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Department of Internal Medicine (W.-S.Y., C.-L.C., T.-Y.T., L.-M.C.), Graduate Institute of Clinical Medicine (W.-S.Y., L.-M.C.), College of Medicine, and Institute of Epidemiology (C.-L.C.), College of Public Health, National Taiwan University, Taipei 100; Department of Surgery (W.-J.L.), En Chu Kong Hospital, Taipei Hsien 237, Taiwan; and Department of Internal Medicine and Molecular Science (T.F., S.T., Y.M.), Graduate School of Medicine, Osaka University, 565-0871, Osaka, Japan
Address all correspondence and requests for reprints to: Lee-Ming Chuang, M.D., Ph.D., Department of Internal Medicine, National Taiwan University Hospital, 7 Chung-Shan South Road, Taipei 100, Taiwan. E-mail: leeming{at}ha.mc.ntu.edu.tw
Abstract
Adiponectin, an adipose tissue-specific plasma protein, was recently revealed to have anti-inflammatory effects on the cellular components of vascular wall. Its plasma levels were significantly lower in men than in women and lower in human subjects with obesity, type 2 diabetes mellitus, or coronary artery disease. Therefore, it may provide a biological link between obesity and obesity-related disorders such as atherosclerosis, against which it may confer protection. In this study, we observed the changes of plasma adiponectin levels with body weight reduction among 22 obese patients who received gastric partition surgery. A 46% increase of mean plasma adiponectin level was accompanied by a 21% reduction in mean body mass index. The change in plasma adiponectin levels was significantly correlated with the changes in body mass index (r = -0.5, P = 0.01), waist (r = -0.4, P = 0.04) and hip (r = -0.6, P = 0.0007) circumferences, and steady state plasma glucose levels (r = -0.5, P = 0.04). In multivariate linear regression models, the increase in adiponectin as a dependent variable was significantly related to the decrease in hip circumference (ß = -0.16, P = 0.028), after adjusting body mass index and waist circumference. The change in steady state plasma glucose levels as a dependent variable was related to the increase of adiponectin with a marginal significance (ß = -0.92, P = 0.053), after adjusting body mass index and waist and hip circumferences. In conclusion, body weight reduction increased the plasma levels of a protective adipocytokine, adiponectin. In addition, the increase in plasma adiponectin despite the reduction of the only tissue of its own synthesis suggests that the expression of adiponectin is under feedback inhibition in obesity.
OBESITY IS A pan-endemic health problem in both developed and developing countries. It increases risk for many common diseases, including coronary artery disease (CAD), type 2 diabetes mellitus (DM), hypertension, gallbladder disease, and osteoarthritis (1). Consequently, obesity increases total mortality (2, 3). Despite that its deleterious health effects are well recognized, how obesity is biologically linked to the pathogenesis of these disorders, especially atherosclerosis, remains obscure.
Adipose tissue, long being misconstrued as a mere tissue of fat
storage, is now acknowledged to be an active participant in energy
homeostasis and other physiological functions. The term
"adipocytokines" was recently coined to describe the
adipose-derived bioactive factors that modulate the physiological
functions of the other tissues in our body (4, 5). Some
well known examples among these factors include leptin, plasminogen
activator inhibitor-1, and TNF
(6, 7, 8). It is
highly possible that some of the adipocytokines may, in fact, mediate
the systemic effects of obesity on health.
One of the most abundant adipose tissue-specific adipocytokines,
adiponectin, was recently shown to modulate a wide array of biological
functions (9, 10). Adiponectin has been shown to reduce
TNF-induced monocyte attachment to cultured human aortic endothelial
cells by inhibiting the expression of vascular cell adhesion
molecule, intercellular adhesion molecule, and E-selectin in
endothelial cells (11). A cross-talk between adiponectin
and TNF-induced nuclear factor 
B signaling may be mediated
through cAMP-protein kinase A pathway (12).
Furthermore, adiponectin was demonstrated to suppress phagocytic
activity and lipopolysaccharide-induced TNF production in cultured
macrophages (13). It may also induce apoptosis of cells in
myelomonogenic lineages (13). Taken together, these
studies suggest that adiponectin may have anti-inflammatory effects,
especially in endothelial cells and macrophages. In animal model,
adiponectin was detected only in catheter-injured vessel wall, but not
in intact vessels (14). The plasma levels of adiponectin
were also demonstrated to be lower in men than in women and lower in
subjects with obesity, CAD, and type 2 DM as well (11, 15, 16). For example, mean plasma adiponectin levels were 3.7
µg/ml and 8.9 µg/ml, respectively, for obese [mean body mass index
(BMI), 31.9 kg/m2] and nonobese (mean BMI, 22.8
kg/m2) subjects in a previous study
(15). These observations indicate that adiponectin may be
a protective adipocytokine against atherosclerosis. Therefore, any
measure that could be taken to increase adiponectin may be
beneficial.
Expression of adipoQ, the mouse homologue of adiponectin, was
detectable by Northern blot on d 4 during the differentiation of 3T3-L1
fibroblasts into adipocytes (17). We have also shown that
the steady state mRNA of adipoQ was increased in 3T3-L1 adipocytes
after 24-h treatment of a peroxisome proliferator-activated receptor
agonist, rosiglitazone (18). However, plasma
adiponectin levels were found to be lower in obese human subjects
(15). In ob/ob mice, the steady state mRNA of adipoQ was
found to be down-regulated as well (17). It is
plausible that the expression of adiponectin is activated during
adipogenesis, but a feedback inhibition on its production may be
imposed in the development of obesity. In fact, the expression of
adipogenic genes was recently reported to decrease in the development
of obesity in mice (19).
In this study, we have intended to observe the changes of plasma adiponectin levels with body weight loss in obese patients who received gastric partition surgery (20). First, we argued that a significant increase of this anti-inflammatory protein might at least partially explain the beneficial effects of weight reduction (21, 22). Second, we argued that if adiponectin were under feedback inhibition in obesity, body weight loss would also result in an increase of its plasma levels, despite losing the tissue of synthesis.
Subjects and Methods
Subjects
Twenty-two severely obese patients (age, 34.0 ± 11.4 yr old; 15 females and 7 males) who met the criteria for surgery according to the NIH consensus were recruited for this study (23). All patients were evaluated with series of physical examination and routine tests for hematology, biochemistry, electrolytes, cardiopulmonary functions, and endocrine functions (including thyroid-stimulating hormone, T4), and plasma glucose concentrations. Gastric partition surgery was performed at En-Chu-Kong Hospital, Taipei Hsien, as described previously (20). Written informed consent was obtained from each individual, and the study was reviewed and approved by the Institutional Review Board.
Biochemical measurements
A 75-g oral glucose tolerance test (OGTT) and an insulin suppression test were given to all subjects before and 3–12 months after the surgery on two separate days after overnight fasting. The insulin suppression test was used to assess insulin-mediated glucose disposal as reflected by the steady state plasma glucose (SSPG) as described previously (24). The concentrations of plasma glucose, total cholesterol, and triglyceride were measured in fasting samples by an autoanalyzer (Hitachi 7250 special; Hitachi, Tokyo, Japan). Serum insulin levels were determined by a microparticle enzyme immunoassay using AxSYM system from Abbott Diagnostics (Abbott Laboratories, Dainabot Co. Ltd., Tokyo, Japan). The homeostasis model assessment is applied to estimate the degree of insulin resistance [HOMA IR = Insulin/22.5e-In(Glucose)] and ß cell function [HOMA ß = 20x Insulin/(Glucose - 3.5)], where insulin in pmol/liter and glucose in mM (25). Plasma levels of adiponectin were determined by an ELISA system as described (15). All the measurements, except those of adiponectin, were presented in System International units because the molecular weight of adiponectin has not been precisely determined.
Statistical analyses
Data were presented in means and SD. Statistical analyses including paired t test, correlation analysis, and multivariate linear regression analysis were performed by using the PC version of the Statistical Analysis System (6.12 edition; SAS Institute, Inc., Cary, NC). Differences in selected clinical characteristics between those before and after the gastric partition surgery were tested by paired t test. Correlation matrix of all the changes in clinical characteristics and changes in plasma adiponectin levels before and after the surgery was performed. Several multivariate linear regression models were performed that included age, gender, changes in plasma adiponectin levels, BMI, waist circumference, and hip circumference as independent variables; and changes in plasma adiponectin levels and SSPG as dependent variables, respectively.
Results
Twenty-two obese patients received gastric partition surgery and
were followed for a mean of 7.7 (±3.5) months. The changes of selected
characteristics in these patients are shown in Table 1
. Reductions in body weight, BMI, waist
circumference, hip circumference, and waist to hip ratio were 23.3 kg
(±11.5), 8.35 kg/m2 (±3.8), 19.5 cm (±13.0),
13.9 cm (±7.6), and 0.02 (±0.02), respectively. The differences
between the means of these variables before and after surgery were
highly significant.
|
). Mean fasting plasma
insulin level (119.8 ± 80.4 pmol/liter) was significantly
reduced, whereas the changes of 2-h postglucose load plasma insulin and
AUC of plasma insulin were not statistically significant. In fact, the
AUC of plasma insulin slightly increased with body weight loss, mainly
due to the elevated insulin levels at 1 h during an OGTT. This
indicates that insulin secretion in response to glucose stimulation was
not impaired with weight reduction. On the other hand, the significant
decrease both in insulin resistance index (7.46 ± 6.53) by HOMA
and in SSPG (1.54 ± 3.38 mmol/liter) was consistent with
increased insulin sensitivity with weight reduction among these obese
subjects. Significant changes with weight loss among the other
variables included reduction in plasma triglyceride levels and systolic
blood pressure.
Along with all the changes described above, plasma levels of
adiponectin were increased by a mean of 2.1 (±1.8) µg/ml (46% of
the mean presurgical level) with a 21% reduction in BMI (Table 1). The
change in plasma levels of adiponectin was significantly correlated
with those of BMI ( = -0.5, P = 0.01), waist
circumference ( = -0.4, P = 0.04), hip
circumference ( = -0.6, P = 0.0007), and SSPG
( = -0.5, P = 0.04) (Fig. 1). In a multivariate linear regression
model, the change of plasma adiponectin levels as a dependent variable
was significantly related to hip circumference only, while adjusting
age, sex, changes in BMI, and waist circumference (Table 2). Before adjusting changes in waist and
hip circumferences, the change in BMI was also significantly related to
that of plasma adiponectin (data not shown). On the other hand, the
change in SSPG as the dependent variable was related to the change of
plasma adiponectin with a marginal statistical significance, while
adjusting age, sex, and changes in BMI, and waist and hip
circumferences (Table 2).
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Adiponectin is an adipose tissue-specific plasma protein. It was
recently demonstrated to modulate a variety of biological functions
(11, 12, 13). It decreased TNF-induced macrophage
attachment to endothelial cells by reducing the expression of adhesion
molecules in endothelial cells through protein kinase A-mediated
interference of nuclear factor B signaling (11, 12). It
was also shown to suppress TNF production and phagocytic activity in
macrophages (13). These indicate that adiponectin has
anti-inflammatory properties. In addition, adiponectin was detectable
in catheter-injured vessel wall, rather than in intact vessels in
animal models (14). This suggests that it may participate
in the pathogenesis of atherosclerosis. In fact, it was documented that
lower levels of plasma adiponectin was associated with CAD and risk
factors of CAD, including male sex, obesity, and type 2 DM (11, 15, 16). Therefore, adiponectin provides a direct biological
link between obesity and atherosclerosis. Body weight loss, a common
medical practice to reduce the risk of CAD, type 2 DM, and
hypertension, would be expected to increase plasma adiponectin levels,
if it were to mediate the beneficial effects of weight reduction. In
this study, we demonstrated that this was indeed the case.
Recently, it was demonstrated that iv injection of the C-terminus globular domain of the mouse homologue of adiponectin reduced plasma fatty acid levels and diet-induced weight gain in mice (26). This indicates that adiponectin may participate in fatty acid and energy homeostasis. We observed a significant decrease in triglyceride levels after weight reduction in this study. Whether this is in part caused by altered fatty acid metabolism secondary to the increase in plasma adiponectin remains unknown. We did not assay plasma fatty acid levels in this study.
In obesity, plasma adiponectin levels were lower despite that adipose tissue is the only tissue of its synthesis, suggesting a negative feedback on its production. Consequently, body weight reduction would result in at least transient disinhibition, therefore, an elevation of plasma adiponectin. Recent demonstration by microarray that the expression of adipogenic genes was suppressed in the development of obesity and DM in mice argues for the existence of a feedback inhibitory pathway (19). In addition, the expression of adipoQ, the mouse homologue of adiponectin, and adiponectin was down-regulated, respectively, in ob/ob obese mice and in obese human subjects (17). This is also consistent with the existence of a negative feedback pathway.
The mechanisms of regulating plasma adiponectin levels by body weight change are still not known. The fact that the steady state mRNA of adipoQ (the mouse homologue of adiponectin) decreased in ob/ob mice compared with those of wild type indicates that the level of regulation is, in part, at transcription or mRNA stability (17). It was also shown that the steady state mRNA of adiponectin in adipose tissue seems to be reduced in obese human subjects (17). Because the weight reduction in this study was accomplished by gastric partition surgery, it is highly possible that some neuro-hormonal factors, especially gut peptides like gastrin, cholecystokinin, and so on, may be involved in regulating the expression of adiponectin expression. Exactly what biological signals that modulate the expression of adiponectin during weight reduction merit further studies. So far, the only hormone known to regulate adiponectin expression is insulin (27).
In this study, we also showed that elevation of plasma adiponectin
levels was correlated with the change in SSPG. In multivariate linear
regression model, the change of plasma adiponectin was related to the
change in SSPG with a marginal statistical significance, after those of
BMI and waist and hip circumferences were adjusted. This implies that
adiponectin may have a direct effect on insulin sensitivity or vice
versa. Adiponectin was clearly demonstrated to reduce TNF production
and TNF-induced biological effects on certain cells. Therefore, it
is highly plausible that it may enhance insulin sensitivity by
interfering with TNF production and signaling. This awaits further
investigation.
In conclusion, we have convincingly showed that body weight reduction increased plasma adiponectin levels. This provides a novel biological explanation for the beneficial effect of body weight loss on reducing cardiovascular risk in obese patients. The result is also compatible with the speculation that adiponectin might be under a strict feedback regulation by body fat mass.
Footnotes
This work was supported by Program for Promoting Academic Excellence of Universities (89-B-FA01-1-4) from the Department of Education and a grant from the National Science Council (NSC89-2314-B-002-065) of the Republic of China.
Abbreviations: AUC, Area under curve; BMI, body mass index; CAD, coronary artery disease; DM, diabetes mellitus; HOMA, homeostasis model assessment; OGTT, oral glucose tolerance test; SSPG, steady state plasma glucose.
Received February 12, 2001.
Accepted April 27, 2001.
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P. HARLE and R. H. STRAUB Leptin Is a Link between Adipose Tissue and Inflammation Ann. N.Y. Acad. Sci., June 1, 2006; 1069(1): 454 - 462. [Abstract] [Full Text] [PDF]
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N. Bansal, V. Charlton-Menys, P. Pemberton, P. McElduff, J. Oldroyd, A. Vyas, A. Koudsi, P. E. Clayton, J. K. Cruickshank, and P. N. Durrington Adiponectin in Umbilical Cord Blood Is Inversely Related to Low-Density Lipoprotein Cholesterol But Not Ethnicity J. Clin. Endocrinol. Metab., June 1, 2006; 91(6): 2244 - 2249. [Abstract] [Full Text] [PDF]
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X. Guo, M. F. Saad, C. D. Langefeld, A. H. Williams, J. Cui, K. D. Taylor, J. M. Norris, S. Jinagouda, C. H. Darwin, B. D. Mitchell, et al. Genome-Wide Linkage of Plasma Adiponectin Reveals a Major Locus on Chromosome 3q Distinct From the Adiponectin Structural Gene: The IRAS Family Study Diabetes, June 1, 2006; 55(6): 1723 - 1730. [Abstract] |
) of plasma adiponectin levels
before and after gastric partition surgery plotted against the changes
(