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Original Studies |
Clinical Diabetes and Nutrition Section (C.W., R.E.P., P.A.T.), National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Phoenix, Arizona 85016; and Department of Internal Medicine and Molecular Science (T.F., S.T., K.H., Y.M.), Graduate School of Medicine, Osaka University, Osaka, Japan
Address all correspondence and requests for reprints to: Christian Weyer, M.D., Clinical Diabetes and Nutrition Section, National Institutes of Health, 4212 North 16th Street, Room 5-41, Phoenix, Arizona 85016. E-mail: cweyer{at}phx.niddk.nih.gov
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Abstract |
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To further characterize the relationship between adiponectinemia and adiposity, insulin sensitivity, insulinemia, and glucose tolerance, we measured plasma adiponectin concentrations, body composition (dual-energy x-ray absorptiometry), insulin sensitivity (M, hyperinsulinemic clamp), and glucose tolerance (75-g oral glucose tolerance test) in 23 Caucasians and 121 Pima Indians, a population with a high propensity for obesity and type 2 diabetes.
Plasma adiponectin concentration was negatively correlated with percent body fat (r = -0.43), waist-to-thigh ratio (r = -0.46), fasting plasma insulin concentration (r = -0.63), and 2-h glucose concentration (r = -0.38), and positively correlated with M (r = 0.59) (all P < 0.001); all relations were evident in both ethnic groups. In a multivariate analysis, fasting plasma insulin concentration, M, and waist-to-thigh ratio, but not percent body fat or 2-h glucose concentration, were significant independent determinates of adiponectinemia, explaining 47% of the variance (r2 = 0.47). Differences in adiponectinemia between Pima Indians and Caucasians (7.2 ± 2.6 vs. 10.2 ± 4.3 µg/ml, P < 0.0001) and between Pima Indians with normal, impaired, and diabetic glucose tolerance (7.5 ± 2.7, 6.1 ± 2.0, 5.5 ± 1.6 µg/ml, P < 0.0001) remained significant after adjustment for adiposity, but not after additional adjustment for M or fasting insulin concentration.
These results confirm that obesity and type 2 diabetes are associated with low plasma adiponectin concentrations in different ethnic groups and indicate that the degree of hypoadiponectinemia is more closely related to the degree of insulin resistance and hyperinsulinemia than to the degree of adiposity and glucose intolerance.
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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(TNF) (6, 7), plasminogen activator inhibitor
type 1 (8), interleukin 6 (9, 10), and
complement C3 (11) may also have a role. This is in part
based on experimental evidence that these adipocytokines have direct
effects on the insulin signaling cascade (TNF) (7), the
fibrinolytic system (plasminogen activator inhibitor type 1)
(8), and endothelial cell adhesion (interleukin 6)
(9). Furthermore, clinical studies have shown that the
plasma concentrations of several of these adipocytokines correlate with
measures of adiposity, insulin sensitivity, and endothelial function in
humans (8, 9, 10, 11).
More recently, a novel adipose-specific protein, adiponectin, has been
discovered (12, 13, 14, 15). Adiponectin, the gene product of the
adipose most abundant gene transcript-1 (apM1) gene which is
exclusively and abundantly expressed in white adipose tissue, is a
244-amino acid protein with high structural homology to collagen VIII,
X, and complement C1q (12, 13, 14, 15) as well as TNF
(16). Although the physiological role of adiponectin is
yet to be fully determined, experimental findings that this protein
accumulates in injured vessel walls (17) and
dose-dependently inhibits TNF-induced cell adhesion in human aortic
endothelial cells (18, 19), have led to the proposal that
adiponectin may have an antiatherogenic effect. Moreover, adiponectin
has recently been reported to have an inhibitory effect on the
proliferation of myelomonocytic progenitors as well as on phagocytic
activity and TNF production by macrophages (20),
findings consistent with an antiinflammatory effect of this protein.
Finally, recent findings of markedly reduced adipose tissue
apM1 gene expression in ob/ob mice (14) and in
obese Caucasians with type 2 diabetes (21) has led to the
hypothesis that adiponectin may have a role in the pathogenesis of
obesity and type 2 diabetes (21). Using an
adiponectin-specific enzyme-linked immunosorbent assay, Arita et
al. (22) have demonstrated that adiponectin is
abundant in the circulation in humans, with plasma levels in the
microgram per ml range, thus accounting for approximately 0.01% of
total plasma protein. In contrast to all other adipocytokines known to
date, plasma adiponectin concentrations were found to be decreased, not
increased, in Japanese individuals with obesity (22), type
2 diabetes (23), and cardiovascular disease (18, 23), conditions commonly associated with insulin resistance and
hyperinsulinemia.
To gain further insights into the anthropometric and metabolic determinants of adiponectinemia in humans, it would be useful to examine the relationship between the plasma adiponectin concentration and direct measures of adiposity, body fat distribution, insulin sensitivity, insulinemia, and glucose tolerance. Moreover, comparative studies of adiponectinemia in populations with different propensity for obesity, insulin resistance, type 2 diabetes, and atherosclerosis are warranted. The Pima Indians of Arizona are interesting in this respect, because they have among the highest reported prevalence rates of obesity, insulin resistance, and type 2 diabetes in the world (24, 25), but a relatively low incidence of cardiovascular disease (26).
In the present study, we examined the relationship between the plasma adiponectin concentration and adiposity, body fat distribution, insulin sensitivity, insulinemia, and glucose tolerance in a large group of Pima Indians and Caucasians covering a wide range of glucose tolerance.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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) who had participated in ongoing
studies of the pathogenesis of obesity and type 2 diabetes (27, 28) and of whom frozen plasma samples had been stored were
included in this analysis. All subjects were between 18 and 50 yr of
age, nonsmokers at the time of the study, and, except for type 2
diabetes in 17 Pima Indians, healthy according to a physical
examination and routine laboratory tests. No subject had clinical or
laboratory signs of acute infection and none had a history of, or
presence of, clinically evident cardiovascular disease. Subjects were
admitted for 8–10 days to the NIH Clinical Research Unit in Phoenix,
Arizona, where they were fed a weight-maintaining diet (50% of
calories as carbohydrate, 30% as fat, and 20% as protein) and
abstained from strenuous exercise. After at least 3 days on the diet,
subjects underwent a series of tests for the assessment of body
composition, glucose tolerance, and insulin sensitivity. The protocol
was approved by the Tribal Council of the Gila River Indian Community
and by the Institutional Review Board of the National Institute of
Diabetes and Digestive and Kidney Diseases and all subjects provided
written informed consent before participation.
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Body composition was estimated by total body dual energy x-ray absorptiometry (DPX-L; Lunar Corp., Madison, WI) with calculation of percent body fat, fat mass, and fat-free mass as described (29). Waist and thigh circumferences were measured at the level of umbilicus and the gluteal fold in the supine and standing position, respectively, and the waist-to-thigh ratio was calculated as an index of body fat distribution.
Oral glucose tolerance test (OGTT) and analytic procedures
After a 12-h overnight fast, subjects underwent a 75-g OGTT (30). Baseline blood samples were drawn for determination of the fasting plasma glucose, insulin, and adiponectin concentrations. Plasma glucose concentrations were determined by the glucose oxidase method (Beckman Coulter, Inc. Instruments, Fullerton, CA) and were also measured at 2 h after glucose ingestion for assessment of glucose tolerance according to the 1985 WHO diagnostic criteria (30). Plasma insulin concentrations were determined by an automated immunoassay (Access; Beckman Coulter, Inc.). The fasting plasma insulin concentration from the OGTT was averaged with two additional fasting plasma insulin concentrations determined on separate days during the same admission to obtain a more robust measure of fasting insulinemia. Blood samples for measurement of fasting plasma adiponectin concentrations were drawn with prechilled syringes, transferred into prechilled EDTA tubes, and immediately placed on ice. All tubes were cold-centrifuged (+4 C) within several minutes of collection and stored at -70 C until assay at the Department of Internal Medicine and Molecular Sciences, Osaka University (Osaka, Japan). Fasting plasma adiponectin concentrations were determined using a validated sandwich enzyme-linked immunosorbent assay employing an adiponectin-specific antibody (intraassay and interassay coefficients of variation 3.3% and 7.4%, respectively) (16, 21, 22).
Two-step hyperinsulinemic euglycemic glucose clamp
Insulin sensitivity was assessed at physiologic and supraphysiologic insulin concentrations during a two-step hyperinsulinemic euglycemic glucose clamp as described (27, 28). In brief, after an overnight fast, a primed continuous iv insulin infusion was administered for 100 min at a constant rate of 240 nmol/m2 body surface area per minute (low dose), followed by a second 100-min infusion at a rate of 2,400 nmol/m2·min (high dose). These infusions achieved steady-state plasma insulin concentrations of 840 ± 4,252 pmol/L and 13,320 ± 3,480 pmol/L (mean ± SD), respectively. Plasma glucose concentrations were maintained at approximately 5.5 mmol/L with a variable infusion of a 20% glucose solution. The rate of total insulin-stimulated glucose disposal (M) was calculated for the last 40 min of the low-dose (M-low) and high-dose (M-high) insulin infusion. As described previously (27, 28), M-low was corrected for the rate of endogenous glucose output [measured by a primed (30 µCi), continuous (0.3 µCi/min) 3-3H-glucose infusion, Refs. 27 and 28 ] and adjusted for the steady-state plasma glucose and insulin concentrations. M-low and M-high were normalized to estimated metabolic body size (EMBS = fat-free mass + 17.7 kg) (27, 28). Five of the 23 Caucasian subjects had no assessment of insulin sensitivity.
Statistical analyses
Statistical analyses were performed using the software of the SAS Institute, Inc. (Cary, NC). M-low and the fasting plasma insulin and adiponectin concentrations were all log-transformed to achieve a more normal distribution. General linear regression models with adjustment for age and sex were used to compare anthropometric and metabolic characteristics between Caucasians and Pima Indians and between subjects with normal glucose tolerance (NGT), impaired glucose tolerance (IGT), and diabetes.
Adiponectinemia in relation to anthropometric and metabolic variables in nondiabetic Caucasians and Pima Indians
In a first analysis, we examined the relationship of the plasma adiponectin concentration to selected anthropometric and metabolic variables in Caucasians and Pima Indians carefully matched for body mass index (BMI) and glucose tolerance. Because no samples of diabetic Caucasians were available and to control for the confounding effect of frank hyperglycemia, results from the 17 diabetic Pima Indians were excluded from this analysis. Univariate linear regression models were used to examine the simple relationships of adiponectin to selected variables. Stepwise and general multivariate regression analyses were used to identify independent determinants of adiponectin and the percentage of variance in adiponectin that they explained (r2).
Adiponectinemia in Pima Indians with NGT, IGT, and diabetes
In a second analysis, we compared the mean plasma adiponectin concentration between Pima Indians with NGT, IGT, and diabetes. General linear regression models with computation of least square means were used to compare the mean plasma adiponectin concentration between the three glucose tolerance groups after adjustment for covariates.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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, subjects covered a wide range of body size
and composition, glucose tolerance, and insulin sensitivity. Despite
having similar BMI and glucose tolerance, nondiabetic Pima Indians had
a higher waist-to-thigh ratio and were markedly more insulin resistant
and hyperinsulinemic than nondiabetic Caucasians. As expected, Pima
Indians with IGT and diabetes were more obese, hyperinsulinemic, and
insulin resistant than those with NGT (Table 1). Adiponectinemia in relation to anthropometric and metabolic variables in nondiabetic Caucasians and Pima Indians
Figure 1 and Table 2 show the simple relationships between
the plasma adiponectin concentration and selected anthropometric and
metabolic variables for the entire study population (Fig. 1) and
separately for the two ethnic groups (Table 2). The plasma adiponectin
concentration was negatively correlated with BMI, percent body fat,
waist-to-thigh ratio, and the fasting plasma insulin and 2-h plasma
glucose concentrations in both Caucasians and Pima Indians (Fig. 1, A
and B, and Table 2). In contrast, plasma adiponectin concentration was
positively correlated with M-low and M-high (Fig. 1, C and D, and
Table 2). In a multivariate analysis, the fasting plasma insulin
concentration, M-low, and waist-to-thigh ratio, but not percent body
fat or the 2-h glucose concentration, were significant independent
determinants of the plasma adiponectin concentration, explaining a
total of 47% of the variance in this measure (r2
= 0.47). The mean plasma adiponectin concentration was lower in Pima
Indians than in Caucasians, a difference that remained significant
after adjustment for percent body fat, but not after additional
adjustment for M and/or the fasting plasma insulin concentration (Fig. 1E). Although females had higher percent body fat than males (39%
vs. 27%, P < 0.001), adiponectin levels
did not differ between females (6.9 µg/ml) and males (7.7 µg/ml)
(P = 0.98 and P = 0.54 with and without
adjustment for the aforementioned determinants).
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The plasma adiponectin concentration was negatively correlated
with the 2-h plasma glucose concentration (Fig. 2A) and accordingly, was lower not only
in individuals with diabetes, but also, to a similar extent, in
individuals with IGT compared with those with NGT (Fig. 2B). As with
the ethnic comparison, differences in mean plasma adiponectin
concentration between glucose tolerance groups remained significant
after adjustment for percent body fat, but not after additional
adjustment for M and/or the fasting plasma insulin concentration (Fig. 2B).
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Discussion |
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Previous studies in Japanese individuals have shown that the plasma adiponectin concentration is negatively correlated with body mass index (BMI) and accordingly, lower in obese than in lean subjects (18, 22, 23). The present results extend this finding by demonstrating that plasma adiponectin concentrations are inversely related to percent body fat, a direct measure of adiposity, and that this is consistent across different ethnic groups. Our results thus confirm that adiponectin is the only adipose-specific protein known to date that, despite its exclusive production in white adipose tissue, is negatively regulated in obesity. This agrees with findings in rodents where the murine homologue of adiponectin, adipoQ, is also down-regulated in obesity (14) and with a recent report of decreased apM1 gene expression in sc and visceral adipose tissue of obese humans (21).
We also found that the mean plasma adiponectin concentration was lower in nondiabetic Pima Indians than in Caucasians and in subjects with IGT and diabetes compared with those with NGT. The fact that these differences were not explained by differences in percent body fat indicates that factors other than adiposity must play a role in determining adiponectinemia. Our finding that the plasma adiponectin concentration was more closely related to fasting insulinemia and to the rate of insulin-stimulated glucose disposal, a direct measure of insulin sensitivity, than to percent body fat and the 2-h glucose concentration suggested that hyperinsulinemia and/or insulin resistance might be major determinants of the hypoadiponectinemia in obesity and type 2 diabetes. This was supported by the finding that differences in adiponectinemia between Pima Indians and Caucasians and between glucose tolerance groups were almost completely explained by differences in insulin sensitivity and/or fasting insulinemia, but not by differences in percent body fat.
The mechanism underlying the observed close association between plasma adiponectin concentration and insulin sensitivity/insulinemia are presently unknown. A direct effect of hyperinsulinemia to down-regulate apM1 gene expression in adipose tissue is an unlikely explanation, given that insulin appears to up-regulate apM1 in rodents (13, 14) and that plasma adiponectin concentrations do not decrease postprandially in humans (23). Interestingly, two recent genomic scan studies have independently revealed linkage of insulinemia to a region on chromosome 3 that harbors the apM1 gene (28, 31). Studies of the regulation of adiponectin gene expression are now warranted.
Although there is currently no experimental evidence to support this,
it is at least possible that adiponectin itself may affect insulin
sensitivity and/or insulinemia. For instance, adiponectin has recently
been shown to inhibit both the production (in macrophages) and action
(in endothelial cells) of TNF (18, 20), a cytokine
which has direct effects on the insulin signaling cascade and has long
been implicated as a possible link between obesity and insulin
resistance/hyperinsulinemia (6, 7). Alternatively, it has
been suggested (14) that adiponectin, which also shares
striking structural homology to collagens VII and X and is thus assumed
to be a matrix-forming protein, may affect intermediate metabolism by
forming matrixes in the interstitium of different tissues. Clearly,
experimental studies of the in vitro and in vivo
effects of adiponectin on insulin signaling and glucose metabolism are
needed to establish the role of adiponectin, if any, as a molecular
link between obesity, insulin resistance, hyperinsulinemia, type-2
diabetes, and atherosclerosis.
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Acknowledgments |
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Received November 20, 2000.
Revised January 11, 2001.
Accepted January 24, 2001.
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S. S. Deepa and L. Q. Dong APPL1: role in adiponectin signaling and beyond Am J Physiol Endocrinol Metab, January 1, 2009; 296(1): E22 - E36. [Abstract] [Full Text] [PDF]
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 F M E Franssen, D E O'Donnell, G H Goossens, E E Blaak, and A M W J Schols Obesity and the lung: 5 {middle dot} Obesity and COPD Thorax, December 1, 2008; 63(12): 1110 - 1117. [Abstract] [Full Text] [PDF]
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C. Snehalatha, A. Yamuna, and A. Ramachandran Plasma Adiponectin Does Not Correlate With Insulin Resistance and Cardiometabolic Variables in Nondiabetic Asian Indian Teenagers Diabetes Care, December 1, 2008; 31(12): 2374 - 2379. [Abstract] [Full Text] [PDF]
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N. Rasouli and P. A. Kern Adipocytokines and the Metabolic Complications of Obesity J. Clin. Endocrinol. Metab., November 1, 2008; 93(11_Supplement_1): s64 - s73. [Abstract] [Full Text] [PDF]
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 J. E. Mallewa, E. Wilkins, J. Vilar, M. Mallewa, D. Doran, D. Back, and M. Pirmohamed HIV-associated lipodystrophy: a review of underlying mechanisms and therapeutic options J. Antimicrob. Chemother., October 1, 2008; 62(4): 648 - 660. [Abstract] [Full Text] [PDF]
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S. A. Phillips, T. P. Ciaraldi, Deborah. K. Oh, M. K. Savu, and R. R. Henry Adiponectin secretion and response to pioglitazone is depot dependent in cultured human adipose tissue Am J Physiol Endocrinol Metab, October 1, 2008; 295(4): E842 - E850. [Abstract] [Full Text] [PDF]
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G. Maiolino, M. Cesari, D. Sticchi, M. Zanchetta, L. Pedon, K. Antezza, A. C. Pessina, and G. P. Rossi Plasma Adiponectin for Prediction of Cardiovascular Events and Mortality in High-Risk Patients J. Clin. Endocrinol. Metab., September 1, 2008; 93(9): 3333 - 3340. [Abstract] [Full Text] [PDF]
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P. Perez-Martinez, J. Lopez-Miranda, C. Cruz-Teno, J. Delgado-Lista, Y. Jimenez-Gomez, J. M. Fernandez, M. J. Gomez, C. Marin, F. Perez-Jimenez, and J. M. Ordovas Adiponectin Gene Variants Are Associated with Insulin Sensitivity in Response to Dietary Fat Consumption in Caucasian Men J. Nutr., September 1, 2008; 138(9): 1609 - 1614. [Abstract] [Full Text] [PDF]
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 S. J. Peterson, G. Drummond, D. H. Kim, M. Li, A. L. Kruger, S. Ikehara, and N. G. Abraham L-4F treatment reduces adiposity, increases adiponectin levels, and improves insulin sensitivity in obese mice J. Lipid Res., August 1, 2008; 49(8): 1658 - 1669. [Abstract] [Full Text] [PDF]
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H. Leth, K. K. Andersen, J. Frystyk, L. Tarnow, P. Rossing, H.-H. Parving, and A. Flyvbjerg Elevated Levels of High-Molecular-Weight Adiponectin in Type 1 Diabetes J. Clin. Endocrinol. Metab., August 1, 2008; 93(8): 3186 - 3191. [Abstract] [Full Text] [PDF]
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T. M. Barber, M. Hazell, C. Christodoulides, S. J. Golding, C. Alvey, K. Burling, A. Vidal-Puig, N. P. Groome, J. A. H. Wass, S. Franks, et al. Serum Levels of Retinol-Binding Protein 4 and Adiponectin in Women with Polycystic Ovary Syndrome: Associations with Visceral Fat But No Evidence for Fat Mass-Independent Effects on Pathogenesis in This Condition J. Clin. Endocrinol. Metab., July 1, 2008; 93(7): 2859 - 2865. [Abstract] [Full Text] [PDF]
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H. Pinar, S. Basu, K. Hotmire, L. Laffineuse, L. Presley, M. Carpenter, P. M. Catalano, and S. Hauguel-de Mouzon High Molecular Mass Multimer Complexes and Vascular Expression Contribute to High Adiponectin in the Fetus J. Clin. Endocrinol. Metab., July 1, 2008; 93(7): 2885 - 2890. [Abstract] [Full Text] [PDF]
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L. M Ritland, D L. Alekel, O. A Matvienko, K. B Hanson, J. W Stewart, L. N Hanson, M. B Reddy, M. D Van Loan, and U. Genschel Centrally located body fat is related to appetitive hormones in healthy postmenopausal women. Eur. J. Endocrinol., June 1, 2008; 158(6): 889 - 897. [Abstract] [Full Text] [PDF]
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M. Li, D. H. Kim, P. L. Tsenovoy, S. J. Peterson, R. Rezzani, L. F. Rodella, W. S. Aronow, S. Ikehara, and N. G. Abraham Treatment of Obese Diabetic Mice With a Heme Oxygenase Inducer Reduces Visceral and Subcutaneous Adiposity, Increases Adiponectin Levels, and Improves Insulin Sensitivity and Glucose Tolerance Diabetes, June 1, 2008; 57(6): 1526 - 1535. [Abstract] [Full Text] [PDF]
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S. E. Recabarren, R. Smith, R. Rios, M. Maliqueo, B. Echiburu, E. Codner, F. Cassorla, P. Rojas, and T. Sir-Petermann Metabolic Profile in Sons of Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., May 1, 2008; 93(5): 1820 - 1826. [Abstract] [Full Text] [PDF]
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C Joaquin, E Aguilera, M L Granada, M C Pastor, I Salinas, N Alonso, and A Sanmarti Effects of GH treatment in GH-deficient adults on adiponectin, leptin and pregnancy-associated plasma protein-A. Eur. J. Endocrinol., April 1, 2008; 158(4): 483 - 490. [Abstract] [Full Text] [PDF]
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M. Kyriakakou, A. Malamitsi-Puchner, H. Militsi, T. Boutsikou, A. Margeli, D. Hassiakos, C. Kanaka-Gantenbein, I. Papassotiriou, and G. Mastorakos Leptin and adiponectin concentrations in intrauterine growth restricted and appropriate for gestational age fetuses, neonates, and their mothers Eur. J. Endocrinol., March 1, 2008; 158(3): 343 - 348. [Abstract] [Full Text] [PDF]
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Y. Tabara, H. Osawa, R. Kawamoto, R. Tachibana-Iimori, M. Yamamoto, J. Nakura, T. Miki, H. Makino, and K. Kohara Reduced High-Molecular-Weight Adiponectin and Elevated High-Sensitivity C-Reactive Protein Are Synergistic Risk Factors for Metabolic Syndrome in a Large-Scale Middle-Aged to Elderly Population: the Shimanami Health Promoting Program Study J. Clin. Endocrinol. Metab., March 1, 2008; 93(3): 715 - 722. [Abstract] [Full Text] [PDF]
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 R. W. Nesto and K. Mackie Endocannabinoid system and its implications for obesity and cardiometabolic risk Eur. Heart J. Suppl., March 1, 2008; 10(suppl_B): B34 - B41. [Abstract] [Full Text] [PDF]
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S. T. Boyd Management Through Risk Factor Modification The Diabetes Educator, March 1, 2008; 34(Supplement_2): 42S - 48S. [Abstract] [Full Text] [PDF]
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 M. K. Ohman, Y. Shen, C. I. Obimba, A. P. Wright, M. Warnock, D. A. Lawrence, and D. T. Eitzman Visceral Adipose Tissue Inflammation Accelerates Atherosclerosis in Apolipoprotein E-Deficient Mice Circulation, February 12, 2008; 117(6): 798 - 805. [Abstract] [Full Text] [PDF]
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 M. Poulain, M. Doucet, V. Drapeau, G. Fournier, A. Tremblay, P. Poirier, and F. Maltais Metabolic and inflammatory profile in obese patients with chronic obstructive pulmonary disease Chronic Respiratory Disease, February 1, 2008; 5(1): 35 - 41. [Abstract] [PDF]
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 J. Koska, N. Stefan, P. A Permana, C. Weyer, M. Sonoda, C. Bogardus, S. R Smith, D. R Joanisse, T. Funahashi, J. Krakoff, et al. Increased fat accumulation in liver may link insulin resistance with subcutaneous abdominal adipocyte enlargement, visceral adiposity, and hypoadiponectinemia in obese individuals Am. J. Clinical Nutrition, February 1, 2008; 87(2): 295 - 302. [Abstract] [Full Text] [PDF]
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E. L Madsen, A. Rissanen, J. M Bruun, K. Skogstrand, S. Tonstad, D. M Hougaard, and B. Richelsen Weight loss larger than 10% is needed for general improvement of levels of circulating adiponectin and markers of inflammation in obese subjects: a 3-year weight loss study Eur. J. Endocrinol., February 1, 2008; 158(2): 179 - 187. [Abstract] [Full Text] [PDF]
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M. E. Spurlock and N. K. Gabler The Development of Porcine Models of Obesity and the Metabolic Syndrome J. Nutr., February 1, 2008; 138(2): 397 - 402. [Abstract] [Full Text] [PDF]
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S. H. S. Santos, L. R. Fernandes, E. G. Mario, A. V. M. Ferreira, L. C. J. Porto, J. I. Alvarez-Leite, L. M. Botion, M. Bader, N. Alenina, and R. A. S. Santos Mas Deficiency in FVB/N Mice Produces Marked Changes in Lipid and Glycemic Metabolism Diabetes, February 1, 2008; 57(2): 340 - 347. [Abstract] [Full Text] [PDF]
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 A. M.J. Wassink, Y. van der Graaf, J. K. Olijhoek, F. L.J. Visseren, and for the SMART Study Group Metabolic syndrome and the risk of new vascular events and all-cause mortality in patients with coronary artery disease, cerebrovascular disease, peripheral arterial disease or abdominal aortic aneurysm Eur. Heart J., January 2, 2008; 29(2): 213 - 223. [Abstract] [Full Text] [PDF]
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J. Saltevo, M. Vanhala, H. Kautiainen, and M. Laakso Levels of adiponectin, C-reactive protein and interleukin-1 receptor antagonist are associated with the relative change in body mass index between childhood and adulthood Diabetes and Vascular Disease Research, December 1, 2007; 4(4): 328 - 331. [Abstract] [PDF]
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 I. A. Harsch Metabolic disturbances in patients with obstructive sleep apnoea syndrome Eur. Respir. Rev., December 1, 2007; 16(106): 196 - 202. [Abstract] [Full Text] [PDF]
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 S. E. Yeo, N. P. Hays, R. A. Dennis, P. M. Kortebein, D. H. Sullivan, W. J. Evans, and R. H. Coker Fat Distribution and Glucose Metabolism in Older, Obese Men and Women J. Gerontol. A Biol. Sci. Med. Sci., December 1, 2007; 62(12): 1393 - 1401. [Abstract] [Full Text] [PDF]
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T. Sir-Petermann, M. Maliqueo, E. Codner, B. Echiburu, N. Crisosto, V. Perez, F. Perez-Bravo, and F. Cassorla Early Metabolic Derangements in Daughters of Women with Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., December 1, 2007; 92(12): 4637 - 4642. [Abstract] [Full Text] [PDF]
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 M. K. Sinha, T. Songer, Q. Xiao, J. H. Sloan, J. Wang, S. Ji, W. E. Alborn, R. A. Davis, M. M. Swarbrick, K. L. Stanhope, et al. Analytical Validation and Biological Evaluation of a High Molecular-Weight Adiponectin ELISA Clin. Chem., December 1, 2007; 53(12): 2144 - 2151. [Abstract] [Full Text] [PDF]
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L. Hojbjerre, M. Rosenzweig, F. Dela, J. M Bruun, and B. Stallknecht Acute exercise increases adipose tissue interstitial adiponectin concentration in healthy overweight and lean subjects Eur. J. Endocrinol., November 1, 2007; 157(5): 613 - 623. [Abstract] [Full Text] [PDF]
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M. H Rokling-Andersen, J. E Reseland, M. B Veierod, S. A Anderssen, D. R Jacobs Jr, P. Urdal, J.-O. Jansson, and C. A Drevon Effects of long-term exercise and diet intervention on plasma adipokine concentrations Am. J. Clinical Nutrition, November 1, 2007; 86(5): 1293 - 1301. [Abstract] [Full Text] [PDF]
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T. W.K. Ng, G. F. Watts, P. H. R. Barrett, K.-A. Rye, and D. C. Chan Effect of Weight Loss on LDL and HDL Kinetics in the Metabolic Syndrome: Associations with changes in plasma retinol-binding protein-4 and adiponectin levels Diabetes Care, November 1, 2007; 30(11): 2945 - 2950. [Abstract] [Full Text] [PDF]
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A. Galler, G. Gelbrich, J. Kratzsch, N. Noack, T. Kapellen, and W. Kiess Elevated serum levels of adiponectin in children, adolescents and young adults with type 1 diabetes and the impact of age, gender, body mass index and metabolic control: a longitudinal study Eur. J. Endocrinol., October 1, 2007; 157(4): 481 - 489. [Abstract] [Full Text] [PDF]
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K. A. Varady, D. J. Roohk, Y. C. Loe, B. K. McEvoy-Hein, and M. K. Hellerstein Effects of modified alternate-day fasting regimens on adipocyte size, triglyceride metabolism, and plasma adiponectin levels in mice J. Lipid Res., October 1, 2007; 48(10): 2212 - 2219. [Abstract] [Full Text] [PDF]
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S. Murosaki, T. R. Lee, K. Muroyama, E. S. Shin, S. Y. Cho, Y. Yamamoto, and S. J. Lee A Combination of Caffeine, Arginine, Soy Isoflavones, and L-Carnitine Enhances Both Lipolysis and Fatty Acid Oxidation in 3T3-L1 and HepG2 Cells in Vitro and in KK Mice in Vivo J. Nutr., October 1, 2007; 137(10): 2252 - 2257. [Abstract] [Full Text] [PDF]
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 D. M. Maahs, L. G. Ogden, J. K. Snell-Bergeon, G. L. Kinney, R. P. Wadwa, J. E. Hokanson, D. Dabelea, A. Kretowski, R. H. Eckel, and M. Rewers Determinants of Serum Adiponectin in Persons with and without Type 1 Diabetes Am. J. Epidemiol., September 15, 2007; 166(6): 731 - 740. [Abstract] [Full Text] [PDF]
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 Y.-F. Tian, C.-H. Chu, M.-H. Wu, C.-L. Chang, T. Yang, Y.-C. Chou, G.-C. Hsu, C.-P. Yu, J.-C. Yu, and C.-A. Sun Anthropometric measures, plasma adiponectin, and breast cancer risk Endocr. Relat. Cancer, September 1, 2007; 14(3): 669 - 677. [Abstract] [Full Text] [PDF]
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L. Cong, J. Gasser, J. Zhao, B. Yang, F. Li, and A. Z Zhao Human adiponectin inhibits cell growth and induces apoptosis in human endometrial carcinoma cells, HEC-1-A and RL95 2 Endocr. Relat. Cancer, September 1, 2007; 14(3): 713 - 720. [Abstract] [Full Text] [PDF]
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M. Bullo, M. R Peeraully, P. Trayhurn, J Folch, and J. Salas-Salvado Circulating nerve growth factor levels in relation to obesity and the metabolic syndrome in women Eur. J. Endocrinol., September 1, 2007; 157(3): 303 - 310. [Abstract] [Full Text] [PDF]
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D. Barb, C. J Williams, A. K Neuwirth, and C. S Mantzoros Adiponectin in relation to malignancies: a review of existing basic research and clinical evidence Am. J. Clinical Nutrition, September 1, 2007; 86(3): 858S - 866S. [Abstract] [Full Text] [PDF]
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W.-S. Yang, Y.-C. Yang, C.-L. Chen, I-L. Wu, J.-Y. Lu, F.-H. Lu, T.-Y. Tai, and C.-J. Chang Adiponectin SNP276 is associated with obesity, the metabolic syndrome, and diabetes in the elderly Am. J. Clinical Nutrition, August 1, 2007; 86(2): 509 - 513. [Abstract] [Full Text] [PDF]
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A. E Schutte, H. W Huisman, R. Schutte, L. Malan, J. M van Rooyen, N. T Malan, and P. E H Schwarz Differences and similarities regarding adiponectin investigated in African and Caucasian women Eur. J. Endocrinol., August 1, 2007; 157(2): 181 - 188. [Abstract] [Full Text] [PDF]
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A Klamer, K Skogstrand, D M Hougaard, B Norgaard-Petersen, A Juul, and G Greisen Adiponectin levels measured in dried blood spot samples from neonates born small and appropriate for gestational age Eur. J. Endocrinol., August 1, 2007; 157(2): 189 - 194. [Abstract] [Full Text] [PDF]
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G. Yuan, X. Chen, Q. Ma, J. Qiao, R. Li, X. Li, S. Li, J. Tang, L. Zhou, H. Song, et al. C-reactive protein inhibits adiponectin gene expression and secretion in 3T3-L1 adipocytes J. Endocrinol., August 1, 2007; 194(2): 275 - 281. [Abstract] [Full Text] [PDF]
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T. Josephs, H. Waugh, I. Kokay, D. Grattan, and M. Thompson Fasting-induced adipose factor identified as a key adipokine that is up-regulated in white adipose tissue during pregnancy and lactation in the rat J. Endocrinol., August 1, 2007; 194(2): 305 - 312. [Abstract] [Full Text] [PDF]
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L. J. Moran, M. Noakes, P. M. Clifton, G. A. Wittert, D. P. Belobrajdic, and R. J. Norman C-Reactive Protein before and after Weight Loss in Overweight Women with and without Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., August 1, 2007; 92(8): 2944 - 2951. [Abstract] [Full Text] [PDF]
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M. Cesari, K. Narkiewicz, R. De Toni, E. Aldighieri, C. J. Williams, and G. P. Rossi Heritability of Plasma Adiponectin Levels and Body Mass Index in Twins J. Clin. Endocrinol. Metab., August 1, 2007; 92(8): 3082 - 3088. [Abstract] [Full Text] [PDF]
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A. J. G. Hanley, D. Bowden, L. E. Wagenknecht, A. Balasubramanyam, C. Langfeld, M. F. Saad, J. I. Rotter, X. Guo, Y.-D. I. Chen, M. Bryer-Ash, et al. Associations of Adiponectin with Body Fat Distribution and Insulin Sensitivity in Nondiabetic Hispanics and African-Americans J. Clin. Endocrinol. Metab., July 1, 2007; 92(7): 2665 - 2671. [Abstract] [Full Text] [PDF]
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T. Sir-Petermann, B. Echiburu, M M. Maliqueo, N. Crisosto, F. Sanchez, C. Hitschfeld, M. Carcamo, P. Amigo, and F. Perez-Bravo Serum adiponectin and lipid concentrations in pregnant women with polycystic ovary syndrome Hum. Reprod., July 1, 2007; 22(7): 1830 - 1836. [Abstract] [Full Text] [PDF]
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J. Jurimae and T. Jurimae Plasma adiponectin concentration in healthy pre- and postmenopausal women: relationship with body composition, bone mineral, and metabolic variables Am J Physiol Endocrinol Metab, July 1, 2007; 293(1): E42 - E47. [Abstract] [Full Text] [PDF]
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J.A. Paniagua, A. G. de la Sacristana, I. Romero, A. Vidal-Puig, J.M. Latre, E. Sanchez, P. Perez-Martinez, J. Lopez-Miranda, and F. Perez-Jimenez Monounsaturated Fat-Rich Diet Prevents Central Body Fat Distribution and Decreases Postprandial Adiponectin Expression Induced by a Carbohydrate-Rich Diet in Insulin-Resistant Subjects Diabetes Care, July 1, 2007; 30(7): 1717 - 1723. [Abstract] [Full Text] [PDF]
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L. A. Barbour, C. E. McCurdy, T. L. Hernandez, J. P. Kirwan, P. M. Catalano, and J. E. Friedman Cellular Mechanisms for Insulin Resistance in Normal Pregnancy and Gestational Diabetes Diabetes Care, July 1, 2007; 30(Supplement_2): S112 - S119. [Full Text] [PDF]
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R. K. Stoving, J.-W. Chen, D. Glintborg, K. Brixen, A. Flyvbjerg, K. Horder, and J. Frystyk Bioactive Insulin-Like Growth Factor (IGF) I and IGF-Binding Protein-1 in Anorexia Nervosa J. Clin. Endocrinol. Metab., June 1, 2007; 92(6): 2323 - 2329. [Abstract] [Full Text] [PDF]
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N. R. Poa and P. F. Edgar Insulin Resistance Is Associated With Hypercortisolemia in Polynesian Patients Treated With Antipsychotic Medication Diabetes Care, June 1, 2007; 30(6): 1425 - 1429. [Abstract] [Full Text] [PDF]
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C. M. de Souza Batista, R.-Z. Yang, M.-J. Lee, N. M. Glynn, D.-Z. Yu, J. Pray, K. Ndubuizu, S. Patil, A. Schwartz, M. Kligman, et al. Omentin Plasma Levels and Gene Expression Are Decreased in Obesity Diabetes, June 1, 2007; 56(6): 1655 - 1661. [Abstract] [Full Text] [PDF]
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L. Qi, A. Doria, E. Giorgi, and F. B. Hu Variations in Adiponectin Receptor Genes and Susceptibility to Type 2 Diabetes in Women: A Tagging-Single Nucleotide Polymorphism Haplotype Analysis Diabetes, June 1, 2007; 56(6): 1586 - 1591. [Abstract] [Full Text] [PDF]
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 W.-S. Chow, B. M.Y. Cheung, A. W.K. Tso, A. Xu, N. M.S. Wat, C. H.Y. Fong, L. H.Y. Ong, S. Tam, K. C.B. Tan, E. D. Janus, et al. Hypoadiponectinemia as a Predictor for the Development of Hypertension: A 5-Year Prospective Study Hypertension, June 1, 2007; 49(6): 1455 - 1461. [Abstract] [Full Text] [PDF]
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) and Caucasians
(•). E, Mean fasting plasma adiponectin concentration in nondiabetic
Pima Indians vs. Caucasians with and without adjustment
for age, sex, percent body fat, and/or insulin sensitivity. To convert
adiponectin concentrations to micromoles per L, divide by 30.
), or diabetes (•). B, Mean fasting plasma adiponectin
concentration in Pima Indians with NGT, IGT, and diabetes (DIA) with
and without adjustment for age, sex, percent body fat and/or insulin
sensitivity. To convert adiponectin concentrations to micromoles per L,
divide by 30.