotes the significance of differences in means of the characteristic among the four subgroups by one-way ANOVA.
b
P value indicates the significance of differences in gender distribution among the four subgroups by 2 test.
c
P 0.001 by Tukeys post hoc test for the comparison of SSPG concentration between IR smokers and IS smokers and between IR nonsmokers
and IS nonsmokers.

Consistent with prior reports (10 13), the plasma adiponectin concentrations [mean (95% CI)] were lower in smokers
[8.6 g/ml (6.9 10.8)] than nonsmokers [11.7 g/ml (9.2
15.0)]. Adiponectin levels were also lower in IR individuals
[7.8 g/ml (6.29.7)], compared with those who were IS [13.0
g/ml (10.516.2)]. Differences in means among these
groups were compared using two-factor ANOVA with interaction. The results showed that smokers had significantly
lower (F 4.2, P 0.046) average adiponectin concentrations, compared with nonsmokers, after taking into account
differences in their insulin resistance status (significant main
effect of smoking). IR subjects on average also had significantly lower (F 11.7, P 0.001) adiponectin concentrations,
compared with IS subjects, after controlling for differences in
their smoking status (significant main effect of insulin resistance). Moreover, the differences in mean adiponectin concentrations between smokers and nonsmokers did not depend on the insulin resistance status (F 0.46, P 0.50) of
the subjects (nonsignificant smoking and insulin resistance
interaction effect). When gender and BMI were included as
covariates in the ANCOVA, the main effects of smoking and
insulin resistance on adiponectin levels remained significant
(P 0.037 and 0.008, respectively), whereas the effects of BMI
and the interaction between insulin resistance and smoking
were not. This finding indicated that after adjustment for
differences in gender, BMI, and insulin resistance status, the
mean adiponectin levels continued to be significantly lower
in smokers. Furthermore, this analysis confirmed that on
FIG. 1. Plasma adiponectin (A) and CRP concentrations (B) in
smokers (n 30) and nonsmokers (n 30). Individual (nontransformed) data for each subject are shown with IR smokers (F), IS
smokers (E), IR nonsmokers (), and IS nonsmokers () identified.
Adiponectin and CRP values were log transformed for statistical
analysis. The horizontal lines represent the geometric means of the
IR (solid line) and IS (broken line) subgroups within the main groups
of smokers and nonsmokers. a, P value indicates the significance of
the effect of smoking on adiponectin (A) and CRP (B) concentrations
after controlling for differences in insulin resistance status by twofactor ANOVA; b, P value indicates the significance of the effect of
insulin resistance on adiponectin (A) and CRP (B) concentrations
after adjustment for differences in smoking status by two-factor
ANOVA. The following data are geometric means, and their 95%
CIs are in parentheses. The adiponectin concentrations were 7.0
g/ml (4.910.1) in IR smokers, 10.6 g/ml (8.213.7) in IS smokers,
8.6 g/ml (6.311.7) in IR nonsmokers, and 15.9 g/ml (11.222.6)
in IS nonsmokers; whereas the CRP concentrations were 1.90 g/ml
(1.163.10) in IR smokers, 1.37 g/ml (1.011.84) in IS smokers,
1.43 g/ml (0.802.56) in IR nonsmokers, and 0.99 g/ml (0.59
1.65) in IS nonsmokers.

average women had higher adiponectin levels, compared

with men (P 0.002), as previously reported (35).
Figure 1B displays the CRP concentrations in smokers and
nonsmokers, again subdivided based on their classification
as IR or IS. In contrast to the data shown in Fig. 1A, the
variability in the individual values seemed comparable in
nonsmokers and smokers. The CRP values [mean (95% CI)]
were somewhat higher in the smokers [1.61 g/ml (1.22
2.12)] than nonsmokers [1.19 g/ml (0.821.72)], and there
was also a trend toward higher values among the IR subjects
[1.65 g/ml (1.152.36)], compared with those who were IS
[(1.16 g/ml (0.871.54)]. Two-factor ANOVA showed that
the average CRP concentrations were not significantly different between the smokers and nonsmokers (F 1.8, P
0.18), even after controlling for differences in their insulin
resistance status. There were also no significant differences
in average CRP concentrations between the IR and IS subjects
despite dissimilarity in their smoking status (F 2.4, P
0.13). Finally, there was no significant effect (F 0.01, P
0.92) of an interaction between smoking and insulin resistance on CRP levels.
The contribution of inflammation toward adiponectin levels was evaluated by examining the correlation coefficients
between CRP and adiponectin concentrations. The results of
this analysis showed there was no significant relationship
between adiponectin and CRP levels among smokers (r
0.05, P 0.78), nonsmokers (r 0.03, P 0.86), or the
whole group (r 0.04, P 0.74) of subjects.

Abbasi et al. Smoking, Adiponectin, and Insulin Resistance

The results in Fig. 2 display the effects of administering

pioglitazone to the two groups of smokers. By selection,
pretreatment SSPG concentrations in the IR and IS smokers
were quite different (198 42 vs. 79 13 mg/dl, P 0.001).
However, there were no differences in the age (50 10 vs.
51 5 yr, P 0.90), gender distribution (female/male, 4/8
vs. 6/2; P 0.17), or BMI (29.3 3.6 vs. 26.7 4.1 kg/m2,
P 0.15) of the two groups. After pioglitazone therapy, SSPG
significantly decreased to 142 70 mg/dl (P 0.001) in the
IR smokers but remained unchanged in the IS smokers (78
30 mg/dl, P 0.99). Plasma adiponectin levels [mean (95%
CI)] increased by 9.5 g/ml (5.516.2, P 0.001) in IR smokers and 10.0 g/ml (4.0 25.0, P 0.001) in IS smokers. It
should also be noted that the average posttreatment adiponectin concentrations in both IR smokers [14.7 g/ml (8.9
24.3)] and IS smokers [22.7 g/ml (13.737.6)] were similar
to or greater than the value in IS nonsmokers [15.9 g/ml
(11.222.6)].
Discussion

Although not a major goal of this study, we demonstrated

that the IR individuals have significantly lower plasma adiponectin concentrations than their IS counterparts, a finding
consistent with previous publications (2, 7, 36). Because there
is evidence suggesting that the prevalence of insulin resistance is increased in smokers (24, 25), it was possible that
reports of lower adiponectin concentrations in smokers (10
13) was not related to smoking, per se, but to the concomitant
presence of insulin resistance in smokers. The results of the
current study argue against this possibility and provide evidence that plasma adiponectin levels are on the average
lower in smokers and demonstrate less interindividual variability than in nonsmokers.
At the simplest level, our results are consistent with previous reports that plasma adiponectin concentrations are
lower in cigarette smokers, compared with nonsmokers (10
13). In contrast to these earlier studies, we quantified insulinmediated glucose disposal with the insulin suppression test
(30 32), a method shown to provide essentially identical

FIG. 2. Plasma adiponectin concentrations before and after

administration of pioglitazone for 3 months to IR and IS
smokers. Individual (nontransformed) data for each subject
are shown, as are the arithmetic means (bars) for the IR
smokers (A) and IS smokers (B). The change in adiponectin
concentrations was log transformed and evaluated using
paired t test in both groups.

J Clin Endocrinol Metab, December 2006, 91(12):50025007

5005

values for insulin action as the euglycemic, hyperinsulinemic

clamp technique (32), thus allowing us to account more precisely for the effect of insulin resistance when assessing the
role of cigarette smoking. The fact that mean adiponectin
concentrations in smokers were lower by 26% in the present
study, a decrease similar to the 20% decrement in adiponectin concentrations in the 311 smokers studied by Iwashima
et al. (11), lends further support for the notion that plasma
adiponcentin concentrations are lower in smokers.
Our data provide substantial evidence that differences in
the degree of insulin sensitivity have a powerful impact on
plasma adiponectin concentrations with the levels in IS individuals essentially 1.5-fold higher than those in IR subjects.
Smoking also appears to have a distinct negative effect on
plasma adiponectin concentrations because these levels were
lower in smokers than nonsmokers. Furthermore, the lower
plasma adiponectin concentrations in smokers were not dependent on the insulin resistance status of the subjects. This
indicates that the effect of smoking independently attenuates
the differences in plasma adiponectin concentrations normally present between IR and IS individuals. Finally, when
we evaluated the effects of gender and BMI on adiponectin
in ANCOVA, the mean adiponectin levels continued to be
significantly lower in smokers, compared with nonsmokers,
even after controlling for differences in gender, BMI, and
insulin resistance status.
In contrast to the impact of smoking on plasma adiponectin concentrations, we could not discern an adverse effect of
smoking on CRP concentration. Thus, although the CRP
concentrations in smokers were somewhat higher than in
nonsmokers, the differences were not statistically significant,
even after controlling for differences in their insulin resistance status. Moreover, there was no relationship between
concentrations of CRP and adiponectin in smokers. Although
these data suggest that lower adiponectin concentrations in
IR and IS smokers are not a consequence of greater systemic
inflammation, we cannot rule out the possibility that a relationship between CRP and adiponectin concentrations
might have emerged if our study population had been larger.

5006 J Clin Endocrinol Metab, December 2006, 91(12):50025007

Furthermore, we recognize that other inflammatory factors

such as TNF- and IL-6 have been associated with lower
adiponectin levels (37, 38) and may directly reduce adiponectin secretion (14 16); however, our data would appear to
indicate that if these factors are indeed relevant, they may be
operating not through systemic inflammation but via local
induction of adipose tissue inflammation.
Because cigarette smoke contains thousands of potentially
bioactive constituents, including free radicals, it is quite possible that one or more of these factors may lower adiponectin
production or release from adipocytes. For example, several
studies demonstrated that nicotine, a major component of
cigarette smoke, promotes inflammation and appears to have
direct effects on adipose tissue, inducing adipose tissue lipolysis via enhanced release of catecholamines (39 42). Consistent with this, addition of nicotine (as well as hydrogen
peroxide) to 3T3-L1 adipocytes reduced expression of adiponectin in a dose-dependent fashion (11).
Finally, the result of administrating pioglitazone to smokers once again shows that thiazolidinedione compounds will
enhance insulin sensitivity when given to nondiabetic, insulin-resistant individuals (26, 27), even if, as in this instance,
they continue to smoke. Not surprisingly, there was no significant change in SSPG concentrations in the IS smokers. In
contrast, plasma adiponectin concentrations increased significantly in both IS and IR smokers, indicating that this
therapy, whether by antiinflammatory effects on adipose
tissue or direct regulation of adiponectin gene expression
(43), can overcome the detrimental effects of smoking on
adiponectin concentrations.
In summary, at a pathophysiological level, the data presented support the concept that adiponectin concentrations
are lower in smokers (10 13), and this phenomenon does not
seem to be due to the concomitant presence of insulin resistance. These data, and other examples of discordance between adiponectin concentrations and extent of IR (26, 44
47), must be kept in mind when considering adiponectin as
a marker of IR. At a clinical level, it is obvious that smoking
cessation is the most effective way to overcome the harmful
effects of smoking. On the other hand, there are individuals
who are either unwilling or unable to stop smoking, and our
findings raise the possibility that thiazolidinedione administration may be of some clinical benefit in these situations.
This may be particularly important if future studies confirm
recent findings indicating that individuals who smoke and
have low adiponectin levels are at a substantially greater risk
for cardiovascular disease than individuals with either of
these risk factors alone (28).
Acknowledgments
Received February 23, 2006. Accepted September 19, 2006.
Address all correspondence and requests for reprints to: Peter
Reaven, M.D., Division of Endocrinology and Metabolism, Department
of Medicine (CS-111E), Carl T. Hayden Veterans Affairs Medical Center,
650 East Indian School Road, Phoenix, Arizona 85012. E-mail:
peter.reaven@med.va.gov.
This work was supported by the Tobacco-Related Disease Research
Program (12RT-0159), the National Insitutes of Health/Stanford Vascular Biology and Medicine Training Grant (5 T32 HL07708), Grant
RR-00070 from the National Institutes of Health, and resources and use

Abbasi et al. Smoking, Adiponectin, and Insulin Resistance

of the facilities at the Carl T. Hayden Veterans Affairs Medical Center

(Phoenix, Arizona).
Disclosure statement: The authors have no potential conflicts of interest to disclose.

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