Glucose and homeostasis model assessment of insulin resistance

Int. j. Adv. Lif. Sci., Available online on at www.
Int. J. Adv. Lif. Sci., Available online on at www. ijals.com Page 610
International Journal of Advanced Life Sciences (IJALS)
ISSN
2277 – 758X
Husseini Masoomeh et al., IJALS, Volume (7) Issue (4) November - 2014. RESEARCH ARTICLE
Introduction
Prevalence of smoking tobacco products,
especially cigarettes, is increasing in the majority of
the developed or developing countries. In this regard,
literature greatly emphasizes the potential role of
cigarette in the development of chronic diseases
associated with metabolic disorders (Arnson et al.,
2010). Cardiovascular diseases, type II diabetes, athero-
sclerosis, high blood pressure, osteoporosis, and
respiratory diseases like chronic obstructive pulmonary
and asthma followed by detrimental effects on systemic
inflammation have been reported to be some of
the consequences of smoking (Karadag et al.,
2008; Groenewegen et al., 2008; Virginia et al., 2011).
Although most studies have pointed to the
reduced pulmonary performance (Kiter et al., 2000)
and metabolic disorders in smokers and also have
supported a relationship between smoking and total
cholesterol (TC) low density lipoprotein cholesterol
(LDL), and high density lipoprotein cholesterol (HDL)
(Mohiuddin et al., 2007) or other cardiovascular risk
factors like C-Reactive protein (CRP) (Karadag
et al., 2008), its role as an important indicator in
the development of type II diabetes has attracted the
attention of many health sciences researchers in recent
decades. Such that, the scientific references have
reported that smokers show higher levels of glucose,
insulin, and insulin resistance compared with non-
Abstract
Regular exercise training is associated with improved metabolic
markers in chronic diseases such as metabolic syndrome and diabetes, although
the role of acute exercise has not been thoroughly investigated. Our study
aimed to assess acute response of diagnosis markers of type II diabetes in
smokers. For this purpose, fifteen smoker men were completed an exercise test
with moderate intensity. Serum insulin, glucose were measured before and
at the end of the exercise. Insulin and glucose levels were used for the
homeostasis model assessment of insulin resistance. Pre- and post-test values
were determined with the Student ‘t’ test. Compared with pre test, glucose
concentration, serum insulin and insulin resistance were decreased
significantly (p < 0.05). Our findings state that indicator markers of type II
diabetes can be influenced by short time moderate-intensity exercise session in
smokers.
Keywords: Exercise, diabetes, insulin resistance and smoking
Glucose and homeostasis model assessment of insulin resistance responses to
exercise in smokers
Husseini Masoomeh*
, Reza Behdari* and Nooraei Farahnaz**
*Department of Exercise Physiology, East Tehran Branch, Islamic Azad University, Tehran, Iran,
**Department of Biology, North Tehran Branch, Islamic Azad University, Tehran, Iran
Email : mhbisadi@yahoo.com
Corresponding Author
Husseini Masoomeh
*Department of Exercise
Physiology, East Tehran Branch,
Islamic Azad University,
Tehran, Iran,
Email : mhbisadi@yahoo.com
Article History
Received on 08 August, 2014;
Received in revised form 04
September, 2014; Accepted 01
October, 2014

ISSN
2277 – 758X
smokers (Gupta et al., 2006). However, the main
molecular mechanisms responsible for this relationship
have not been fully recognized so far. In addition, the
assumption that smoking affects some cellular
metabolisms like changes in the sensitivity of target
cells to insulin have been argued in some studies, as
they have considered smoking as a risk factor for type
II diabetes (Foy et al., 2005 and Sairenchi et al., 2004).
Increasing pieces of evidence suggest that active or
inactive smoking is associated with insulin resistance
and reduced glucose tolerance (Tsujii et al., 2004 and
Nakanishi et al., 2000).
However, the role of internal or external
interventions in reducing the harmful effects of
cigarette should not be overlooked. Meanwhile, the
role of exercise in reducing the fasting blood glucose
and also increasing the insulin sensitivity in the mice
exposed to smoke has been reported in some recent
studies (Patrícia et al., 2011). It seems that muscular
activities, as an important interventional method
for coping with abnormalities or disorders caused by
smoking such as insulin resistance, are associated
with reduced prevalence of diabetes in susceptible
individuals or severity of disease and also improved
cardiovascular capacity of such people (Patrícia et al.,
2011). However, the effect of exercise on metabolic
disorders caused by smoking has been mainly restricted
to long-term training programs and few studies
have been conducted on acute responses of metabolic
markers to short-term or single session exercise
trainings. Hence, the present study aimed to study
the acute response of type II diabetes determinant
indicators to a single aerobic exercise session in male
smokers.
Methods
Human subjects
A total of 15 adult men participants with an
average age of 44 ± 2.5 years cigarette smoke,
voluntarily enrolled in this study. Subjects were
asked to complete questionnaires on anthropometric
characteristics, general health, smoking and present
medications. All participants had not participated in
regular exercise/diet programs for the preceding 6
months. Those with a history of metabolic diseases
were excluded. After the nature of the study was
explained in detail, informed consent was obtained
from all participants.
Obesity or overweight were measured by body
mass index (BMI). Body mass index (BMI) was
calculated by dividing body mass (kg) by height in
meters squared (m2). Height was measured without
shoes on standing while the shoulders were tangent
with the wall. Body weight was measured in the
morning following a 12-h fast. Body fat percentage
was determined using body composition monitor
(OMRON, Finland). Abdominal circumference and
hip circumference were measured in the most
condensed part using a non-elastic cloth meter.
Biochemistry and exercise test
All subjects underwent an exercise test included
40 min running, pre and post exercise glucose and
insulin were measured. Glucose was determined by
the oxidase method (Pars Azmoun, Tehran, Iran).
Plasma insulin was determined by ELISA method
(Demedite,German). Insulin resistance was determined
according to the HOMA-IR as the product of plasma
glucose (mM) and insulin (µU/ml) divided by the
constant 22.5 (Afreen and Krishnananda, 2013).
Exercise test was similar for all subjects, so they
exercised at 68 % of maximal heart rate. Subjects asked
to refrain from any severe physical activity 48 h before
measurements.
Data analysis
Data were analyzed using the program SPSS 11.0

ISSN
2277 – 758X
for Windows (Chicago, IL, USA). Values are presented
as mean ± standard deviation. The Kolmogorov-
Smirnov test was used to determine of normal status of
the data. Paired t test was used to determine the mean
differences between baseline and post-test values on all
metabolic variables. A probability level of p<0.05
was used to indicate statistical significance.
Result
This study aimed to determine the acute response
to glucose, insulin and insulin resistance to exercise
test in males with cigarette smoking. Table 1 shows the
descriptive anthropometric features of the study
subjects. All data represent are mean and SD.
Compared to pre-test, glucose concentration
decreased significantly (p = 0.000) after the exercise
test in studing subjects (from 93 ± 6 to 87 ± 6.8, mg/dl,
Fig.- 1).
A significant decrease was also found in insulin
resistance by an exercise test (from 3.71 ± 0.83; t - 2.81
± 0.89, Fig.- 2).
Insulin levels were significantly decreased after
the exercise test when compared with pre-test (from
16.2 ± 3.44 to 13 ± 4.52, µIU/ml, Fig.- 3 )
Discussion
The findings showed that a single session of
moderate-intensity in aerobic exercise is followed
by acute responses of glucose, insulin, and insulin
resistance in male smokers had a sedentary lifestyle
previously. In other words, blood glucose levels and
Table - 1. Mean and standard deviation of anthro-
pometrical markers of studied subjects
Variables Mean SD
Age (year) 43.8 2.54
Weight (kg) 90.2 5.56
Height (cm) 176.9 2.28
Body Fat (%) 28.5 2.11
Body mass index (kg/m2
) 28.8 2.06
Abdominal circumference
(cm)
97.7 5.22
Hip circumference (cm) 95.1 4.7
Fig. – 1. Glucose concentration in pre and post
training men
70
75
80
85
90
95
100
105
110
115
Pre-test Post-test
Glucoseconcentration(mg/dl)
Fig.- 2. Insulin resistance in pre and post training
men
0.00
1.00
2.00
3.00
4.00
5.00
6.00
7.00
Pre-test Post-test
Insulinresistance(HOMA-IR)
Fig.- 3. Serum insulin concentration in pre and post
training men
0.00
1.00
2.00
3.00
4.00
5.00
6.00
7.00
Pre-test Post-test
Insulinresistance(HOMA-IR)

ISSN
2277 – 758X
insulin resistance significantly decreased in male
smokers in response to a single session of aerobic
exercise (40 minutes running with a relatively moderate
intensity).
Previous studies have reported the increased
number of white blood cells (WBC) and leukocytes
in response to smoking (Frohlich et al., 2003 and
Wannamethee et al., 2005). There are pieces of
evidence indicating that the disorder or secretion of
inflammatory cytokines has a key role in insulin
resistance. In addition, recent studies have revealed
that inflammatory reactions caused by increased
cytokines such as IL-6, TNF-α, and IL-1 have a special
role in the prevalence, spread, and pathogenesis of
type II diabetes (Fernández-Real and Ricart, 2003;
Shulman, 2000). In this regard, several studies have
shown that inflammatory cytokines such as CRP
and tumor necrosis factor-alpha (TNF-α) increase
in response to smoking, which is associated with
the prevalence of COPD and cardiovascular diseases
(Karadag et al., 2008 and Groenewegen et al., 2008).
Recent studies have revealed that even the
second-hand smokers may be afflicted with type II
diabetes (Foy et al., 2005). Type II diabetes is a
common disease that its mechanism has not been fully
known yet. For a long time, it seemed that this disease
occurs only in genetically susceptible people, but
it has been found that, in addition to genetic reasons,
several dimensions of the modern lifestyle, especially
inactivity and high calorie intake cause an increase
in blood sugar and pancreatic malfunction. It seems
that tobacco consumption, specifically cigarette, is
also involved in the prevalence of type II diabetes. In
recent years, some studies have demonstrated that
smoking can considerably increase the risk of affliction
with type II diabetes (Sairenchi et al., 2004). Studies
have shown that smoking of more than 40 cigarettes a
day increases the risk of diabetes by 45% in men and
74% in women. Recent studies have shown that
smoking can gradually raise the blood sugar level and
also reduce the sensitivity of body organs to insulin.
Compared with non-smokers, the body of
professional smokers is less sensitive to insulin and,
interestingly, this sensitivity would return several
weeks or months after quitting smoking. On the
other hand, scientific studies have reported the
improvement of blood glucose levels and insulin
resistance in smokers, although the majority of these
studies have employed exercise sessions or long-
term training programs and the effects of short-term
trainings on the level of blood glucose and insulin
resistance has been rarely studied. However, in the
present study, a significant reduction in both glucose
level and insulin resistance in response to a single,
relatively long exercise session at relatively moderate
intensity was observed in adult male smokers.
References
Afreen, A.C. and Krishnananda, P. 2013. An Association
of High Sensitive C Reactive Protein and Lipid
Profile Parameters in South Indian Population.
International Journal of Scientific and Research
Publications., 3(7): 1 - 3.
Arnson, Y., Shoenfeld, Y. and Amital, H. 2010. Effects
of tobacco smoke on immunity, inflammation
and autoimmunity. J. Autoimmun., 34(3): 258 -
65.
Fernández-Real, J.M. and Ricart, W. 2003. Insulin
resistance and chronic cardiovascular inflamma-
tory syndrome Endocr. Rev., 24: 278 - 301.
Foy, C.P., Bell, R.A., Farmer, D.F., Goff, D.C. and
Wagenknecht, L.E. 2005. Smoking and Incidence
of Diabetes Among U.S. Adults. Findings from
the Insulin Resistance Atherosclerosis Study.
Diabetes Care., 28: 2501 – 7.

ISSN
2277 – 758X
Frohlich, M., Sund, M. and Frolich M. 2003.
Independent association of various smoking
characteristics with markers of systemic
inflammation in men: results from a representative
sample of the general population (MONICA
Augsburg Suvey 1994/95). Eur. Heart. J., 24 :
1365 - 1372.
Groenewegen, K.H., Postma, D.S. and Hop, W.C.
2008. Increased systemic inflammation is a
risk factor for COPD exacerbations. Chest., 133:
350 – 357.
Gupta, V., Tiwari, S., Agarwal, C.G., Shukla, P.,
Chandra, H. and Sharma, P. 2006. Effect of
short-term cigarette smoking on insulin
resistance and lipid profile in asymptomatic
adults. Indian J. Physiol. Pharmacol., 50(3): 285
- 90.
Karadag, F., Kirdar, S. and Karul, A.B. 2008. The value
of C-reactive protein as a marker of systemic
inflammation in stable chronic obstructive
pulmonary disease. Eur. J. Intern. Med., 19:104–
108.
Kiter, G., Ucan, E.S., Cylan, E. and Kilinic, C. 2000.
Water-pipe smoking and pulmonary function.
Respire. Med. J., 44 (9): 891 - 4.
Mohiuddin, S.M., Mooss, A.N. and Hunter, C.B.
2007. Intensive smoking cessation intervention
reduces mortality in high-risk smokers with
cardio vascular disease. Chest., 131: 446– 452.
Nakanishi, N., Nakamura, K., Matsuo, Y., Suzuki, K.
and Tatara, K. 2000. Cigarette Smoking and
Risk for Impaired Fasting Glucose and Type 2
Diabetes in Middle-Aged Japanese Men. Ann.
Intern. Med., 133: 183-91.
Patrícia, E.S. 2011. Physical Exercise Improves Insulin
Sensitivity of Rats Exposed to Cigarette Smoke.
Rev. Bras. Med. Esporte., 17(3): 202 - 206.
Sairenchi, T., Iso, H., Nishimura, A., Hosoda, T., Irie,
F. and Saito, Y. 2004. Cigarette Smoking
and Risk of Type 2 Diabetes Mellitus among
Middle-aged and Elderly Japanese Men and
Women. Am. J. Epidemiol., 160 : 158 - 62.
Shulman, G.I. 2000. Cellular mechanisms of insulin
resistance. J. Clin. Invest.,106: 171 - 6.
Tsujii, S. and Kuzuya, H. 2004. The significance of
lifestyle as a factor for the metabolic syndrome.
Nippon Rinsho., 62(6): 1047 - 1052.
Virginia, R., Xiangying, X., Diane, B., Daniel, J.,
Christine, F. and Patricia, F. 2011. A Pilot Study
to Examine the Effects of Smoking Cessation
on Serum Markers of Inflammation in Women
at Risk for Cardiovascular Disease. Chest.,
212 - 219.
Wannamethee, S.G., Lowe, G.D. and Shaper, A.G.
2005. Associations between cigarette smoking,
pipe/cigar smoking, and smoking cessation, and
haemostatic and inflammatory markers for
cardiovascular disease. Eur. Heart. J., 26:1765–
1773.
Weitzman M, Cook S, Auinger P, Florin TA, Daniels S,
Nguyen M, Winickoff JP. 2005. Tobacco smoke
exposure is associated with the metabolic
syndrome in adolescents. Circulation., 112(6):
862 - 269.
Corresponding Author : Husseini Masoomeh, Department of Exercise Physiology, East Tehran Branch, Islamic Azad
University, Tehran, Iran, Email : mhbisadi@yahoo.com © 2014, IJALS. All Rights Reserved.

Glucose and homeostasis model assessment of insulin resistance

Recomendados

Recomendados

Mais conteúdo relacionado

Mais procurados

Mais procurados (19)

Semelhante a Glucose and homeostasis model assessment of insulin resistance

Semelhante a Glucose and homeostasis model assessment of insulin resistance (19)

Glucose and homeostasis model assessment of insulin resistance