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ORIGINAL ARTICLE
Adipokines in Patients With Cancer
Anorexia and Cachexia
Joanna Smiechowska, MD,*Þ Anne Utech, MS, RD, LD,Þþ George Taffet, MD,*Þ
Teresa Hayes, MD, PhD,Þ§ Marco Marcelli, MD,Þþ and José M. Garcia, MD*Þþ
Background: Anorexia, cachexia, and insulin resistance are com-
monly seen in patients with cancer. Adipocyte-derived hormones or
adipokines play a role in the regulation of appetite, body weight, and
insulin sensitivity. However, their role in cancer-induced cachexia has
not been well-established. The objective of this study was to determine
the levels of adipokines and their relation to appetite, weight loss, insulin
resistance, and other hormones in cancer cachexia.
Methods: We measured adiponectin, resistin, and leptin plasma levels
in 21 men with cancer cachexia, 24 noncachectic cancer subjects, and 25
noncancer controls matched by age, sex, and pre-illness body weight.
Body weight change, appetite scores, insulin resistance assessed by
homeostasis model assessment, and other cytokines and hormones were
also measured. Differences between groups were measured by analysis
of covariance. Relations between variables were examined by linear
regression analyses.
Results: Adiponectin levels were similarly elevated in cachectic and
noncachectic cancer patients compared with noncancer controls. Leptin
levels were significantly decreased in cancer cachexia and were directly
associated with appetite and insulin resistance, explaining 37% and 19%
of the variance seen in cancer patients, respectively. Resistin levels were
not different between groups.
Conclusions: Leptin may play a role in the increased insulin resistance
seen in cancer patients. However, these patients are resistant to the
orexigenic effects of hypoleptinemia. Other mechanisms besides weight
loss are responsible for the increased adiponectin level seen in cancer
patients. It is unlikely that resistin plays a major metabolic role in this
setting.
Key Words: weight loss, cytokines, IL-6, TNF->, ghrelin, leptin,
adiponectin, resistin
(J Investig Med 2010;58: 554Y559)
BACKGROUND
Adipose tissue is increasingly being recognized as an im-
portant endocrine organ that plays a role in the regulation of
body weight, food intake, and insulin resistance by producing
hormones known collectively as adipokines. In healthy individ-
From the *The Huffington Center on Aging, Baylor College of Medicine;
†Michael E. DeBakey Veterans Affairs Medical Center; and ‡Division of
Diabetes, Endocrinology and Metabolism, Department of Medicine, and
§Department of Oncology, Baylor College of Medicine, Houston, TX.
Received August 18, 2009, and in revised form November 2, 2009.
Accepted for publication December 12, 2009.
Reprints: José M. Garcia, MD, MEDVA Medical Center, 2002 Holcombe
Blvd, Houston, TX 77030. E-mail: jgarcia1@bcm.edu.
This work is partly supported by The Huffington Center on Aging, Baylor
College of Medicine. Dr Garcia receives support from a MERIT Review
Entry Program Grant from the Department of Veterans Affairs and a
South Central VA Healthcare Network Career Development Award from
the Department of Veterans Affairs.
The authors have no financial disclosures related to this work.
Copyright * 2010 by The American Federation for Medical Research
ISSN: 1081-5589
DOI: 10.231/JIM.0b013e3181cf91ca
554 Journal of Investigative Medicine
Copyright @ 2010 American Federation for Medical Research. Unauthorized reproduction of this article is prohibited.
uals, a decrease in fat mass induced by caloric restriction (diet)
or by an increase in energy expenditure (ie, exercise) improves
insulin sensitivity. However, this is also accompanied by a com-
pensatory increase in appetite that often leads to weight regain.
These changes in insulin sensitivity and appetite are thought to be
mediated at least partially by changes in inflammatory markers
and the adipokines leptin, adiponectin, and resistin.1,2
Leptin is a known satiety factor secreted proportionally to the
amount of fat mass and related to insulin resistance.3 Moreover,
leptin administration induces anorexia and weight loss. In contrast,
adiponectin has been shown to stimulate appetite in rodents, and
its circulating levels are inversely related to body weight.1 Resistin
is known to stimulate insulin resistance in mice. The role of resistin
is less clear in humans, but it has been suggested that it also plays a
role in energy homeostasis.4
Cachexia (a complex metabolic syndrome associated with
underlying illness and characterized by loss of muscle with or
without loss of fat mass5) is common in patients with cancer,6 and
it is usually the result of lean and fat mass losses. Unlike what is
seen in diet-induced weight loss, cancer cachexia patients have
diminished appetite, food intake, and insulin sensitivity.7 Despite
the significant impact that cachexia and anorexia have on these
patients’ quality of life, the mechanisms underlying these symp-
toms are not fully understood.
In this study, we sought to determine the levels of adipokines
and the relation between adipokines, insulin resistance, and other
inflammatory markers in subjects with cancer anorexia and ca-
chexia compared with noncachectic cancer patients and non-
cancer controls.
MATERIALS AND METHODS
Protocol and Experimental Subjects
The protocol was approved by the Baylor College of
Medicine Institutional Review Board. All clinical investigation
described was in accordance with the Declaration of Helsinki.
Informed consent was obtained from subjects before enrollment.
The study included 3 groups:
1. Patients with cancer and cachexia, defined as an uninten-
tional weight loss of at least 5% of their pre-illness body
weight over the previous 6 months (n = 21).
2. Noncachectic cancer patients, with stable body weight,
matched by age, sex, race, pre-illness body mass index
(BMI), and cancer staging to the previous group (n = 24).
3. Subjects without cancer with a stable body weight, matched
by age, sex, race, and BMI to the other 2 groups (n = 25).
The inclusion criteria were male sex, 18 years or older,
weight loss of 5% or more over the previous 6 months for the
cachectic subjects and 2% or less for the other groups, and
diagnosis of cancer other than nonmelanoma skin cancer for the
cancer groups.
The exclusion criteria were blood malignancies or can-
cer involving the upper airway or upper gastrointestinal tract,
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Journal of Investigative Medicine & Volume 58, Number 3, March 2010 Adipokines in Cancer Cachexia

dysphagia, substance abuse, heart failure, severe liver disease, groups were measured by analysis of covariance. Relations
chronic obstructive pulmonary disease, diabetes with hemo- between continuous variables were examined by linear regres-
globin level A1c higher than 7%, fasting glucose level higher than sion analyses. P values were 2-sided, and a P e 0.05 was
140 mg/dL or random glucose level higher than 200 mg/dL, thy- considered statistically significant. All the calculations were
roid disease, renal failure, active infection, use of glucocorticoids, performed using SPSS version 12.00 (SPSS Inc, Chicago, IL).
use of progesterone, testosterone or other orexigenic agents, his- Linear regression was used to test weight change pro-
tory of eating disorders, and history of cancer other than non- spectively (expressed as percentage of change from baseline
melanomatous skin cancer for the control group. to 12 months) as a secondary analysis. Weight change percent
Appetite was measured fasting in the morning at the time of was conceptualized as the outcome, and the predictors leptin,
blood draw by a visual analogue scale taken from the Edmonton adioponectin, and resistin levels were individually entered into the
Symptom Assessment System: BHow would you describe your regression analyses. Other predictors (TNF->, IL-6, HOMA-IR,
appetite?[ that ranged from 0 to 100 mm with words anchored at ghrelin, and IGF-1) were added in a separate stepwise fashion to
each end, expressing the most positive and negative ratings test for significance. Inclusion was set at probability F G 0.05, and
(where 0 was Bno appetite[ and 100 was Bvery good appetite[). exclusion was set at F 9 0.10. One-tailed correlations were used
This visual analogue scale for appetite is used extensively in the during these tests, with > = 0.05.
setting of cancer-induced cachexia and correlates well with 1-
and 7-day scores in test-retest evaluations.8Y10 RESULTS
Fasting blood samples were obtained by 0900 hours. Insu- All the groups were matched for age, BMI 6 months before
lin sensitivity was assessed using the homeostasis model assess- recruitment, race, and proportion of subjects with diabetes.
ment (HOMA-IR = fasting glucose (mmol/L)  fasting insulin Results for acylated ghrelin, peptide YY, IGF-1, IL-6, TNF->,
[KU/mL] / 22.5) as previously described. These estimates correlate insulin, HOMA-IR, appetite, and weight loss have been
well with the criterion standard hyperinsulinemic euglycemic published previously.12 The groups differed in their BMI at the
clamp method (r = 0.88, P G 0.0001).11 time of recruitment because weight loss was an inclusion
criterion for the cachectic group and an exclusion criterion for
Hormone Assays the other groups (Table 1). The cancer diagnoses for the
Blood was collected in EDTA-containing tubes and kept at cachectic group were small cell carcinoma of the lung (SCLC,
4-C during processing. Plasma was stored at j80-C until n = 8), colon cancer (n = 4), adenocarcinoma of the prostate
assayed. Adiponectin level was measured by radioimmunoassay (n = 3), nonYSCLC (NSCLC, n = 2), renal cell carcinoma
(RIA) with a commercially available kit purchased from Linco (n = 1), fibrosarcoma (n = 1), adenocarcinoma of unknown
Research (St Charles, MO) in diluted plasma samples (1:450) as origin (n = 1), and squamous cell carcinoma of unknown origin
indicated by the manufacturer. The lower and upper detection
limits were 1.56 and 200 Kg/mL, respectively. Resistin level was
measured by the enzyme-linked immunosorbent assay accord-
ing to the protocol provided by the manufacturer (Biovendor, TABLE 1. Baseline Characteristics
Candler, NC). The lower and upper detection limits were 1 and
50 ng/mL, respectively. Leptin level was measured by RIA Cancer Cancer
(Linco Research) following the manufacturer’s instructions. Cachexia Noncachexia Controls
Acylated ghrelin levels were measured by a commercially (n = 21) (n = 24) (n = 25) P
available RIA kit from Linco Research in plasma treated with 1-N Age, mean (SD), yr 66 (8) 69 (11) 64 (12) 0.67
hydrochloric acid and phenylmethylsulfonyl fluoride added im- Race, n (%) 0.92
mediately after collection. This RIA kit uses an antibody raised
White 12 (57) 14 (58) 17 (68)
in guinea pig against octanoylated ghrelin and 125I-octanoylated
African 8 (38) 8 (33) 6 (24)
ghrelin as the tracer. This assay has been found to be highly
American
specific for acylated ghrelin with lower than 0.1% cross reactivity
Other 1 (4.8) 2 (8.4) 2 (8)
for des-octanoyl ghrelin and no cross reactivity with ghrelin
14Y28, motilin-related peptide, leptin, insulin, glucagon, or glu- Initial BMI, 27.5 (4) 27 (4) 28.5 (3) 0.4
mean (SD)
cagonlike peptide 7Y36. The lower and upper detection limits were
10 and 2000 pg/mL, respectively. The intra-assay coefficient Final BMI, 24 (4) 28 (4) 30 (4) 0.001
mean (SD)
of variation was 5.3%. Insulin levels were measured by a RIA
kit purchased from Linco Research. Insulinlike growth factor Staging, n(%) 0.12
1 (IGF-1) levels were extracted using acid-methanol and measured I 3 (13)
by a RIA kit from Nichols Laboratories (San Juan Capistrano, II 3 (15) 7 (29)
CA). The measurements of the circulating levels of interleukin III 3 (15) 5 (21)
6 (IL-6) and tumor necrosis factor > (TNF->) were performed at IV 14 (70) 9 (38)
the Michael E. DeBakey Veterans Affairs Medical Center as we Chemotherapy*, 14 (67) 18 (75) 0.74
have previously described.12 For all hormones, plasma from an n (%)*
equal number of subjects from each group was included in the first Current 9 (42) 9 (36) 0.59
assay, and the remaining samples were assayed in a second assay chemotherapy,
to minimize interassay variability in hormone levels between the n (%)†
groups. Time to diagnosis, 627 (1018) 1324 (1366) 0.06
mean (SD), d
Statistical Analyses *Patients who had received chemotherapy at any time point before
Continuous variables are expressed as mean (SEM). enrollment.
Nonnormally distributed data (leptin, resistin, and adiponectin) †Patients receiving chemotherapy at the time of enrollment.
were log transformed before analysis. Differences between the

* 2010 The American Federation for Medical Research 555

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Smiechowska et al Journal of Investigative Medicine
(n = 1). For the noncachectic group, the diagnoses were
adenocarcinoma of the prostate (n = 10), NSCLC (n = 6), SCLC
(n = 3), adenocarcinoma of unknown origin (n = 1), bladder
cancer (n = 1), chondrosarcoma (n = 1), breast cancer (n = 1),
and melanoma (n = 1). However, the difference in cancer
diagnoses did not reach significance (P = 0.09). There was also a
trend toward a more advanced stage (P = 0.12) and shorter
duration of disease (P = 0.06) in the cachectic group, although it
did not reach significance. The 2 groups were comparable
regarding the proportion of subjects receiving chemotherapy
(Table 1).
The appetite scores were also lower for cancer cachexia
subjects compared with the cancer noncachexia subjects and the
controls (21.1 [3], 48 [3], and 49 [3], respectively; analysis of
variance, P G 0.001), and insulin resistance as measured by
HOMA-IR was elevated in cancer noncachexia subjects
compared with the other 2 groups (8.5 [0.94%], 4.67 [0.94%],
and 5.22 [0.92%], respectively; analysis of variance, P G 0.02).
Adipokine Levels
The adiponectin levels were significantly higher in both
groups of subjects with cancer when compared with the noncancer
controls. However, there was no difference between the 2 cancer
groups (Fig. 1). The adiponectin levels were not correlated with
IL-6 or TNF-> levels (r = 0.18, P = NS or r = j0.12, P = NS,
respectively). The leptin levels were significantly decreased in
cancer cachexia compared with the other 2 groups (Fig. 2), and
they correlated negatively with IL-6 (r = j0.46, P G 0.005) but not
with TNF-> (r = 0.21, P = NS). The resistin levels were similar
between the groups (Fig. 3, P = 0.14) and were not correlated with
the IL-6 or TNF-> levels (r = 0.25, P = 011 or r = 0.26, P = 0.09,
respectively). These results persisted after adjusting for BMI and
cancer staging.
Adipokines, Body Weight Changes, Appetite,
and Insulin Resistance
We used simple linear regression analyses to establish the
relationship between adipokines and other hormones regarding
body weight, weight loss, appetite, and insulin resistance in the
2 cancer groups (Table 2). Leptin, adiponectin, IGF-1, and
insulin were significantly associated with body weight. Leptin,
IL-6, ghrelin, IGF-1, and insulin were associated with appetite
and weight change, whereas only leptin and IGF-1 were asso-
ciated with insulin resistance. When multiple linear regres-
sion analysis models were used including parameters with
significant correlations in univariate analyses, leptin and IL-6
FIGURE 1. Adiponectin levels in the cancer cachexia, cancer
noncachexia, and noncancer control subjects. *P G 0.05 when
compared with the control group.
556
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& Volume 58, Number 3, March 2010
FIGURE 2. Leptin levels in the cancer cachexia, cancer
noncachexia, and noncancer control subjects. *P G 0.05 when
compared with the control group. §P G 0.05 compared with
the cancer cachexia group.
levels remained significantly associated with anorexia, acylated
ghrelin and IL-6 were associated with weight loss, and only
leptin was associated with body weight and insulin resis-
tance. Adiponectin and resistin were not associated with any of
the 4 dependent variables (body weight, body weight change,
appetite, and insulin resistance) on multiple regression analysis
(Table 3).
Prospectively, the weight change percent between the base-
line and more than 12 months in the cancer cachectic versus
noncachectic groups was not significantly predicted by baseline
levels of leptin (F1,26 = 0.204, P = 0.655), adiponectin
(F1,21 = 3.28, P = 0.084), or resistin (F1,26 = 0.12, P = 0.915).
Baseline adiponectin level was negatively correlated (R = j0.368,
P = 0.42) with weight change percent, however. The stepwise
regression analysis did not find any significant predictive value nor
correlations of TNF->, IL-6, HOMA-IR, ghrelin, nor IGF-1 with
weight change percent (data not shown). Similarly, nonsignificant
results were found when all the 3 subject groups (adding controls)
were entered into the equation (data not shown).
DISCUSSION
Cachexia affects 50% of cancer patients, worsening their
quality of life and survival. Paradoxically, the weight loss seen in
this setting does not cause an increase in appetite and insulin
sensitivity usually seen in noncancer subjects losing weight
voluntarily. It is thought that adipokines play a role in regulating
FIGURE 3. Resistin levels in the cancer cachexia, cancer
noncachexia, and noncancer control subjects. P = 0.14.
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Journal of Investigative Medicine & Volume 58, Number 3, March 2010 Adipokines in Cancer Cachexia

TABLE 2. Simple Linear Regression Analysis Between Adipokines and Body Weight, Weight Loss, Anorexia, and Insulin Resistance

Body Weight Weight Change Appetite Score HOMA-IR

Parameter r P r P r P r P
Leptin 0.87 G0.001 0.55 G0.001 0.60 G0.001 0.44 0.003
Adiponectin j0.36 0.03 j0.19 0.27 j0.23 0.18 j0.18 0.29
Resistin 0.19 0.23 0.16 0.31 j0.21 0.18 0.001 0.99
Acylated ghrelin j0.25 0.1 j0.54 G0.001 j0.37 0.01 j.13 0.39
IL-6 j0.26 0.08 j0.5 G0.001 j0.51 G0.001 j0.16 0.29
TNF-> 0.2 0.18 0.01 0.97 j0.11 0.47 j0.2 0.18
Peptide YY 0.15 0.34 0.18 0.25 0.10 0.53 j0.02 0.88
IGF-1 0.44 0.003 0.38 0.01 0.40 0.008 0.34 0.02
Insulin 0.51 G0.001 0.32 0.03 0.44 0.003
P G 0.05 appear in bold.

appetite and insulin resistance in other settings, but their role in weight loss.22,23 Recently, resistin level was found to be higher in
cancer cachexia is not well defined. cachectic compared with noncachectic lung and stomach cancer
The role of adiponectin in the setting of cancer is contro- patients24 and in esophageal cancer patients compared with non-
versial, and its relationship with anorexia has not been well cancer controls.13,25 In our study, resistin levels were comparable
established. Although subjects with obesity-related cancers have between cancer cachexia, cancer without cachexia, and noncancer
lower adiponectin levels at the time of diagnosis in some but not controls. This discrepancy could be explained by our smaller
all reports,13,14 this is not the case in lung or prostate cancer sample size, but other contributing factors such as the more severe
patients.15,16 In this study, we found increased adiponectin levels anorexia usually seen in esophageal or gastric cancer patients may
in cancer cachexia subjects compared with noncancer controls. have also played a role. Nevertheless, the fact that weight loss,
We expected these changes in cachectic subjects because weight appetite, and insulin resistance were not associated with resistin
loss is associated with increased adiponectin levels in non- levels suggests that it is unlikely that resistin plays a major meta-
cancer subjects.17 However, adiponectin levels were also ele- bolic role in this setting.
vated in cancer subjects without cachexia, suggesting that other
mechanisms besides weight loss are responsible for the in-
creased adiponectin levels in this setting. Although adiponectin
was inversely related to body weight, it was not a significant TABLE 3. Multivariate Analyses for Appetite, Body Weight,
predictor of weight change, appetite, or insulin resistance in this HOMA-IR, and Weight Change in Cancer Patients
population.
Given adiponectin’s antiproliferative properties,18 it is pos- Dependent Regression
sible that this increase in adiponectin levels may represent a Variable Variable Coefficient, A SE P
compensatory response present in subjects with advanced cancer Appetite Constant 2.66 0.77 0.001
aimed at controlling the disease. On the other hand, several Leptin level 0.77 0.31 0.01
publications recently have indicated that adiponectin may have
IL-6 level j0.03 0.01 0.01
proangiogenic properties in animal models of cancer19 or under
caloric restriction.20 Hence, the increase in adiponectin in this IGF-1 level 0.003 0.004 0.52
setting could be a marker of increased proangiogenic environ- Insulin level 0.009 0.014 0.5
ment in the presence of cancer. Further studies are needed to test Body weight Constant 20 2.46 0.001
these hypotheses and to clarify the role of adiponectin in this Leptin level 3.43 0.61 0.001
setting. Adiponectin level j0.78 0.79 0.33
Adiponectin’s orexigenic properties in rodents raise the IGF-1 level 0.01 0.01 0.32
possibility that this pathway may be a therapeutic target for Insulin level 0.01 0.04 0.66
anorexia and cachexia in the setting of cancer.1 Although our HOMA-IR Constant j5.45 45.56 0.9
data does not support the hypothesis that low adiponectin levels Leptin level 55.26 24.47 0.02
contribute to anorexia in this setting given the lack of correlation
IGF-1 level 0.35 0.37 0.34
with anorexia and that endogenous adiponectin levels are
already elevated, investigation of this pathway is warranted Weight change Constant j1.78 3.46 0.61
because further activation of the adiponectin receptor may still Acyl-ghrelin level j0.05 0.01 0.002
prove useful in the same way that exogenous ghrelin adminis- IL-6 level j0.11 0.04 0.01
tration increases appetite and food intake in cancer subjects Leptin level 2.57 1.39 0.07
despite their high endogenous ghrelin levels.12,21 Insulin level j0.02 0.06 0.73
Resistin, a product of white adipose tissue in mice and of IGF-1 level 0.02 0.01 0.21
mononuclear cells in humans, is associated with insulin resistance
Multiple linear regression analysis models include those predictors
and obesity, but its relationship with weight change is not clear. with significant correlations in univariate analyses. Significance appears
Some authors have reported a decrease in circulating resistin level, in bold.
whereas others have found an increase in its levels in response to

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Smiechowska et al Journal of Investigative Medicine
Leptin suppresses appetite in other settings, and lack of
leptin or defects in leptin signaling are associated with hyper-
phagia and massive obesity.26,27 In agreement with previous
reports, the leptin level was significantly lower in our cachectic
patients compared with noncachectic cancer subjects and healthy
controls.28 This is expected because leptin is secreted by adipo-
cytes in proportion to fat mass and excludes leptin excess as
a cause for anorexia in this setting. We also found leptin level
to be directly associated with appetite, explaining 37% of the
variance seen in cancer patients. That these patients are resistant
to the orexigenic effects of hypoleptinemia has been proposed
before.29 Our findings that leptin is inversely associated with
appetite in this setting is novel and further supports this hy-
pothesis. We also found leptin level to be directly associated
with insulin resistance, explaining 19% of the variance seen in
cancer patients. These findings suggest that leptin also may play
a role in the increased insulin resistance seen in noncachectic
cancer subjects.
Several in vivo studies in rodent models suggest that the
increase in proinflammatory cytokines may be responsible for the
decrease in appetite and food intake in this setting by acting
centrally.30,31 Our findings support this hypothesis because IL-6
remained a significant predictor of anorexia in multivariate
analysis. The leptin receptor is part of the cytokine receptor
superfamily and activates several pathways that are normally
activated by IL-6 such as the c-Jun N-terminal kinase pathway.32
It is possible that this increase in cytokines may also be
responsible for the failure of low leptin levels to increase appetite
in this setting.29,33
Baseline laboratory values (leptin, adiponectin, resistin,
TNF->, IL-6, HOMA-IR, ghrelin, and IGF-1) did not predict
weight change percent in the following 12 months after the initial
data collection. These results may be limited to interpretation
because only baseline laboratory values were available, whereas
weights were followed prospectively. Adiponectin level was
negatively correlated with weight change percent, however, when
all the groups were analyzed and when just cancer cachectic
subjects were compared with cancer noncachectic subjects. In the
future, it would be useful to measure changes in adiponectin
levels over time to study this relationship further, for reasons
previously explained.
Limitations of our study include the small sample size
and the heterogeneity in cancer diagnosis that could explain
the lack of difference in resistin levels. Given the biological
differences between visceral and subcutaneous fat regard-
ing production of adipokines, assessing body composition by
computed tomography or magnetic resonance imaging would
have been useful in determining the association between dif-
ferent fat deposits and the level of these hormones. Although
HOMA-IR correlates well with hyperinsulinemic euglycemic
clamp, most of the data comes from large epidemiological
studies. The use of the clamp technique would have provided
stronger support to the clinical relevance of the HOMA-IR
data. These issues should be considered in the design of future
studies.
In summary, adiponectin level was not associated with
appetite or insulin resistance in this group of men with cancer, but
it was higher in the cachectic and noncachectic cancer patients
compared with that in the noncancer controls. This suggests that
other mechanisms besides weight loss are responsible for these
differences. Leptin is a marker for anorexia and insulin resistance
in cancer patients. It is unlikely that resistin plays a major
metabolic role in this setting.
A better understanding of the mechanisms regulating
appetite and body weight may help with the development of
558
Copyright @ 2010 American Federation for Medical Research. Unauthorized reproduction of this article is prohibited.
& Volume 58, Number 3, March 2010
new therapies that could prolong survival and increase quality of
life in these patients.
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Adipokines in Patients With Cancer

Anorexia and Cachexia
Joanna Smiechowska, Anne Utech, George Taffet, Teresa Hayes,
Marco Marcelli and José M. Garcia

J Investig Med 2010 58: 554-559

doi: 10.2310/JIM.0b013e3181cf91ca

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