Science & Sports (2013) 28, 75—80

Disponible en ligne sur

www.sciencedirect.com

ORIGINAL ARTICLE

Effects of training on body composition, blood lipids,

and glucose homeostasis assessed by the homeostasis
model assessment
Effets de l’entraînement sur la composition corporelle, les lipides
plasmatiques et l’homéostasie du glucose

M. Eizadi a,∗, G. Bagheri b, J.M. Kasparast c, F. Zahedmanesh d, Z. Afsharmand d

a
Laboratory of Exercise physiology, Department of physical Education and Sport Science, Saveh Branch, Islamic Azad University,
Saveh, Iran
b
Department of Physical Education and Sport Science, Tehran university, Qom college, Iran
c
Department of physical Education and Sport Science, Karaj Branch, Islamic Azad University, Karaj, Iran
d
Department of physical Education and Sport Science, Islamshahr Branch, Islamic Azad University, Islamshahr, Iran

Received 27 August 2011; accepted 9 January 2012

Available online 16 February 2012

KEYWORDS Summary
Glycemic control; Objective. — To determine effect of aerobic exercise training on glucose homeostasis, body
Exercise training; composition and lipid profile in presence of obesity.
Diabetes; Methods. — A total 34 middle-aged (43 ± 3 years) obese men (BMI = 32.1 ± 2.9 kg/m2 ) were
Obesity divided into exercise (3 months aerobic exercise, three times weekly) or control (detraining)
group. Fasting glucose, triglyceride (TG), high-density lipoprotein (HDL), beta-cell function and
anthropometrical indexes measured before and after aerobic exercise intervention or detrain-
ing in exercise and control group respectively. Statistical analysis was performed with the SPSS
software version 15.0 using an independent paired t-test. The P-value < 0.05 was considered
statistically significant.
Results. — There are no differences in anthropometrical or biochemical variables in baseline
in two groups (P ≥ 0.05). Exercise intervention led to significant decrease in fasting glucose,
TG, TG/HDL ratio, systolic blood pressure and all anthropometrical indexes in exercise group
(P < 0.05). Insulin concentrations of exercise group increased significantly after intervention
(P < 0.05). There were no significant changes in insulin resistance by exercise intervention
in exercise group. But, beta-cell function increased significantly (P < 0.05). No changes were
observed in all variables in control group (P ≥ 0.05).

∗
Corresponding author.
E-mail addresses: izadimojtaba2006@yahoo.com (M. Eizadi), ghbagheri@ut.ac.ir (G. Bagheri), kasbparast@yahoo.co.uk
(J.M. Kasparast), Zahedmanesh2006@yahoo.com (F. Zahedmanesh), Afsharmand ro@yahoo.com (Z. Afsharmand).

0765-1597/$ – see front matter © 2012 Elsevier Masson SAS. All rights reserved.
doi:10.1016/j.scispo.2012.01.001
76 M. Eizadi et al.

Conclusion. — Despite no significant change on insulin resistance in response to aerobic exercise

training in middle-aged obese males, but was associated with an improvement in body composi-
tion and lipid profile and particularly fasting glucose in these subjects. It seems that reduction
in blood glucose has occurred in response to increased insulin secretion of pancreas beta-cells.
© 2012 Elsevier Masson SAS. All rights reserved.

Résumé
MOTS CLÉS Objectif. — Il s’agit de déterminer l’effet de l’entraînement physique aérobie sur l’homéostasie
Contrôle de la du glucose, la composition corporelle et le profil lipidique chez des patients obèses.
glycémie ; Méthodes. — Un total de 34 hommes d’âge moyen (43 ± 3 ans), obèses (IMC = 32,1 ± 2,9 kg/m2 )
Entraînement ont été répartis en deux groupes, l’un soumis à un programme d’activité physique (trois mois
physique ; d’exercices de type aérobie, trois fois par semaine), l’autre constituant le groupe témoin (sans
Diabète ; programme d’activité physique). Différents indices anthropométriques, la glycémie à jeun, les
Obésité triglycérides (TG) et lipoprotéines de haute densité (HDL) plasmatiques, ainsi que la fonction
des cellules bêta du pancréas ont été mesurés avant et après l’intervention du programme
d’activité physique. L’analyse statistique a été réalisée avec la version du logiciel SPSS 15,0 en
utilisant un test-t de Student pour effectifs appariés. La valeur p < 0,05 a été considérée comme
statistiquement significative.
Résultats. — Il n’y a pas de différences significatives dans les variables anthropométriques et
biochimiques de base entre les deux groupes. Le suivi du programme d’activité physique s’est
traduit par une diminution significative de la glycémie à jeun, des TG, du ratio TG/HDL, de la
pression artérielle systolique et de tous les indices anthropométriques (p < 0,05). Les concen-
trations d’insuline plasmatique ont été augmentées de façon significative après l’intervention
par le programme d’entraînement physique (p < 0,05). Il n’y a eu aucune amélioration de la
sensibilité à l’insuline dans le groupe exercice. Mais, la fonction des cellules bêta a augmenté
significativement (p < 0,05). Les variables anthropométriques et biologiques étudiées n’ont pas
été affectées dans le groupe témoin.
Conclusion. — Malgré l’absence d’amélioration de la sensibilité à l’insuline en réponse à
l’entraînement physique chez des sujets obèses d’âge moyen, on retient une amélioration de
la composition corporelle, du profil lipidique et de la glycémie à jeun. Il est probable que la
réduction de la glycémie soit liée à une meilleure réponse insulinique.
© 2012 Elsevier Masson SAS. Tous droits réservés.

1. Introduction habits, insulin secretion is not sufficient to compensate

Initial studies have reported both hyperinsulinemia and
insulin resistance simultaneously in obese individuals [1].
Obesity which is identified by increased body fat tissue is
one of the most important risk factors for type II diabetes,
hypertension, hyperlipidaemia, and arteriosclerosis diseases
such as coronary vascular disease [2]. Impairment of insulin
secretion in obese adults also has been frequently observed
[3,4]. Longitudinal studies have shown that the development
of impaired beta-cell function is especially important in
the prevalence of diabetes [5]. Factors promoting beta-cell
dysfunction and increased incidence of diabetes in obese
people are not fully understood. [6]. On the other hand,
some studies suggest that damage to the pancreatic beta-
cell sensitivity to glucose and the inability of these cells to
compensate for insulin resistance are apparent in healthy
older people, particularly in obese individuals [4].
Based on observations in the past decade, it is generally
accepted that obesity is associated with an impaired utiliza-
tion of fat as a fuel. A number of studies have demonstrated
that raised levels of fatty acids, cytosolic triglycerides or
hyperglycemia associated with obesity and insulin resis-
tance may affect beta-cell function in those predisposed
to diabetes [7—8]. Scientific sources have revealed that
when insulin resistance is elevated by the increased con-
sumption of fat and simple sugars associated with dietary
for insulin resistance [9]. Although some studies have also
stated that the acute increase in insulin resistance leads
to increased beta-cell mass or increased insulin secretion
to compensate for insulin resistance [10—11]. Conversely,
severe or prolonged insulin resistance in obese or diabetic
patients is associated with decline in beta-cell prolifera-
tion and impaired beta-cell function. Consequently, as a
result in response to long-term insulin resistance, beta-
cell expansion cannot be sustained for long periods [11],
which ultimately results in reduced secretion of insulin and
increased blood glucose concentration in these subjects.
While these reports have been as recent studies on labora-
tory animals have shown that inadequate secretion of insulin
due to destruction of pancreatic beta-cells in response to
prolonged insulin resistance with increased prevalence of
the disease in people with type II diabetes and is associated
with [11—12].
Hence, extensive studies aimed at reducing the glucose
concentration by improving insulin function, are underway
by health researchers. In this regard, longitudinal studies
have shown that prolonged exercise leads to improved
insulin and insulin resistance [13]. Recent studies suggest
that exercise; especially prolonged activities lead to
increased insulin sensitivity, reduced insulin resistance and
improved lipid profile and obesity related diseases in obese
individuals [14—15]. On the other hand, although some
Exercise, obesity and beta-cell function
studies have focused on mechanisms of insulin function in
animal models and more or less human populations [6,14],
but the role of physical activity or long-term exercise in this
area in humans has received limited attention. This study,
therefore, is aimed at the response of insulin function and
blood glucose concentration also body composition and lipid
profile to prolonged aerobic exercise in obese middle-aged
men.
2. Methods
2.1. Subjects
This randomized controlled trail study was approved by
the ethics committee of Saveh Azad University. This
study investigated the effects of a three-month aerobic
training program on glucose homeostasis, body compo-
sition and lipid profile in obese middle-aged men. For
this purpose, thirty-four middle-aged (43 ± 3 years) obese
(BMI = 32.1 ± 2.9 kg/m2 ) men participated in the study. Sub-
jects included in the study were divided into two groups
(experimental or control). Demographic characteristics of
patient and control groups were similar. All participants gave
informed consent before recruitment.
2.2. Inclusion or exclusion criteria
Subjects with a history or clinical evidence of impaired
fasting glucose or diabetes, recent myocardial infarction,
congestive heart failure, active liver or kidney disease,
growth hormone deficiency or excess, neuroendocrine
tumor, anemia or who were on medications known to alter
insulin sensitivity were excluded. Neither the control nor
experimental subjects had participated in regular exercise
for the preceding 6 months, nor did all subjects have sta-
ble body weight. All subjects were non-smokers. In addition,
exclusion criteria included supplementations that alter car-
bohydrate metabolism.
2.3. Anthropometric measures
Anthropometric measurements of height, weight, percent
body fat, body mass index and circumference measurements
were taken pre- and postexercise training. Waist circum-
ference was measured at the level of the umbilicus using
a nonelastic tape to the nearest 0.1 cm. Height and body
mass were measured using a wall- mounted stadiometer and
a digital scale, respectively. Body mass index was calcu-
lated as body mass (in kilograms) divided by height squared
(in square meters). Blood pressure was measured using the
left arm after the subject had been sitting comfortably for
5 minutes, using a blood pressure device (Alpikado, Japan).
2.4. Blood sampling and exercise program
A venous blood sample was collected from all the subjects
who came after a 12-hour overnight fast for measuring of
glucose and insulin concentration. Serums were immediately
separated and stored at —80◦ until the assays were per-
formed. Then, the experimental group performed an aerobic
77
exercise program in 60—80% maximal heart rate. Exercise
training duration was 3 months (three times, weekly). Typ-
ical exercise sessions consisted of a 5-minute warm-up;
45 minutes of aerobic training consist of running on tread-
mill or stationary cycling, and 5—10 minutes of cool down
activity. Polar heart rate (HR) monitors were worn by the
subjects during every exercise session. Finally, 48 hours after
the last exercise session, the blood sampling repeated after
overnight fast. Also, blood sampling at all time stages was
performed on the control group except that they did not
participate in long-time aerobic exercise program. Glu-
cose oxidase method (Pars Azmun, Tehran, Iran) was used
for measuring blood glucose and insulin was measured by
Elisa method (Demeditec, Germany). Triglyceride concen-
tration was measured by Pars Azmoon commercial kits using
Kobas Mira auto-analyzer made in Germany. The anthro-
pometric measurements repeated after a 3-month training
period again. The HOMA1-IR index was calculated by the for-
mula: HOMA1-IR = fasting plasma insulin (␮U/mL) × fasting
plasma glucose (mmol/L) /22.5 [16]. The HOMA2-IR index
was obtained by the program HOMA Calculator v2.2.2 [17].
2.5. Statistical analysis
Data were expressed as individual values or the mean ± SD
for groups. Data were analyzed by computer using the Statis-
tical Package for Social Sciences (SPSS) for Windows, version
15. Independent samples t-test was used to compare base-
line levels of anthropometric and biochemical variables of
control and experimental groups. Paired Student t-test was
used to determine significance levels of changes in any of
the variables compared to baseline conditions after exer-
cise interventions. A Pearson correlation method were used
to determine the associations between change in beta-
cell function and change in concentrations of Triglyceride
changes by exercise training. The differences between the
groups were considered to be significant at a P-value ≤ 0.05.
3. Results
There were 34 obese middle-aged men (43 ± 3 years) in
this study and they had mean body mass index upper
than 30 kg/m2 (range 30—36 kg/m2 ). Anthropometric and
metabolic characteristics of the study participants in the
control and exercise groups are shown in Table 1. The
findings of the independent t-test showed no significant dif-
ferences in the baseline anthropometric and biochemical
parameters between control and exercise groups which indi-
cates similarity between the exercise and control groups
in all variables before the training program (P ≥ 0.05).
Comparison of mean changes in beta-cell function before
and after the exercise intervention showed that aerobic
exercise training significantly increased beta-cell func-
tion in the exercise group (P < 0.01) while no change was
observed in the control group (P = 0.211). The three-month
exercise intervention significantly reduced fasting glucose
concentration (P < 0.05, Fig. 2), serum triglyceride levels
(P < 0.05) and TG/HDL ratio (P < 0.05, Fig. 1) in the exer-
cise group while there was no change in the control group
after detraining intervention compared to baseline lev-
els (P ≥ 0.05). Exercise intervention significantly decreased
 78 M. Eizadi et al.

Table 1 Anthropometrical and biochemical characteristics in the baseline and after interventions of two groups.

Variable Exercise group Control group

Pretest Post-test Pretest Post-test

Weight (kg) 102 ± 11a 97 ± 9 101 ± 9 100 ± 9

WC (cm) 107 ± 10a 103 ± 11 106 ± 9 106 ± 11
BMI (kg/m2 ) 32.1 ± 2.9a 30.8 ± 3.4 32.2 ± 2.3 31.9 ± 1.8
BF (%) 31.6 ± 2.14a 27.3 ± 3.21 31.1 ± 3.23 30.9 ± 3.68
Systolic pressure (mmHg) 128 ± 21a 116 ± 15 126 ± 17 121 ± 13
Diastolic pressure (mmHg) 89 ± 9 84 ± 8 85 ± 8 82 ± 9
Glucose (mg/dL) 103 ± 12a 89 ± 8 105 ± 11 101 ± 7
Insulin (␮U/mL) 7.97 ± 2.01a 9.42 ± 2.14 7.78 ± 1.68 7.65 ± 1.23
TG (mg/dL) 178 ± 18a 132 ± 12 174 ± 11 168 ± 10
TG/HDL 3.83 ± 0.22a 2.75 ± 0.21 3.77 ± 0.31 3.68 ± 0.28
HOMA1-IR 2.02 ± 0.23 2.07 ± 0.39 2.01 ± 0.29 1.90 ± 0.36
HOMA2-IR 1.1 ± 0.09 1.2 ± 1.11 1 ± 0.08 1 ± 0.11
HOMA2-(%B) 75 ± 8a 112 ± 17 71 ± 9 75 ± 11
Data represent mean ± standard deviation.
a Represent significant changes compared to baseline levels; Pretest: baseline; Post-test: after intervention; WC: waist circumference;

BMI: body mass index; BF: body fat percentage; TG/HDL: triglyceride to low-density lipoprotein ratio; HOMA-(%B): beta-cell function
index.

5 Pre systolic blood pressure in exercise group (P < 0.05), while

Post-test no change observed in diastolic blood pressure in these
4 subjects (P = 0.124). Exercise training resulted in signif-
icant increase in serum insulin (P < 0.05). A significant
*
TG / HDL

3 decrease was observed in body weight (P < 0.05) and body

fat percentage (P < 0.01) after exercise intervention in the
2 exercise group. No significant change in insulin resistance
(either HOMA-1 or HOMA-2) was observed after exercise
1
intervention in exercise group (P ≥ 0.05). There is a high neg-
ative correlation between change in beta-cell function and
0
change in concentrations of triglyceride changes by exercise
Control Exercise
intervention in exercise group (P < 0.05, r = —0.55).
Figure 1 The triglyceride high-density lipoprotein (TG/HDL)
ratio data in pre-(baseline) and post-test (intervention) of con- 4. Discussion
trol and exercise group. The three-month exercise intervention
significantly decreased TG/HDL ratio in the exercise group What is certain is the primary cause of type II diabetes is
(P = 0.014) while no change was observed in the control group insulin resistance phenomenon and beta-cell dysfunction is
compared to pre-test levels (P ≥ 0.05). the secondary cause. Nonetheless, some Asian studies have
140
Pre reported beta-cell dysfunction as the primary factor in the
Post-test
pathogenesis of type II diabetes [18—19]. The findings of this
120 study showed that prolonged exercise by obese adults leads
* to decreased fasting glucose, body weight, TG, TG/HDL
Glucose (mg/dL)

100
ratio and increase beta-cell function (%B). Accumulating evi-
80 dence indicates that lifestyle changes such as weight loss
60 and regular physical activity are recognized as effective
none-pharmacological interventions with beneficial effects
40
on metabolic and cardiovascular risk factors [20—21]. Insulin
20 functional falls with increasing obesity, especially central
obesity, and there is associated impairment of glucose tol-
0
Control Exercise erance, dyslipidaemia and systemic hypertension. These
features constitute the metabolic syndrome, and each is
Figure 2 Fasting glucose concentration in pre-(baseline) and known to be associated with increased cardiovascular risk
post-test (intervention) of control and exercise group. The [22]. In healthy individuals, insulin secretion from pancre-
three-month exercise intervention significantly reduced fasting atic is related to peripheral insulin sensitivity through a
glucose concentration (P = 0.011) in the exercise group while postulated negative feedback loop which enables beta-cells
there was no change in the control group compared to pre-test to compensate for any change in total body sensitivity to
levels (P ≥ 0.05). insulin by a proportionate and reciprocal change in insulin
Exercise, obesity and beta-cell function
secretion [23]. It was observed that exercise increases
insulin sensitivity under normal conditions and to ameliorate
impaired insulin action in insulin-resistant humans and ani-
mals [24]. However, the role of exercise training on beta-cell
function and mass in obese or obesity-induced diseases has
not drawn much attention. Although, several studies have
suggested that regular exercise decreases insulin secretion
by insulin secretagogues [25—26]. But, our study showed
that after exercise training was completed, serum insulin
levels increased significantly in exercise group. Consistent
with our findings, some studies have demonstrated that long-
term exercise enhances glucose-stimulated insulin secretion
in humans and experimental [27—28]. In confirmation of
the findings of the present study, the findings of a recent
study showed that seven sessions of aerobic exercise leads
to significant improvement of beta-cell function in older
people with glucose tolerance impairment [15]. Although
in the said study, increase in beta-cells function was not
associated with changes in body weight and blood glu-
cose concentrations [15], but enhanced beta-cell function in
obese patients in our present was accompanied with weight
loss, decreased body fat percentage and a decrease in blood
glucose concentration and serum triglycerides. In this area,
a recent study demonstrated that improved beta-cell secre-
tion or increased circulating insulin indicates that, to some
extent, beta-cell dysfunction is reversible with weight loss
[29]. In obese people, weight reduction is associated with a
reduced risk of developing chronic diseases such as type 2
diabetes, improved glycemic control and, with considerable
weight loss, remission of type 2 diabetes [30—31]. Although
insulin resistance remained without significant change in our
study but fasting glucose decreased significantly in studied
subject. On the other hand, insulin levels were significantly
increased in response to exercise intervention. Therefore,
it seems that reduced glucose has occurred in response to
increased insulin secretion of pancreas beta-cells.
This study also showed that there is a significant rela-
tionship between the increase in beta-cell function and
reduced blood glucose concentrations in the study subjects.
In this regard, some studies in rats and in humans have also
revealed that the decline in beta-cell function has a strong
correlation with decreased levels of glucose transporter-2
(GLUT2) mRNA and protein levels [32—33]. In addition, some
authors noted a role for molecular candidates/markers in
the control of the relationship between net beta-cell growth
and net beta-cell death. One such study indicates a role of
the insulin/insulin-like growth factor I signaling pathway in
the adaptive ß -cell response to insulin resistance [10]. Exer-
cise training is associated with increased beta-cell function
[14]. Also, in people with diabetes, regular exercise train-
ing increases insulin response to hyperglycemia which refers
to the effect of exercise on beta-cell function [27]. In spite
of the increase in beta-cell function and reduced blood glu-
cose concentrations in this study, effective mechanisms in
decline of beta-cell function due to aging or obesity, and the
role of exercise in beta-cell function can not be explained
based merely on findings of the recent study.
It is possible that exercise-induced weight loss affected
insulin secretion or circulation glucose levels indirectly
or by affecting improvement in circulating levels of some
adipocyte-secreted cytokines such as leptin, adiponectin,
resistin or interleukins. However, the exact molecular
79
mechanisms of these changes remain to be clarified. In this
area, a number of studies have demonstrated that there
are receptors of these cytokines in pancreas beta-cells, and
any improvement in these cytokines in result of weight loss
is accompanied with improvement in circulation glucose
and insulin balance in obese or type 2 diabetic patients
[15,34—39]. For example, increased serum adiponectin in
response to exercise training leads to glucose reduction
or glycemic control by decreasing hepatic glucose produc-
tion through direct inhibition of hepatic gluconeogenesis
enzymes i.e. phosphoenolpyruvate carboxykinase and
Glucose 6-phosphate [40]. Lack measuring these cytokines
is a limitation of our study.
5. Conclusion
Our study demonstrates that exercise training for 3 months
is accompanied with weight loss. Although insulin did not
change in response to exercise intervention, but exercise-
induced weight loss leads to an improvement in glucose
homeostasis and lipid profile. It seems that blood glucose
reduction in response to exercise training in these middle-
aged obese males has occurred in response to increased
insulin secretion of pancreas beta-cells. Also, since the exer-
cise intervention was associated with decrease in body fat
percentage, it is likely that improved glucose homeosta-
sis after exercise intervention was related to improvement
in adipocyte-secreted cytokines. Of course, the lack of
cytokine measure is a limitation of our study.
Disclosure of interest
The authors declare that they have no conflicts of interest
concerning this article.
Acknowledgements
The authors thank all of the obese men who participated in
the study. Thanks are due to assistant Professor Dr. Sohaily
Shahram for valuable suggestions and statistical analyses.
We acknowledge the excellent laboratory assistance of Dr.
Zaryfyan Asghar.
References
[1] Muller EE, Locatelli V, Cocchi D. Neuroendocrine control of
growth hormone secretion. Physiol Rev 1999;79(2):511—607.
[2] Yukihiro Y, Hiroshi H, Ikuo S, Motowo T, Matsuo T, Koichi M, et al.
Correlation of the adipocyte-derived protein adiponectin with
insulin resistance index and serum high-density lipoprotein-
cholesterol, independent of body mass index, in the Japanese
population. Clin Sci 2002;103(2):137—42.
[3] Basu R, Breda E, Oberg AL, Powell CC, Dalla Man C, Basu A,
et al. Mechanisms of the age-associated deterioration in glu-
cose tolerance: contribution of alterations in insulin secretion,
action, and clearance. Diabetes 2003;52(7):1738—48.
[4] Chang AM, Smith MJ, Galecki AT, Bloem CJ, Halter JB.
Impaired ß-cell function in human aging: response to nico-
tinic acid-induced insulin resistance. J Clin Endocrinol Metab
2006;91(9):3303—9.
80
[5] Weyer C, Bogardus C, Mott DM, Pratley RE. The natural his-
tory of insulin secretory dysfunction and insulin resistance in
the pathogenesis of type 2 diabetes mellitus. J Clin Invest
1999;104(6):787—94.
[6] Morioka T, Asilmaz E, Hu J, Dishinger JF, Kurpad AJ, Elias CF,
et al. Disruption of leptin receptor expression in the pancreas
directly affects ␤ cell growth and function in mice. J Clin Invest
2007;117(10):2860—8.
[7] Gleason CE, Gonzalez M, Harmon JS, Robertson RP. Determi-
nants of glucose toxicity and its reversibility in the pancreatic
islet beta-cell line HIT-T15. Am J Physiol Endocrinol Metab
2000;279(5):997—1002.
[8] Bakker SJ, Rg IJ, Teerlink T, Westerhoff HV, Gans RO, Heine
RJ. Cytosolic triglycerides and oxidative stress in central
obesity: the missing link between excessive atherosclerosis,
endothelial dysfunction, and beta-cell failure? Atherosclerosis
2000;148(1):17—21.
[9] Cockram CS. The epidemiology of diabetes mellitus in the Asia-
Pacific region. Hong Kong Med J 2000;6(1):43—52.
[10] Jetton TL, Lausier J, LaRock K, Trotman WE, Larmie B,
Habibovic A, et al. Mechanisms of compensatory beta-cell
growth in insulin-resistant rats: roles of Akt kinase. Diabetes
2005;54(8):2294—304.
[11] Weir GC, Bonner-Weir S. Five stages of evolving ß-
cell dysfunction during progression to diabetes. Diabetes
2004;53(3):16—21.
[12] Withers DJ, Gutierrez JS, Towery H, Burks DJ, Ren JM, Previs
S, et al. Disruption of IRS-2 causes type 2 diabetes in mice.
Nature 1998;391(6670):900—4.
[13] Kirwan JP, Kohrt WM, Wojta DM, Bourey RE, Holloszy JO.
Endurance exercise training reduces glucose-stimulated insulin
levels in 60- to 70-year-old men and women. J Gerontol
1993;48(3):84—90.
[14] Király MA, Bates HE, Kaniuk NA, Yue JT, Brumell JH, Matthews
SG, et al. Swim training prevents hyperglycemia in ZDF rats:
mechanisms involved in the partial maintenance of beta-cell
function. Am J Physiol Endocrinol Metab 2008;294(2):271—83.
[15] Bloem CJ, Chang AM. Short-term exercise improves B-cell
function and insulin resistance in older people with impaired
glucose tolerance. J Clin Endocrinol Metab 2008;93(2):
387—92.
[16] Marita AR, Sarkar JA, Rane S. Type 2 diabetes in non-
obese Indian subjects is associated with reduced leptin
levels: study from Mumbai Western India. Mol Cell Biochem
2005;275(1—2):143—51.
[17] Diabetes Trials Unit, Oxford University. HOMA-2 Calcula-
tor. Available at: www.dtu.ox.ac.uk/homa Accessed 27 Oct
2004.
[18] Kim DJ, Lee MS, Kim KW, Lee MK. Insulin secretory dysfunc-
tion and insulin resistance in the pathogenesis of Korean type
2 diabetes mellitus. Metabolism 2001;50(5):590—3.
[19] Matsumoto K, Miyake S, Yano M, Ueki Y, Yamaguchi Y, Akazawa
S, et al. Glucose tolerance, insulin secretion, and insulin sensi-
tivity in no obese and obese Japanese subjects. Diabetes Care
1997;20(10):1562—8.
[20] Ryan AS. Insulin resistance with aging. Effects of diet and exer-
cise. Sports Med 2000;30(5):327—46.
[21] Braith RW, Stewart KJ. Resistance exercise training: its
role in the prevention of cardiovascular disease. Circulation
2006;113(22):2642—50.
[22] Timar O, Sestier F, Levy E. Metabolic syndrome X: A review. Can
J Cardiol 2000;16(6):779—89.
[23] Retnakaran R, Hanley AJ, Raif N, Hirning CR, Connelly PW,
Sermer M, et al. Adiponectin and beta cell dysfunction
M. Eizadi et al.
in gestational diabetes: pathophysiological implications.
Diabetologia 2005;48(5):993—1001.
[24] Perrini S, Henriksson J, Zierath JR, Widegren U. Exercise-
induced protein Kinase C isoform-specific activation in human
skeletal muscle. Diabetes 2004;53(1):21—4.
[25] Dela F, Mikines KJ, Tronier B, Galbo H. Diminished arginine-
stimulated insulin secretion in trained men. J Appl Physiol
1990;69(1):261—7.
[26] King DS, Staten MA, Kohrt WM, Dalsky GP, Elahi D, Hol-
loszy JO. Insulin secretory capacity in endurance-trained
and untrained young men. Am J Physiol Endocrinol Metab
1990;259(2):155—61.
[27] Dela F, von Linstow ME, Mikines KJ, Galbo H. Physical training
may enhance beta-cell function in type 2 diabetes. Am J Physiol
Endocrinol Metab 2004;287(5):E1024—31.
[28] Farrell PA, Caston AL, Rodd D. Changes in insulin response to
glucose after exercise training in partially pancreatectomized
rats. J Appl Physiol 1991;70(4):1563—8.
[29] Dixon JB, Dixon AF, O’Brien PE. Improvements in insulin sen-
sitivity and beta-cell function (HOMA) with weight loss in the
severely obese. Homeostatic model assessment. Diabet Med
2003;20(2):127—34.
[30] Dixon JB, O’Brien PE. Health outcomes of severely obese type
2 diabetic subjects 1-year after laparoscopic adjustable gastric
banding. Diabetes Care 2002;25(2):358—62.
[31] Heymsfield SB, Segal KR, Hauptman J, Lucas CP, Boldrin MN,
Rissanen A, et al. Effects of weight loss with orlistat on glucose
tolerance and progression to type 2 diabetes in obese adults.
Arch Intern Med 2000;160(9):1321—6.
[32] Harmon JS, Gleason CE, Tanaka Y, Poitout V, Robertson RP.
Antecedent hyperglycemia, not hyperlipidemia, is associated
with increased islet triacylglycerol content and decreased
insulin gene mRNA level in Zucker diabetic fatty rats. Diabetes
2001;50(11):2481—6.
[33] Tanaka Y, Gleason CE, Tran PO, Harmon JS, Robertson RP.
Prevention of glucose toxicity in HIT-T15 cells and Zucker dia-
betic fatty rats by antioxidants. Proc Natl Acad Sci U S A
1999;96(19):10857—62.
[34] Wang C, Guan Y, Yang J. Cytokines in the progression of pan-
creatic b-cell dysfunction. Int J Endocrinol 2010;2010:515136.
Epub.
[35] Zhao YF, Feng DD, Chen C. Contribution of adipocyte-derived
factors to beta-cell dysfunction in diabetes. Int J Biochem Cell
Biol 2006;38(5—6):804—19.
[36] Park S, Hong SM, Sung SR, Jung HK. Long-term effects of central
leptin and resistin on body weight insulin resistance and ß-cell
function and mass by the modulation of hypothalamic leptin
and insulin signaling. Endocrinology 2008;149(2):445—54.
[37] Monzillo LU, Hamdy O, Horton ES, Ledbury S, Mullooly C,
Jarema C, et al. Effect of lifestyle modification on adipokine
levels in obese subjects with insulin resistance. Obes Res
2003;11(9):1048—54.
[38] Jung SH, Park HS, Kim KS, Choi WH, Ahn CW, Kim BT, et al.
Effect of weight loss on some serum cytokines in human
obesity: increase in IL-10 after weight loss. J Nutr Biochem
2008;19(6):371—5.
[39] Milan G, Granzotto M, Scarda A, Calcagno A, Pagano C,
Federspil G, et al. Resistin and adiponectin expression in
visceral fat of obese rats: effect of weight loss. Obes Res
2002;10(11):1095—103.
[40] Yamauchi T, Kamon J, Minokoshi Y, Ito Y, Waki H, Uchida S,
et al. Adiponectin stimulates glucose utilization and fatty-acid
oxidation by activating AMP-activated protein kinase. Nat Med
2002;8(11):1288—95.