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ISSN: 0963-7486 (print), 1465-3478 (electronic)
Int J Food Sci Nutr, Early Online: 1–6
!2014 Informa UK Ltd. DOI: 10.3109/09637486.2014.880671
RESEARCH ARTICLE
The effect of ginger consumption on glycemic status, lipid profile and
some inflammatory markers in patients with type 2 diabetes mellitus
Tahereh Arablou
1
, Naheed Aryaeian
2
, Majid Valizadeh
3
, Faranak Sharifi
3
, AghaFatemeh Hosseini
4
, and
Mahmoud Djalali
5
1
Department of Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran,
2
Department of
Nutrition, School of Public Health, Iran University of Medical Sciences, Tehran, Iran,
3
Zanjan Metabolic Disease Research Center, Zanjan University
of Medical Sciences, Zanjan, Iran,
4
Department of Statistics and Mathematics, School of Health Management and Information Science, Iran
University of Medical Sciences, Tehran, Iran, and
5
Department of Nutrition and Biochemistry, School of Nutritional Sciences and Dietetics, Tehran
University of Medical Sciences, Tehran, Iran
Abstract
Objective: To assess the effect of ginger consumption on glycemic status, lipid profile and some
inflammatory markers in patients with type 2 diabetes mellitus. Methods: In a double-blinded,
placebo-controlled clinical trial, 70 type 2 diabetic patients were enrolled. They allocated
randomly into ginger group and control group. They consumed 1600 mg ginger versus
1600 mg wheat flour placebo daily for 12 weeks. Serum sugar, lipids, CRP, PGE2 and TNFawere
measured before and after intervention. Results: Ginger reduced fasting plasma glucose, HbA
1C
,
insulin, HOMA, triglyceride, total cholesterol, CRP and PGE
2
significantly compared with
placebo group (p50.05). There were no significant differences in HDL, LDL and TNFabetween
two groups (p40.05). Conclusion: Ginger improved insulin sensitivity and some fractions of lipid
profile, and reduced CRP and PGE
2
in type 2 diabetic patients. Therefore ginger can be
considered as an effective treatment for prevention of diabetes complications.
Keywords
Blood sugar, ginger, inflammation, insulin
sensitivity, serum lipids, type 2 diabetes
History
Received 14 October 2013
Revised 22 December 2013
Accepted 26 December 2013
Published online 4 February 2014
Introduction
Type 2 diabetes, a growing public health problem, is associated
with increased morbidity and mortality (Mahluji et al., 2013).
Cardiovascular diseases are the leading cause of morbidity and
mortality in diabetic patients. Diabetic patients are 2-to-4-folds
more prone to atherosclerosis. Dyslipidemia is the most important
modifiable risk factor for atherosclerosis in diabetic patients.
Glycemic control moderates diabetes-related dyslipidemia
(Bhandari et al., 2005). Insulin sensitivity can control glycemia,
improve endothelial function and reduce the risk of atheroscler-
osis (Mahluji et al., 2013).
Today, many herbs are used to treat diseases worldwide.
Rhizome of ginger (Zingiber officinale Roscoe, Zingiberaceae),
as a spice, is used widely all around the world. For centuries, this
plant has been an important part of Chinese, Ayurvedic and Tibb
Unani herbal medicine to treat cataract, rheumatism, nervous
diseases, gingivitis, toothache, asthma, stroke, constipation and
diabetes (Ali et al., 2008).
Recent studies have shown that ginger has different pharma-
cological effects, due to its different components such as gingerols
and shogaols. So far, more than 40 antioxidant compounds are
also detected in ginger (Shirdel et al., 2009). The main
pharmacological actions of ginger and its isolated compounds
include immunomodulatory, antitumorogenesis, antiinflamma-
tory, antiapoptosis, glucose and lipid lowering effect and
antiemetic (Ali et al., 2008).
To date, several studies have investigated the effect of ginger
on blood glucose and lipids.
Mahluji et al. (2013) studied the effect of daily intake of 2 g of
powdered ginger in type 2 diabetic patients. After 2 months,
insulin, HOMA, TG and LDL decreased significantly in ginger
group compared with placebo group, no significant changes were
observed in FPG, HbA
1C
, total cholesterol and HDL levels.
Also, in another study (Bordia et al., 1997), 4 g of ginger
powder, were given to healthy subjects, patients with CAD and
type 2 diabetic patients with or without CAD. After 3 months, no
significant changes were observed in blood sugar and serum
lipids.
Diabetes can be considered as an inflammatory disease that is
associated with metabolic disorders (Navarro & Mora, 2006).
Mild chronic inflammation associated with increased levels of
circulating inflammatory cytokines may increase insulin resist-
ance in the liver, skeletal muscles and vascular endothelium
(Simin et al., 2007).
The antiinflammatory effect of ginger is possibly through
inhibition of cyclooxygenase, inducible nitric oxide synthase
and lipoxygenase activity and suppression of prostaglandin
synthesis and interference in cytokine signaling and this is
attributed to gingerols, shogaols and diarylheptanoids in ginger
(Singletary, 2010).
Correspondence: Naheed Aryaeian, PhD, MS, Department of Nutrition,
School of Public Health, Iran University of Medical Sciences, Hemmat
Broadway, Tehran, Iran. Tel: +982186704750. Fax: +982188622707. E-
mail: aryaeian.n@iums.ac.ir, nah_arya2002@yahoo.com
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To the best of our knowledge, there is no performed research
assessing the effect of ginger on inflammatory markers in diabetic
patients and because of insufficient information on the effects of
ginger on blood glucose and lipid profile, this study was
performed to investigate the effect of ginger supplementation on
glycemic status, lipid profile and CRP, PGE
2
and TNFaas
inflammatory markers in patients with type 2 diabetes.
Methods and materials
Study design
This is a double-blinded, placebo-controlled clinical trial. The
study was approved by Medical Ethics Committee of Tehran
University of Medical Sciences and Zanjan Metabolic Disease
Research Center which conform to the provision of Helsinki in
1995 (as revised in 2000) and recorded by the identification code
of IRCT201204159472N1 in clinical trials registry of Iran. Prior
to the study, informed written consents were obtained from all of
the participants.
Study population and intervention
Seventy patients 30–70 years old with type 2 diabetes included
after baseline assessments. Eligibility criteria included: treated
with oral hypoglycemic agents, HbA
1C
between 7% and 10%,
BMI between 20 and 35 kg/m
2
, no pregnancy and lactation, no use
of tobacco or alcohol, any renal, liver, thyroid and parathyroid
disorders, cancer, infection, inflammation and fever.
Participants allocated randomly into two groups receiving
ginger or placebo. Neither researcher nor the patients were aware
whether the patients belong to ginger or placebo group. They
consumed 1600 mg of powdered rhizome of ginger or wheat flour
placebo (one 800 mg capsule before lunch and one 800 mg
capsule before dinner) per day. The participants were asked not to
change their regular diet and physical activity during the study
period and report any particular disease or any other abnormal
sensations immediately. The intervention lasted for 12 weeks.
During the study period, two patients in ginger group (one due to
heartburn and one due to unwillingness to cooperation) and five
patients in placebo group (three due to unwillingness to cooper-
ation, one due to pregnancy and one due to recurrence of disease
and the need for insulin therapy) were excluded from the study
and the study ended with 63 patients (33 in ginger group and 30 in
placebo group).
Supplement preparation
Dried rhizomes of Z. officinale were purchased from local market
and ground into fine particles and capsules containing 800 mg of
powdered ginger were prepared. Weight of empty and filled
capsules was measured using high precision balance (HR202i,
A&D company, Japan) at nutrition and biochemistry laboratory
(School of Health, Tehran University of Medical Sciences,
Tehran, Iran). Placebo containing wheat flour was prepared in
the same color and package and they were placed in a container of
ginger powder for 2 weeks to give ginger odor to all placebo
capsules.
Analytical procedures
To control the confounding effects of dietary intake and physical
activity, energy intake, macronutrients and some micronutrients
(vitamins A, C and E, zinc and selenium), 24-h recall question-
naire (1 day) and food diary (2 days) and International physical
activity questionnaire-short form (IPAQ-S), were recorded for
each person at the beginning and end of the study. Dietary
intake were analyzed by Nutritionist IV software (version 3.5.2,
The Hearst Corporation, San Bruno, CA). Body weight was
measured in the fasting state with light clothing and without shoes
using Seca scale (Seca, Hamburg, Germany) and height was
measured without shoes using a stadiometer attached to the scale.
Blood samples (10 ml) were taken in a 12- to 14-h fasting state at
the beginning and after 12 weeks of intervention. Sera were
obtained by high-speed centrifugation and stored at 70 C.
Fasting blood glucose, HbA
1C
, TG, total cholesterol and HDL
levels were determined by enzymatic colorimetric method with
commercial kits (Pars Azmun Co, Iran) on an automatic analyzer
(Abbott, model Alcyon 300, Abbott Park, IL). Serum LDL was
calculated using Friedewald formula:
LDL ¼Total cholestrol HDL TG=5
Serum insulin was measured by radioimmunoassay kit (Mono
bind Inc, 2425-300A, Insulin AccuBind, Lake Forest, CA) using
ELISA method. HOMA was calculated using the US formula:
fasting blood glucose ðmg=dlÞ
fasting serum insulin ðU=mlÞ=405
Plasma PGE
2
was determined by enzyme immunoassay using
ELISA kit (Cayman Chemical, Item Number 514010, Ann Arbor,
MI). Serum TNFaand quantitative CRP were measured by
enzyme-linked immunosorbent assay and enzyme immunoassay
using ELISA kit (Orgenium, product code TNFa021, Vantaa,
Finland and Cayman Chemical, Item Number 10011236, Ann
Arbor, MI, respectively).
Statistical analysis
Statistical analysis was performed using SPSS software (version
16; SPSS Inc., Chicago, IL). Kolmogorov–Smirnov test was used
to determine data compliance with the normal distribution.
Quantitative variables were compared between two groups at
baseline and at the end of the study using an independent t-test or
Mann–Whitney test. Quantitative variables before and after
treatment within each group were compared with paired t-test
or Wilcoxon test. Qualitative variables were analyzed with chi-
squared and McNemar tests. All values are reported based on
mean ± SD. pValue 50.05 was considered as the statistical
significance level.
Results
Baseline characteristics of study participants are presented in
Table 1. Comparisons showed no significant differences in age,
body weight, duration of illness, sex and physical activity levels
between two groups at baseline.
Statistical analysis of energy, macronutrients and some
micronutrients intake showed no significant differences between
two groups and within each group at the beginning and end of the
study (Tables 2 and 3). Also, there is no significant changes in
type and dose of medications and physical activity levels between
two groups before and after intervention (date not shown).
Table 4 shows the mean and standard deviation of anthropo-
metric indices, glycemic status and lipid profile in both groups
before and after intervention. There were no significant changes
in body weight and BMI between two groups before and after
intervention. Results showed that despite no significant differ-
ences in FPG in ginger and placebo groups before and after
intervention, changes in FPG were statistically significant
compared between two groups (p¼0.02).
Ginger also caused a significant decrease in HbA
1C
(p¼0.001), insulin (p¼0.01), HOMA (p¼0.000),TG
(p¼0.001) and total cholesterol (p¼0.02) and significant
increase in HDL/total cholesterol ratio (p¼0.02) in ginger
2T. Arablou et al. Int J Food Sci Nutr, Early Online: 1–6
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group compared with placebo group, but had no significant effect
on HDL (p¼0.97), LDL (p¼0.16) and LDL/HDL ratio
(p¼0.29).
Also results showed significant reduction in serum CRP
(p¼0.01) and plasma PGE
2
(p¼0.000) levels in ginger group
compared with placebo group after 12 weeks (Table 5). Although
serum TNFalevels was significantly decreased in ginger group
compared with placebo group after 12 weeks (p¼0.005),
statistical analysis showed no significant changes in serum
TNFalevels within groups (Table 5).
Discussion
In this study, the effect of ginger on glycemic status, plasma lipids
and some inflammatory markers in patients with type 2 diabetes
were examined.
Results showed that ginger reduced FPG and insulin and
increased insulin sensitivity. Mahluji et al. (2013) found that
taking 2 g of ginger per day for 2 months has no effect on FPG and
HbA
1C
, but can reduce serum insulin and HOMA. This difference
is attributable to longer duration of our study.
Bordia et al. (1997) observed no significant changes in blood
sugar levels in healthy individuals and patients with CAD and
type 2 diabetes with or without CAD.
Animal studies had conflicting results. Shanmugam et al.
(2011) showed that ginger decreased blood glucose significantly
in diabetic rats compared with diabetic controls. Although Islam
& Choi (2008) observed no effect of ginger on blood sugar and
insulin levels in diabetic rats, Nammi et al. (2009) and Goyal &
Kadnur (2006), observed the effect of ginger on reduction of
blood glucose and insulin, in their studies on rats receiving the
high-fat diet and obese rats, respectively.
Many researchers speculate that hypoglycemic and other
pharmacological activities of ginger is due to its phenols,
polyphenols and flavonoids (Shanmugam et al., 2011). It seems
that ginger decreases blood glucose by antagonistic activity
against serotonin receptors and its blockage (Al-Amin et al., 2006;
Goyal & Kadnur, 2006). Also ginger may inhibit the intestinal
glucosidase and amylase enzymes activity and thereby reduce
absorption of glucose (Li et al., 2012).
Many studies have shown that treatment with antioxidants
improves glucose transport and tolerance in type 2 diabetic
patients and animals with insulin resistance. Ginger contains lots
of antioxidants including gingerols, shogaols, paradols and
zingerones. It is possible that they act by increasing the GLUT4
protein, insulin receptors and improving b-cells function (Mahluji
et al., 2013).
Table 2. Energy and macronutrients intake in ginger and placebo groups
before and after intervention.
Variable Ginger group (n¼33) Placebo group (n¼30) p*
Energy (kcal)
Before 1517.3 ± 352.7 1537.7 ± 287.7 0.8
After 1514.2 ± 355.8 1540.7 ± 290.5 0.74
py0.84 0.83
Carbohydrate (g)
Before 194.4 ± 57.9 193.5 ± 46.8 0.95
After 195.2 ± 57.3 192.7 ± 46.1 0.85
py0.87 0.91
Protein (g)
Before 57.6 ± 18.6 61.3 ± 20.1 0.45
After 59.6 ± 18.2 62.7 ± 20.7 0.52
py0.5 0.75
Total fat (g)
Before 56.9 ± 14.5 58.8 ± 18.0 0.65
After 55.3 ± 13.6 58.2 ± 18.5 0.48
py0.49 0.87
SAFA (g)
Before 18.7 ± 1.9 18.9 ± 1.9 0.7
After 18.8 ± 2.0 18.5 ± 2.1 0.73
py0.79 0.35
MUFA (g)
Before 15.2 ± 1.6 14.4 ± 3.6 0.39
After 15.5 ± 1.8 15.4 ± 1.7 0.86
py0.27 0.27
PUFA (g)
Before 16.1 ± 1.5 16.4 ± 1.6 0.63
After 16.2 ± 1.7 16.3 ± 1.6 0.88
py0.76 0.84
Data are presented as mean ± SD.
p* Between group comparison (independent t-test or Mann–Whitney
test).
pyWithin group comparison (paired t-test or Wilcoxon test).
pValue 50.05 is significant.
Table 3. Some micronutrients intake in ginger and placebo groups before
and after intervention.
Variable Ginger group (n¼33) Placebo group (n¼30) p*
Vitamin A (mg)
Before 831.1 ± 773.6 660.0 ± 676.6 0.21
After 831.9 ± 818.3 679.4 ± 661.7 0.39
py0.7 0.057
Vitamin C (mg)
Before 44.6 ± 16.8 39.1 ± 21.6 0.26
After 45.2 ± 16.4 38.9 ± 21.1 0.19
py0.38 0.63
Vitamin E (mg)
Before 16.72 ± 6.8 16.37 ± 5.3 0.82
After 16.76 ± 6.8 16.36 ± 5.3 0.78
py0.62 0.91
Zinc (mg)
Before 7.9 ± 2.7 8.2 ± 2.8 0.55
After 8.0 ± 2.8 8.4 ± 3.2 0.55
py0.22 0.19
Selenium (mg)
Before 62.7 ± 30.6 63.6 ± 31.9 0.95
After 64.0 ± 32.4 63.3 ± 31.5 0.92
py0.32 0.49
Data are presented as mean ± SD.
p* Between group comparison (independent t-test or Mann–Whitney
test).
pyWithin group comparison (paired t-test or Wilcoxon test).
pValue 50.05 is significant.
Table 1. Baseline characteristics of study participants.
Characteristics
Ginger group
(n¼33)
Placebo group
(n¼30) p
Age (year) 52.6 ± 8.4 52.0 ± 9.0 0.78*
Body weight (kg) 66.2 ± 8.2 66.1 ± 7.8 0.95*
Duration of illness (month) 45.8 ± 25.5 48.5 ± 26.5 0.68*
Sex
Female (%) 25 (75.8) 23 (76.7) 0.93y
Male (%) 8 (24.2) 7 (23.3)
Physical activity
Light (%) 15 (45.5) 14 (46.7) 0.82y
Moderate (%) 13 (39.4) 10 (33.3)
Severe (%) 5 (15.2) 6 (20)
Data of age, body weight and duration of illness are presented as mean
± SD.
*Independent t-test.
yChi-squared test.
pValue 50.05 is significant.
DOI: 10.3109/09637486.2014.880671 Effect of ginger consumption in patients with type 2 diabetes mellitus 3
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It seems that ginger’s effect on insulin sensitivity is through
the activation of PPARgor up regulation of adiponectin. Isa et al.
(2008) stated that the 6-gingerol and 6-shogaol in ginger,
up regulate adiponectin and 6-shogaol has agonistic activity
with PPARg. Plasma adiponectin levels and its RNA
expression are reduced in obesity and insulin resistance, and
increasing adiponectin, improves insulin sensitivity (Nammi
et al., 2009).
In this study, ginger reduced TG and total cholesterol in
diabetic patients but it had no effect on HDL and LDL.
This is consistent with the findings of Alizadeh et al.’s study
(2008) which investigated the effect of taking 3 g of ginger for
45 days on blood lipids in patients with hyperlipidemia. In
Mahluji et al.’s study (2013), ginger reduced LDL and TG
significantly, but it had no significant effect on total cholesterol
and HDL levels.
In another study, taking 4 g of ginger for 3 months caused no
significant changes in blood lipids in healthy subjects, patients
with CAD and type 2 diabetes with or without CAD (Bordia et al.,
1997).
Our finding on the effectiveness of ginger in decreasing serum
TG is consistent with the findings of several animal studies
(Al-Amin et al., 2006; Bhandari et al., 2005; ElRokh et al., 2010;
Goyal & Kadnur, 2006; Nammi et al., 2009; Sharma et al., 1991;
Shirdel et al., 2009).
The hypotriglyceridemic effect of ginger may be due to
increasing lipoprotein lipase enzyme activity and therefore
hydrolysis of circulatory TG and decreasing serum TG (Shirdel
et al., 2009). Ginger also reduces the ChREBP gene expression in
the liver. ChREBP, a transcriptional regulator of lipid and glucose
metabolism, converts excess carbohydrates into TGs. Reduced
ChREBP expression, decreases expression of ACC1, fatty acid
synthase, SCD1, and glucose-6-phosphatase, glucogenic and
lipogenic proteins and decreases fat accumulation in the liver,
reduces serum TG and improves insulin resistance (Gao et al.,
2012).
Based on the findings of the present study, ginger could
decrease serum total cholesterol in diabetic patients.
This effect also was observed by Alizadeh et al. (2008) and
some animal studies (Al-Amin et al., 2006; Bhandari et al., 2005;
ElRokh et al., 2010; Goyal & Kadnur, 2006; Nammi et al., 2009;
Sharma et al., 1991).
Ginger can increase hepatic cholesterol 7a-hydroxylase enzyme
activity and the conversion of cholesterol into bile acids, resulting
in reduced serum cholesterol concentration. Also there are
observations that the compounds in ginger inhibit the biosynthesis
of cholesterol in the liver of rats (Alizadeh et al., 2008). In addition
to the effect of ginger on increasing bile secretion, increased fecal
excretion of cholesterol and phospholipids by ginger can also
reduce cholesterol levels (Sharma et al., 1991).
The findings showed that ginger has no significant effect on
serum HDL, LDL and LDL/HDL ratio. Findings about the effect
Table 4. Anthropometric indices, glycemic and lipid profile in ginger and
placebo groups before and after intervention.
Variable
Ginger group
(n¼33) p*
Placebo group
(n¼30) p*py
Body weight (kg)
Before 66.2 ± 8.2 0.2 66.1 ± 7.8 0.16 0.95
After 66.1 ± 8.2 66.0 ± 7.7 0.95
Differences 0.07 ± 0.3 0.06 ± 0.2 0.9
BMI (kg/m
2
)
Before 26.9 ± 3.6 0.16 26.8 ± 3.4 0.63 0.91
After 26.8 ± 3.5 26.8 ± 3.4 0.93
Differences 0.51 ± 0.2 0.03 ± 0.3 0.82
FPG (mg/dl)
Before 131.0 ± 42.5 0.17 129.0 ± 62.5 0.8 0.88
After 121.9 ± 37.4 145.0 ± 68.4 0.1
Differences 9.1 ± 38.5 16.0 ± 48.5 0.02
HbA
1C
%
Before 8.4 ± 1.6 0.002 8.1 ± 1.5 0.1 0.55
After 7.3 ± 1.3 8.6 ± 2.2 0.01
Differences 1.0 ± 1.7 0.4 ± 1.4 0.001
Insulin (mU/ml)
Before 8.3 ± 8.3 0.000 6.9 ± 4.6 0.66 0.54
After 4.6 ± 1.4 7.0 ± 3.3 0.000
Differences 3.7 ± 8.2 0.1 ± 3.5 0.01
HOMA
Before 3.1 ± 5.1 0.000 2.2 ± 1.5 0.36 0.58
After 1.3 ± 0.5 2.4 ± 1.4 0.01
Differences 1.7 ± 4.9 0.2 ± 1.3 0.000
TG (mg/dl)
Before 187.0 ± 68.9 0.001 187.4 ± 111.4 0.72 0.98
After 141.5 ± 47.4 190.0 ± 115.3 0.03
Differences 45.4 ± 69.6 2.5 ± 38.5 0.001
Total cholesterol (mg/dl)
Before 188.6 ± 35.6 0.01 188.2 ± 45.2 0.4 0.96
After 173.1 ± 28.7 194.0 ± 45.1 0.03
Differences 15.4 ± 34.3 5.8 ± 37.9 0.02
HDL (mg/dl)
Before 44.8 ± 9.1 0.16 42.8 ± 6.4 0.3 0.33
After 46.2 ± 8.3 44.2 ± 7.6 0.32
Differences 1.3 ± 5.5 1.3 ± 7.0 0.97
LDL (mg/dl)
Before 107.7 ± 31.6 0.16 108.6 ± 43.7 0.54 0.93
After 98.9 ± 27.2 112.7 ± 37.0 0.09
Differences 8.8 ± 35.3 4.1 ± 37.3 0.16
HDL/total cholesterol ratio
Before 0.24 ± 0.06 0.005 0.23 ± 0.06 0.92 0.65
After 0.27 ± 0.06 0.23 ± 0.06 0.03
Differences 0.02 ± 0.05 0.0007 ± 0.03 0.02
LDL/HDL ratio
Before 2.4 ± 0.8 0.17 2.58 ± 1.0 0.94 0.67
After 2.2 ± 0.8 2.59 ± 0.9 0.11
Differences 0.2 ± 0.9 0.01 ± 0.9 0.29
Data are presented as mean ± SD.
p* Within group comparison (paired t-test or Wilcoxon test).
pyBetween group comparison (independent t-test or Mann–Whitney
test).
pValue 50.05 is significant.
Table 5. CRP, TNFaand PGE
2
levels in ginger and placebo groups
before and after intervention.
Variable
Ginger group
(n¼33) p*
Placebo group
(n¼30) p*py
CRP (mg/L)
Before 5.2 ± 5.4 0.004 7.1 ± 9.6 0.01 0.99
After 2.6 ± 3.2 6.4 ± 8.4 0.01
Differences 2.5 ± 4.7 0.7 ± 6.5 0.02
TNFa(pg/ml)
Before 17.6 ± 26.3 0.11 23.6 ± 24.6 0.63 0.07
After 11.8 ± 13.5 26.6 ± 26.5 0.005
Differences 5.7 ± 15.8 3.0 ± 18.4 0.12
PGE
2
(pg/ml)
Before 234.9 ± 225.7 0.000 221.9 ± 127.5 0.07 0.42
After 108.1 ± 205.6 200.5 ± 129.6 0.000
Differences 126.7 ± 231.6 21.4 ± 60.4 0.009
Data are presented as mean ± SD.
p* within group comparison (Wilcoxon test).
pybetween group comparison (Mann–Whitney test).
pValue 50.05 is significant.
4T. Arablou et al. Int J Food Sci Nutr, Early Online: 1–6
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of ginger on HDL, are similar to findings of Mahluji et al. (2013),
Alizadeh et al. (2008) and Bordia et al. (1997). Increased levels of
insulin and TG are associated with reduced HDL
2
and HDL
particle size (Pascot et al., 2001). Probably ginger increases HDL
2
and HDL particle size and reduces atherogenesis through
decreasing insulin and TG levels.
Although Mahluji et al. (2013) showed that taking 2 g of ginger
per day for 2 months could reduce LDL in diabetic patients, in our
study, LDL reduced in ginger group compared with placebo group
but it was not statistically significant. It is consistent with the
findings of Alizadeh et al. (2008) and Bordia et al. (1997). Ginger
may increase LDL particle size and reduce uptake of oxidized
LDL by macrophages (Fuhrman et al., 2000).
The results showed that ginger reduced plasma PGE
2
signifi-
cantly in diabetic patients. So far, as our knowledge, the effect of
ginger on PGE
2
levels in diabetic humans has not been studied.
Black et al. (2010) studied the effects of daily consumption of 2 g
of raw or heated ginger on muscle pain and plasma PGE
2
in
participants. After 11 days, there were no significant differences
in plasma levels of PGE
2
between two groups. Ginger’s effect on
PGE
2
have addressed in several animal and cellular studies
(Shen et al., 2005; Shimoda et al., 2010; Thomson et al., 2002).
Lantz et al. (2007) demonstrated that PGE
2
production was
inhibited in U937 cell cultures containing standard compounds of
ginger (6, 8, 10 gingerols and 6-shogaol). It also became clear that
inhibition of PGE
2
production in mixed ginger extract was greater
than either of the compounds alone. Although this study did not
show the suppression of TNFaproduction by ginger, several
cellular studies showed the effect of ginger on TNFareduction
(Habib et al., 2008; Tripathi et al., 2007). Levy & Simon (2009)
found that 6-shogaol can reduce TNFalevels in macrophages
activated with lipopolysaccharide.
However, we showed that consumption of ginger powder for
12 weeks can cause a significant reduction in CRP in patients with
type 2 diabetes. Our result is similar to the result of Atashak et al.
(2010). They showed that consumption of 1 g of powdered ginger
daily for 10 weeks made 27.6% reduction in mean CRP levels in
obese men.
Chronic, low grade inflammation and activation of the innate
immune system are closely involved in the pathogenesis of
diabetes (Navarro & Mora, 2006). Anti-inflammatory properties
of ginger have been known for centuries (Ali et al., 2008). Effect
of ginger on PGE
2
takes place through inhibition of cycloox-
ygenase-2 mRNA expression and direct inhibition of this enzyme
activity (Lantz et al., 2007). It seems that the effect of ginger on
inflammation is also due to the effect of certain active compounds
(gingerols and zerumbone) that inhibit NF-kB. Compounds in
ginger inhibit NF-kB and TNFaexpression in liver cancer cells
(Habib et al., 2008). 6-gingerol and 6-paradol have strong anti-
inflammatory activity and suppress TNFaproduction (Kim et al.,
2004; Park et al., 1998). TNFagene inhibition by ginger, reduces
NF-kB activity and thereby other inflammatory cytokines and so
cyclooxygenase 2 and its related products such as PGE
2
. Acute-
phase proteins such as CRP are also inhibited. This reduces
inflammation and its complications in diabetic patients.
Conclusion
The present study showed that ginger can reduce blood glucose
and insulin levels and improve insulin sensitivity, reduce serum
total cholesterol and TG and decrease inflammation by reducing
CRP and PGE
2
levels in type 2 diabetic patients.
Acknowledgements
We thank the efforts of all the teachers and friends who were with us in
this study, especially the staff of Zanjan Metabolic Disease Research
Center. This is a report of a database from thesis entitled ‘‘The effect of
ginger consumption on glycemic status, lipid profile and some inflam-
matory markers in patients with type 2 diabetes mellitus’’.
Declaration of interest
The authors declare no conflict of interest. The study was funded by
Tehran University of Medical Sciences and Zanjan Metabolic Disease
Research Center, Zanjan University of Medical Sciences.
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