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Departments of 1 Physiology, 2 Exercise and Sport Science Human Performance Laboratory, and 3 Surgery, East Carolina University, Greenville 27858; 4 Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710; and 5 Linco Research Inc., St. Charles, Missouri 63304
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
EXPERIMENTAL PROCEDURES
RESULTS
DISCUSSION
REFERENCES
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Adiponectin is an adipocytokine that is hypothesized to be involved in the regulation of insulin action. The purpose of the present investigation was to determine whether plasma adiponectin is altered in conjunction with enhanced insulin action with exercise training. An insulin sensitivity index (SI) and fasting levels of glucose, insulin, and adiponectin were assessed before and after 6 mo of exercise training (4 days/wk for ~45 min at 65-80% peak O2 consumption) with no loss of body mass (PRE, 91.9 ± 3.8 kg vs. POST, 91.6 ± 3.9 kg) or fat mass (PRE, 26.5 ± 1.8 kg vs. POST, 26.7 ± 2.2 kg). Insulin action significantly (P < 0.05) improved with exercise training (SI +98%); however, plasma adiponectin concentration did not change (PRE, 6.3 ± 1.5 µg/ml vs. POST, 6.6 ± 1.8 µg/ml). In contrast, in a separate group of subjects examined before and after weight loss, there was a substantial increase in adiponectin (+281%), which was accompanied by enhanced insulin action (SI, +432%). These data suggest that adiponectin is not a contributory factor to the exercise-related improvements in insulin sensitivity.
weight loss
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INTRODUCTION |
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ABSTRACT
INTRODUCTION
EXPERIMENTAL PROCEDURES
RESULTS
DISCUSSION
REFERENCES
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ADIPOSE
TISSUE WAS ONCE THOUGHT to simply be a storage depot for energy
surplus; however, it is now known that adipocytes also secrete multiple
proteins that modulate various biological functions. These
proteins are collectively known as adipocytokines and include
leptin, tumor necrosis factor (TNF)-
, plasminogen-activator inhibitor type I, adipsin, and resistin. Recently, an adipocytokine referred to as adiponectin (also known as Acrp 30, AdipoQ, apM-1, and
GBP28) has been independently identified and characterized (14,
16, 18, 22). Unlike other adipocytokines, mRNA expression (14) and adiponectin plasma levels (1) are
reduced with obesity and diabetes. Adiponectin may also be a marker for
coronary artery disease (CAD), as low plasma adiponectin levels are
associated with the presence of CAD (12).
Hu et al. (14) originally demonstrated that adiponectin was reduced in murine models of insulin resistance and obesity, which was subsequently confirmed in humans (12, 25). Recently, Hotta et al. (13) reported parallel decreases in insulin action and plasma levels of adiponectin with the progression of obesity in rhesus monkeys. Yamauchi et al. (27), through the administration of recombinant adiponectin, ameliorated hyperglycemia and hyperinsulinemia and successfully reversed insulin resistance in obese mice. Also, Fruebis et al. (8), using a proteolytic cleavage product of adiponectin, induced an increase in fatty acid oxidation and weight loss in mice. These findings suggest that adiponectin may not be merely a passive factor regulated by insulin resistance and obesity. Additional support for the role of adiponectin in the pathogenesis of insulin resistance comes from two independent genetic studies (4, 24). Vionnet et al. (24) mapped a diabetes susceptibility locus in a native French cohort to human chromosome 3q27, which encodes adiponectin. In addition, Comuzzie et al. (4) demonstrated a quantitative-trait locus on 3q27 strongly linked to the metabolic syndrome in European individuals.
Weight loss (9, 10) and exercise (23, 29) are common clinical interventions for the treatment of insulin resistance. Two recent publications have reported significant increases in plasma adiponectin with weight loss (12, 28). Yang et al. (28) also reported that with weight loss, an increase in adiponectin was associated with enhanced insulin action. However, to date, there are no reports on the effects of exercise training on plasma adiponectin levels. Given that exercise training improves insulin sensitivity, we sought to determine the effects of exercise training on plasma adiponectin. For the purpose of comparison, we also examined adiponectin responses to weight loss where insulin action is also improved.
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EXPERIMENTAL PROCEDURES |
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ABSTRACT
INTRODUCTION
EXPERIMENTAL PROCEDURES
RESULTS
DISCUSSION
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Study groups.
An exercise group and a weight loss group were examined. The exercise
group consisted of 11 previously sedentary, healthy subjects [3
females, 8 males; age, 51.1 ± 6.8 yr; body mass index (BMI),
29.1 ± 0.9 kg/m2] who participated in a 6-mo
endurance training program. The weight loss group consisted of 14 morbidly obese subjects (3 males, 11 females; age, 42.5 ± 10.1 yr; BMI, 46.8 ± 1.2 kg/m2) who underwent gastric
bypass surgery. Of the weight loss subjects, four were classified as
having non-insulin-dependent diabetes mellitus (NIDDM), and ten were
classified as nondiabetic, according to the criteria established by the
National Diabetes Data Group. None of the weight loss subjects had any
disease other than diabetes and/or obesity, and subjects from both the
exercise training and weight loss groups were weight stable for 
2 mo
before entry into the study. The experimental protocol was explained to
each subject, and informed consent was obtained. The project was
approved by the East Carolina University Policy and Review Committee on
Human Research.
Exercise intervention.
The exercise training subjects were selected from a larger, randomized,
controlled clinical trial designed to study the effects of exercise
training regimens differing in dose (kcal/wk) and/or intensity
[relative to peak O2 consumption
(
O2 peak)] on established
cardiovascular risk factors (15). Exercise training was
supervised and included treadmill walking/running, stair climbing, and
cycling. After a 6-wk ramping period, all participants exercised 4 days/wk for ~45 min at 65-80%
O2 peak for 6 mo. Average time and
distance per week were 175 min and 17 miles, respectively. All
physiological measures were assessed 24 h after the last training session. A goal of the exercise training program was to minimize weight
loss in an attempt to focus on the effect of exercise alone.
Weight loss intervention.
Gastric bypass surgery was performed, as previously described
(10), in the weight loss subjects. After surgery, all
patients were followed at 6- to 8-wk intervals for weighing and dietary counseling, and a plateau in weight was declared when three consecutive weights varied by 
1 kg.
Body composition. Body composition was assessed via hydrostatic weighing in the exercise training group but not in the weight loss group. The hydrostatic weighing procedure was offered to all weight loss subjects before gastric bypass surgery, but no patients elected the procedure due to difficulties involved in submersion and fear of water. Thus, for the weight loss subjects, we present BMI, which is obtained consistently.
Residual volume was determined by the O2 dilution method, as described by Wilmore (26). Body density was determined by hydrostatic weighing, with percent body fat calculated using residual volume and body density with the equations of Brozek et al. (3), as described previously (13).Insulin action.
Insulin action was determined with a 3-h intravenous glucose tolerance
test (minimal model) (2). Glucose and insulin dosages were
calculated on the basis of body mass for the exercise training subjects
and body surface area in the weight loss subjects. Dosages were
different between groups due to the high body mass of morbidly obese
subjects (R. N. Bergman, personal communication). After fasting
samples were obtained, glucose (50%) was injected into a catheter
placed in an antecubital vein at a dose of 1.7 mmol/kg (exercise
training subjects) or 12 g/m2 of body surface area (weight
loss subjects). Insulin, at a dose of 150 pmol/kg (exercise training
subjects) or 1.5 U/m2 body surface area (weight loss
subjects), was injected at minute 20. Blood samples were
obtained at minutes 2, 3, 4, 5, 6, 8, 10, 12, 14, 16, 19, 22, 25, 30, 40, 50, 60, 70, 80, 90, 100, 120, 140, 160, and 180 and centrifuged, and plasma was frozen at 
80°C for the subsequent
determination of insulin and glucose. Insulin was determined with
immunoassay (Access Immunoassay System; Beckman Coulter, Fullerton, CA)
and glucose with an oxidation reaction (YSI model 2300 Stat Plus,
Yellow Springs Instrument, Yellow Springs, OH). An insulin sensitivity
index (SI) was calculated on the basis of the minimal model
as described by Bergman et al. (2). SI is an
index of the ability of insulin to promote the disposal of glucose,
with a higher SI indicating enhanced insulin sensitivity.
Plasma adiponectin. Plasma adiponectin was assessed using a commercially available radioimmunoassay kit (cat. no. HADP-61HK, Linco Research, St. Charles, MO).
Statistical analysis.
Differences in all measured variables before and after the exercise and
weight loss interventions were compared by paired t-test.
Pearson correlational analyses were performed for all clinical
characteristics and plasma adiponectin levels before and after the
exercise and weight loss interventions. Statistical analyses were
conducted using the Statistical Package for the Social Sciences (SPSS,
v. 10.0, SPSS, Chicago, IL). Data were presented as means ± SE,
and statistical significance was accepted as P 0.05.
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RESULTS |
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ABSTRACT
INTRODUCTION
EXPERIMENTAL PROCEDURES
RESULTS
DISCUSSION
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Effects of exercise training and weight loss.
PRE and POST values for all measured variables are displayed in Table
1. Six months of exercise training
resulted in significant decreases in fasting insulin (18%) and
significant increases in SI (+98%), with no changes in
body mass, fat mass, BMI, fasting glucose, or adiponectin. Plasma
adiponectin levels were not significantly related (P > 0.05) to BMI (PRE, r = 0.46; POST, r = 0.38), fat mass (PRE, r = 0.06; POST,
r = 0.19), plasma glucose (PRE, r = 0.48; POST, r = 0.51), or SI (PRE,
r = 0.51; POST, r = 0.40) before or
after exercise training. However, plasma levels of adiponectin and
insulin (PRE, r = 0.63, P = 0.04;
POST, r = 0.60, P = 0.05) were
significantly related pre- and postexercise training (Fig. 1).
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40%), BMI
(40%), fasting insulin (78%), and glucose (25%) and
significant increases in SI (+432%) and adiponectin levels (+281%). Plasma adiponectin levels were not significantly related (P > 0.05) to BMI (PRE, r = 0.165;
POST, r = 0.44) or plasma glucose (PRE,
r = 0.07; POST, r = 0.10) before or
after weight loss. SI was significantly related to plasma
adiponectin prior to (r = 0.72, P = 0.004) but not following (r = 0.38) weight loss. Plasma
levels of adiponectin and insulin were not significantly related before
(r = 0.45) weight loss but were significantly related
afterward (r = 0.62, P = 0.02; Fig.
1).
Diabetic and nondiabetic surgery patients differed only in fasting
glucose levels before weight loss (diabetic, 10.0 ± 2.7 mmol/l
vs. nondiabetic, 5.3 ± 0.2 mmol/l), and the presence of diabetes
had no influence on the change in any measured variables with weight
reduction (data not shown).
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DISCUSSION |
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ABSTRACT
INTRODUCTION
EXPERIMENTAL PROCEDURES
RESULTS
DISCUSSION
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Peripheral insulin resistance is a primary disorder in both obesity and NIDDM (19). In animals and humans, plasma adiponectin concentrations are lower in states of insulin resistance compared with healthy controls (12, 14, 25). Weight loss (10) and exercise training (23, 29) are successful and common treatments for insulin resistance. Previous reports (12, 28) demonstrate increased adiponectin concentrations with weight reduction. The effects of exercise training on this novel adipocytokine are unknown. Our data suggest that both weight loss and exercise training significantly improve insulin action, but only the former significantly increases plasma adiponectin.
The weight loss- and exercise-related improvements in insulin sensitivity reported in the present study are in agreement with results from our laboratory (10, 23, 29) and others (9, 28). In addition, our findings of increased plasma adiponectin concentrations with weight reduction support the data of Hotta et al. (12) and Yang et al. (28). However, in contrast to weight loss, exercise training had no effect on circulating adiponectin levels despite significant improvements in insulin action. This novel finding suggests that adiponectin is not a contributory factor to the exercise-related improvements in insulin sensitivity.
There is currently no available literature mechanistically linking
adiponectin to improved insulin sensitivity. TNF--induced defects in
insulin signaling have been implicated in the pathogenesis of insulin
resistance (7, 11, 17). Thus a feasible hypothesis, which
has been proposed previously (10), is that adiponectin may
improve insulin sensitivity by inhibiting the detrimental effects of
TNF- on insulin action. It has been suggested that adiponectin
serves as a protective mechanism against the development of coronary
artery disease, as TNF--induced expression of endothelial molecules
is inhibited by adiponectin (20, 21). The negative correlations between plasma levels of adiponectin and insulin observed
in the present study are in agreement with previous findings (12). Hotta et al. (12) suggested that plasma
insulin levels do not acutely affect plasma adiponectin, as the daily
profile of plasma adiponectin was not altered by food intake. Thus the negative relationship between plasma levels of adiponectin and insulin
may be a result of decreased insulin sensitivity due to TNF--induced
defects in insulin signaling. Investigations examining the effect of
adiponectin on TNF- signaling and insulin sensitivity are warranted.
On the basis of the results of the present study, it is also plausible that exercise and weight loss improve insulin sensitivity either partially or completely via different mechanisms, with adiponectin functioning as a contributing factor to weight loss-associated enhanced insulin action but not exercise-related improvements in insulin action. This notion is supported by previous randomized, controlled trials comparing the effects of weight loss and aerobic exercise on glucose tolerance (5, 6). Dengel and colleagues (5, 6) observed an additive effect of aerobic exercise training and weight loss on glucose tolerance in two separate studies. In older men (5), insulin area during a glucose tolerance test was reduced by 32, 29, and 50% in response to weight loss alone, aerobic exercise training alone, and aerobic exercise training plus weight loss, respectively. In middle aged sedentary men (6), similar results were observed, with 21, 18, and 42% reductions in insulin area during a glucose tolerance test after weight loss alone, aerobic exercise training alone, and aerobic exercise training plus weight loss, respectively. The fact that exercise combined with weight loss results in significantly improved insulin action compared with weight loss alone and exercise alone provides evidence that the effects of exercise and weight loss on insulin sensitivity function via different mechanisms.
In conclusion, there was no change in plasma adiponectin concentration with exercise training that did not alter body mass, despite an improvement in insulin action. In contrast, plasma adiponectin increased in conjunction with insulin action after weight loss. These findings suggest that adiponectin may contribute to improved insulin action with weight loss but not with exercise training.
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ACKNOWLEDGEMENTS |
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This research was supported by funding from National Institute of Diabetes and Digestive and Kidney Diseases Grant DK-56112 (J. A. Houmard) and a clinical research grant from the American Diabetes Association (G. L. Dohm).
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FOOTNOTES |
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Address for reprint requests and other correspondence: M. W. Hulver, Dept. of Physiology, The Brody School of Medicine, 7W-44 Brody Medical Sciences Bldg., East Carolina University, Greenville, NC 27858 (E-mail: hulverm{at}mail.ecu.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
10.1152/ajpendo.00150.2002
Received 20 May 2002; accepted in final form 26 May 2002.
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REFERENCES |
|---|
|
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ABSTRACT
INTRODUCTION
EXPERIMENTAL PROCEDURES
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Arita, Y,
Kihara S,
Ouchi N,
Takahashi M,
Maeda K,
Miyagawa J,
Hotta K,
Shimomura I,
Nakamura T,
Miyaoka K,
Kuriyama H,
Nishida M,
Yamashita S,
Okubo K,
Matsubara K,
Muraguchi M,
Ohmoto Y,
Funahashi T,
and
Matsuzawa Y.
Paradoxical decrease of an adipose-specific protein, adiponectin, in obesity.
Biochem Biophys Res Commun
257:
79-83,
1999[ISI][Medline].
2.
Bergman, RN,
Finegood DT,
and
Ader M.
Assessment of insulin sensitivity in vivo.
Endocr Rev
6:
45-86,
1985[ISI][Medline].
3.
Brozek, J,
Grnade F,
Anderson JT,
and
Keys A.
Densitometric analysis of body composition: revision of some quantitative assumptions.
Ann NY Acad Sci
110:
113-140,
1963.
4.
Comuzzie, AG,
Funahashi T,
Sonnenberg G,
Martin LJ,
Jacob HJ,
Black AE,
Maas D,
Takahashi M,
Kihara S,
Tanaka S,
Matsuzawa Y,
Blangero J,
Cohen D,
and
Kissebah A.
The genetic basis of plasma variation in adiponectin, a global endophenotype for obesity and the metabolic syndrome.
J Clin Endocrinol Metab
86:
4321-4325,
2001
5.
Dengel, DR,
Galecki AT,
Hagberg JM,
and
Pratley RE.
The independent and combined effects of weight loss and aerobic exercise on blood pressure and oral glucose tolerance in older men.
Am J Hypertens
11:
1405-1412,
1998[ISI][Medline].
6.
Dengel, DR,
Pratley RE,
Hagberg JM,
Rogus EM,
and
Goldberg AP.
Distinct effects of aerobic exercise training and weight loss on glucose homeostasis in obese sedentary men.
J Appl Physiol
81:
318-325,
1996
7.
Fang, Q,
Xiang K,
and
Lu J.
[The mechanism of tumor necrosis factor-alpha (TNF-alpha) induced insulin resistance by variation in promoter region of TNF-alpha gene].
Zhonghua Yi Xue Za Zhi
79:
343-345,
1999[Medline].
8.
Fruebis, J,
Tsao TS,
Javorschi S,
Ebbets-Reed D,
Erickson MR,
Yen FT,
Bihain BE,
and
Lodish HF.
Proteolytic cleavage product of 30-kDa adipocyte complement-related protein increases fatty acid oxidation in muscle and causes weight loss in mice.
Proc Natl Acad Sci USA
98:
2005-2010,
2001
9.
Goodpaster, BH,
Kelley DE,
Wing RR,
Meier A,
and
Thaete FL.
Effects of weight loss on regional fat distribution and insulin sensitivity in obesity.
Diabetes
48:
839-847,
1999[Abstract].
10.
Hickey, MS,
Pories WJ,
MacDonald KG, Jr,
Cory KA,
Dohm GL,
Swanson MS,
Israel RG,
Barakat HA,
Considine RV,
Caro JF,
and
Houmard JA.
A new paradigm for type 2 diabetes mellitus: could it be a disease of the foregut?
Ann Surg
227:
637-644,
1998[ISI][Medline].
11.
Hotamisligil, GS.
Mechanisms of TNF-alpha-induced insulin resistance.
Exp Clin Endocrinol Diabetes
107:
119-125,
1999[ISI][Medline].
12.
Hotta, K,
Funahashi T,
Arita Y,
Takahashi M,
Matsuda M,
Okamoto Y,
Iwahashi H,
Kuriyama H,
Ouchi N,
Maeda K,
Nishida M,
Kihara S,
Sakai N,
Nakajima T,
Hasegawa K,
Muraguchi M,
Ohmoto Y,
Nakamura T,
Yamashita S,
Hanafusa T,
and
Matsuzawa Y.
Plasma concentrations of a novel, adipose-specific protein, adiponectin, in type 2 diabetic patients.
Arterioscler Thromb Vasc Biol
20:
1595-1599,
2000
13.
Hotta, K,
Funahashi T,
Bodkin NL,
Ortmeyer HK,
Arita Y,
Hansen BC,
and
Matsuzawa Y.
Circulating concentrations of the adipocyte protein adiponectin are decreased in parallel with reduced insulin sensitivity during the progression to type 2 diabetes in rhesus monkeys.
Diabetes
50:
1126-1133,
2001
14.
Hu, E,
Liang P,
and
Spiegelman BM.
AdipoQ is a novel adipose-specific gene dysregulated in obesity.
J Biol Chem
271:
10697-10703,
1996
15.
Kraus, WE,
Torgan CE,
Duscha BD,
Norris J,
Brown SA,
Cobb FR,
Bales CW,
Annex BH,
Samsa GP,
Houmard JA,
and
Slentz CA.
Studies of a targeted risk reduction intervention through defined exercise (STRRIDE).
Med Sci Sports Exerc
33:
1774-1784,
2001[ISI][Medline].
16.
Maeda, K,
Okubo K,
Shimomura I,
Funahashi T,
Matsuzawa Y,
and
Matsubara K.
cDNA cloning and expression of a novel adipose specific collagen-like factor, apM1 (AdiPose Most abundant Gene transcript 1).
Biochem Biophys Res Commun
221:
286-289,
1996[ISI][Medline].
17.
Moller, DE.
Potential role of TNF-alpha in the pathogenesis of insulin resistance and type 2 diabetes.
Trends Endocrinol Metab
11:
212-217,
2000[ISI][Medline].
18.
Nakano, Y,
Tobe T,
Choi-Miura NH,
Mazda T,
and
Tomita M.
Isolation and characterization of GBP28, a novel gelatin-binding protein purified from human plasma.
J Biochem (Tokyo)
120:
803-812,
1996
19.
Olefsky, JM,
Ciaraldi TP,
and
Kolterman OG.
Mechanisms of insulin resistance in non-insulin-dependent (type II) diabetes.
Am J Med
79:
12-22,
1985[ISI][Medline].
20.
Ouchi, N,
Kihara S,
Arita Y,
Nishida M,
Matsuyama A,
Okamoto Y,
Ishigami M,
Kuriyama H,
Kishida K,
Nishizawa H,
Hotta K,
Muraguchi M,
Ohmoto Y,
Yamashita S,
Funahashi T,
and
Matsuzawa Y.
Adipocyte-derived plasma protein, adiponectin, suppresses lipid accumulation and class A scavenger receptor expression in human monocyte-derived macrophages.
Circulation
103:
1057-1063,
2001
21.
Ouchi, N,
Kihara S,
Arita Y,
Okamoto Y,
Maeda K,
Kuriyama H,
Hotta K,
Nishida M,
Takahashi M,
Muraguchi M,
Ohmoto Y,
Nakamura T,
Yamashita S,
Funahashi T,
and
Matsuzawa Y.
Adiponectin, an adipocyte-derived plasma protein, inhibits endothelial NF-kappaB signaling through a cAMP-dependent pathway.
Circulation
102:
1296-1301,
2000
22.
Scherer, PE,
Williams S,
Fogliano M,
Baldini G,
and
Lodish HF.
A novel serum protein similar to C1q, produced exclusively in adipocytes.
J Biol Chem
270:
26746-26749,
1995
23.
Tanner, CJ,
Koves TR,
Cortright RL,
Pories WJ,
Kim YB,
Kahn BB,
Dohm GL,
and
Houmard JA.
Effect of short-term exercise training on insulin-stimulated PI 3-kinase activity in middle-aged men.
Am J Physiol Endocrinol Metab
282:
E147-E153,
2002
24.
Vionnet, N,
Hani El H,
Dupont S,
Gallina S,
Francke S,
Dotte S,
De Matos F,
Durand E,
Lepretre F,
Lecoeur C,
Gallina P,
Zekiri L,
Dina C,
and
Froguel P.
Genomewide search for type 2 diabetes-susceptibility genes in French whites: evidence for a novel susceptibility locus for early-onset diabetes on chromosome 3q27-qter and independent replication of a type 2-diabetes locus on chromosome 1q21-q24.
Am J Hum Genet
67:
1470-1480,
2000[ISI][Medline].
25.
Weyer, C,
Funahashi T,
Tanaka S,
Hotta K,
Matsuzawa Y,
Pratley RE,
and
Tataranni PA.
Hypoadiponectinemia in obesity and type 2 diabetes: close association with insulin resistance and hyperinsulinemia.
J Clin Endocrinol Metab
86:
1930-1935,
2001
26.
Wilmore, JH.
A simplified method for determination of residual lung volumes.
J Appl Physiol
27:
96-100,
1969
27.
Yamauchi, T,
Kamon J,
Waki H,
Terauchi Y,
Kubota N,
Hara K,
Mori Y,
Ide T,
Murakami K,
Tsuboyama-Kasaoka N,
Ezaki O,
Akanuma Y,
Gavrilova O,
Vinson C,
Reitman ML,
Kagechika H,
Shudo K,
Yoda M,
Nakano Y,
Tobe K,
Nagai R,
Kimura S,
Tomita M,
Froguel P,
and
Kadowaki T.
The fat-derived hormone adiponectin reverses insulin resistance associated with both lipoatrophy and obesity.
Nat Med
7:
941-946,
2001[ISI][Medline].
28.
Yang, WS,
Lee WJ,
Funahashi T,
Tanaka S,
Matsuzawa Y,
Chao CL,
Chen CL,
Tai TY,
and
Chuang LM.
Weight reduction increases plasma levels of an adipose-derived anti-inflammatory protein, adiponectin.
J Clin Endocrinol Metab
86:
3815-3819,
2001
29.
Youngren, JF,
Keen S,
Kulp JL,
Tanner CJ,
Houmard JA,
and
Goldfine ID.
Enhanced muscle insulin receptor autophosphorylation with short-term aerobic exercise training.
Am J Physiol Endocrinol Metab
280:
E528-E533,
2001
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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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V. B. O'Leary, A. E. Jorett, C. M. Marchetti, F. Gonzalez, S. A. Phillips, T. P. Ciaraldi, and J. P. Kirwan Enhanced adiponectin multimer ratio and skeletal muscle adiponectin receptor expression following exercise training and diet in older insulin-resistant adults Am J Physiol Endocrinol Metab, July 1, 2007; 293(1): E421 - E427. [Abstract] [Full Text] [PDF]
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 M. G. Flynn, B. K. McFarlin, and M. M. Markofski State of the Art Reviews: The Anti-Inflammatory Actions of Exercise Training American Journal of Lifestyle Medicine, May 1, 2007; 1(3): 220 - 235. [Abstract] [PDF]
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 R. R. Kraemer and V. D. Castracane Exercise and Humoral Mediators of Peripheral Energy Balance: Ghrelin and Adiponectin Experimental Biology and Medicine, February 1, 2007; 232(2): 184 - 194. [Abstract] [Full Text] [PDF]
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C. R. Bruce, A. B. Thrush, V. A. Mertz, V. Bezaire, A. Chabowski, G. J. F. Heigenhauser, and D. J. Dyck Endurance training in obese humans improves glucose tolerance and mitochondrial fatty acid oxidation and alters muscle lipid content Am J Physiol Endocrinol Metab, July 1, 2006; 291(1): E99 - E107. [Abstract] [Full Text] [PDF]
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 H. Huang, K. T. Iida, H. Sone, T. Yokoo, N. Yamada, and R. Ajisaka The effect of exercise training on adiponectin receptor expression in KKAy obese/diabetic mice. J. Endocrinol., June 1, 2006; 189(3): 643 - 653. [Abstract] [Full Text] [PDF]
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C. Moro, J. Polak, J. Hejnova, E. Klimcakova, F. Crampes, V. Stich, M. Lafontan, and M. Berlan Atrial natriuretic peptide stimulates lipid mobilization during repeated bouts of endurance exercise Am J Physiol Endocrinol Metab, May 1, 2006; 290(5): E864 - E869. [Abstract] [Full Text] [PDF]
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 F. Abbasi, S.-A. Chang, J. W. Chu, T. P. Ciaraldi, C. Lamendola, T. McLaughlin, G. M. Reaven, and P. D. Reaven Improvements in insulin resistance with weight loss, in contrast to rosiglitazone, are not associated with changes in plasma adiponectin or adiponectin multimeric complexes Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2006; 290(1): R139 - R144. [Abstract] [Full Text] [PDF]
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 J. R. Berggren, M. W. Hulver, and J. A. Houmard Fat as an endocrine organ: influence of exercise J Appl Physiol, August 1, 2005; 99(2): 757 - 764. [Abstract] [Full Text] [PDF]
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 F. Guebre-Egziabher, J. Bernhard, T. Funahashi, A. Hadj-Aissa, and D. Fouque Adiponectin in chronic kidney disease is related more to metabolic disturbances than to decline in renal function Nephrol. Dial. Transplant., January 1, 2005; 20(1): 129 - 134. [Abstract] [Full Text] [PDF]
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H. Yokoyama, M. Emoto, T. Araki, S. Fujiwara, K. Motoyama, T. Morioka, H. Koyama, T. Shoji, Y. Okuno, and Y. Nishizawa Effect of Aerobic Exercise on Plasma Adiponectin Levels and Insulin Resistance in Type 2 Diabetes Diabetes Care, July 1, 2004; 27(7): 1756 - 1758. [Full Text] [PDF]
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 F. Abbasi, J. W. Chu, C. Lamendola, T. McLaughlin, J. Hayden, G. M. Reaven, and P. D. Reaven Discrimination Between Obesity and Insulin Resistance in the Relationship With Adiponectin Diabetes, March 1, 2004; 53(3): 585 - 590. [Abstract] [Full Text] [PDF]
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P. J. Havel Update on Adipocyte Hormones: Regulation of Energy Balance and Carbohydrate/Lipid Metabolism Diabetes, February 1, 2004; 53(90001): S143 - 151. [Abstract] [Full Text]
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A. Sierksma, H. Patel, N. Ouchi, S. Kihara, T. Funahashi, R. J. Heine, D. E. Grobbee, C. Kluft, and H. F.J. Hendriks Effect of Moderate Alcohol Consumption on Adiponectin, Tumor Necrosis Factor-{alpha}, and Insulin Sensitivity Diabetes Care, January 1, 2004; 27(1): 184 - 189. [Abstract] [Full Text] [PDF]
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G. Perseghin, G. Lattuada, M. Danna, L. P. Sereni, P. Maffi, F. De Cobelli, A. Battezzati, A. Secchi, A. Del Maschio, and L. Luzi Insulin resistance, intramyocellular lipid content, and plasma adiponectin in patients with type 1 diabetes Am J Physiol Endocrinol Metab, December 1, 2003; 285(6): E1174 - E1181. [Abstract] [Full Text] [PDF]
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M. Chandran, S. A. Phillips, T. Ciaraldi, and R. R. Henry Adiponectin: More Than Just Another Fat Cell Hormone? Diabetes Care, August 1, 2003; 26(8): 2442 - 2450. [Full Text] [PDF]
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