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Correspondence: Javad Mohiti, Yazd Diabetes Research Center, Joomhori Avenue, Yazd, Iran.
E-mail: mohiti_99@yahoo.com
Introduction
Leptin, a 16 kDa circulating hormone produced and released primarily by adipose tissue, exerts a regulatory control mechanism
on food intake via inhibition of neuropeptide
Y and increases the basal metabolism rate
with selectively promoting fat metabolism.1
Leptin has two types of receptors; the long
form and humorous short form. At the beginning direct leptin actions were thought to be
exclusively confined to the central nervous
system (CNS). It is now clear that there are
multiplicities of peripheral target organs such
as the pancreas, skeletal muscle, liver and
gastrointestinal system.2,3
Leptin appears to play a range of roles as a
growth factor in a number of different cell
types, such as a mediator of energy expenditure and most importantly interaction with
other hormonal mediators and regulators of
energy and metabolism such as insulin, glucagon, growth hormone and glucocorticoids.5,6,7
A large body of evidence indicates that
leptin along with insulin exerts an inhibitory
effect on food intake, and an activation effect
ORIGINAL ARTICLE
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J. Mohiti et al.
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Table 1. The characteristic and results analysis of obese and non-obese Type II diabetic patients
Variable
Leptin (g/L)
Insulin (Iu/mL)
FBS (mg/dL)
HbA1c (%)
Cholesterol (mg/dL)
Triglycerides (mg/dL)
Group A
(n=32)
21.811.2
11.445.8
174.629.97
8.760.36
222.1511.82
21911.18
Statistical analysis
Data were analyzed using the SPSS statistical package program. The obese group was
compared to the non-obese group using twotailed students t-test. Correlation between
the groups was tested by the Pearson test. A
P value <0.05 was considered statistically
significant.
Group B
(n=17)
5.161.20
6.751.20
177.5813.25
9.380.56
194.059.38
25441.10
P
0.001
0.078
0.86
0.340
0.053
0.299
Table 2. Correlation between Leptin and Insulin, FBS, HbA1c, Cholesterol, Triglyreceride
(TG), and BMI in group A
Leptin
Insulin
FBS
HbA1c
Cholesterol
TG
BMI
r
-0.089
-0.213
-0.095
0.050
-0.101
0.211
P
0.62
0.242
0.605
0.786
0.582
0.245
Results
As shown in table 1, the mean level of
leptin obtained was 21.811.2 g/L in group
A and 5.161.2g/L in group B. These results show that plasma leptin concentrations
in group A increase with body mass index.
Plasma leptin levels in obese diabetics (group
A) when compared to those of non-obese
diabetic patients (group B) show more than a
four-fold increase (p=0.001, table 1).
Our statistical analysis results show a significantly positive correlation between leptin
and insulin (r=0.59, p=<0.s05) in group B
(table 3), the correlation however in group A
(table 2) between leptin and insulin is negative and not significant (r=-0.089, p=0.62).
The mean insulin levels obtained were
11.45.8 Iu/ml in group A and 6.751.2
Iu/ml in group B (table 1), The mean values
of HbA1c obtained were 8.76 % 0.36 in
Table 3. Correlation between Leptin and Insulin, FBS, HbA1c, Cholesterol, Triglyreceride
(TG), and BMI in group B
Leptin
Insulin
FBS
HbA1c
Cholesterol
TG
BMI
r
0.598
-0.190
-0.273
0.361
-0.032
0.179
p
0.05
0.464
0.289
0.154
0.903
0.327
Discussion
The paradoxical observation contributes to
the question of whether alteration in leptin
action contributes to diabetes caused by obesity or lipodystrophy merely as a correlate
with these phenomena or if they occur as a
consequence of insulin resistance.12,13 The
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J. Mohiti et al.
statistical analysis shows a significantly positive correlation between leptin and insulin in
group B (table 3).
These correlations may express a cooperative effect between these two hormones in the
control of body weight in group B,14 while
the correlation between leptin and insulin is
negative and not significant in group A (table
2) that may express an uncooperative effect
of these two hormones on the control of body
weight in this group.18,19 Our results indicate
that plasma insulin levels are higher in either
obese diabetic patients or obese non-diabetes
individuals (results not shown) when compared to non-obese diabetic patients (table 1).
Since other factors measured are very similar
in the two groups (see table 1), the increase
in insulin levels in group A may be caused by
the impaired action of leptin signaling in
cells.20,21 Kellerer and co-workers21 have assessed the effects of insulin concentration on
the leptin signaling pathway in rat-1 and
HEK293 cells. Their results suggest that insulin concentration may contribute to the
pathogenesis of leptin.21,22 It has also been
reported that leptin effects on glucose metabolism differ between lean mice and hyper-
Acknowledgment
We would like to thank Shahid Sadoughi
University of Medical Science for funding
this project.
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Mantzoros CS, Moschos SJ. Leptin: in search of
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Dhillon H, Kalra SP, Prima V, Zolotukhin S,
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