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Effects of green coffee aqueous extract supplementation on glycemic indices, lipid profile, CRP, and malondialdehyde in patients with type 2 diabetes: a randomized, double-blind, placebo-controlled trial

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Frontiers in Nutrition
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Background/objectives Studies have reported the health benefits of green coffee extract (GCE) in experimental models. In the current study, we aimed to determine whether supplementation with GCE improves glycemic indices, inflammation, and oxidative stress in patients with type 2 diabetes (T2D). Methods and study design This randomized, double-blind, placebo-controlled trial included 44 patients (26 male and 18 female) with T2D and overweight/obesity. After blocked randomization, patients received either capsules containing 400 mg GCE twice per day (n = 22) or a placebo (n = 22) and were followed for 10 weeks. In this study, glycemic indices, lipid profiles, anthropometric examinations, blood pressure, high-sensitivity C-reactive protein (hs-CRP), and malondialdehyde (MDA) were measured twice; at baseline and at the end of the study. Results After 10 weeks of supplementation, GCE supplementation significantly reduced body weight (p = 0.04) and body mass index (BMI) (p = 0.03) compared to the placebo. The intention-to-treat (ITT) analysis indicated patients in the GCE group had a lower fasting blood glucose (FBG) concentration compared to the placebo group; however, this decreasing was marginally significant (8.48 ± 8.41 vs. 1.70 ± 5.82 mg/dL, p = 0.05). There was no significant difference in insulin levels and HOMA-IR between the groups. At the end of the study, significant changes in systolic blood pressure (SBP) (p = 0.01), triglyceride (TG) level (p = 0.02), high-density lipoprotein (HDL) (p = 0.001), and TG-to-HDL ratio (p = 0.001) were found between the intervention and placebo groups. Our trial indicated GCE supplementation had no effect on diastolic blood pressure (DBP), low-density lipoprotein (LDL), or total cholesterol. During the supplementation period, the hs-CRP level significantly decreased in the GCE group compared to the placebo group (p = 0.02). No significant changes were observed in the MDA level between the two groups at the end of the study (p = 0.54). Conclusion Our findings showed beneficial effects of GCE on SBP, TG, hs-CRP, and HDL levels in patients with T2D and overweight/obesity over a 10-week period of supplementation. Clinical trial registration:https://en.irct.ir/trial/48549, identifier [IRCT20090203001640N18].
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Frontiers in Nutrition 01 frontiersin.org
Eects of green coee aqueous
extract supplementation on
glycemic indices, lipid profile, CRP,
and malondialdehyde in patients
with type 2 diabetes: a
randomized, double-blind,
placebo-controlled trial
SajadKhalili-Moghadam
1, MehdiHedayati
2, MahdiehGolzarand
3*
and ParvinMirmiran
1,3*
1 Department of Clinical Nutrition and Dietetics, Faculty of Nutrition and Food Technology, National
Nutrition and Food Technology, Research Institute, Shahid Beheshti University of Medical Sciences,
Tehran, Iran, 2 Cellular and Molecular Endocrine Research Center, Research Institute for Endocrine
Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran, 3 Nutrition and Endocrine
Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical
Sciences, Tehran, Iran
Background/objectives: Studies have reported the health benefits of green
coee extract (GCE) in experimental models. In the current study, we aimed
to determine whether supplementation with GCE improves glycemic indices,
inflammation, and oxidative stress in patients with type 2 diabetes (T2D).
Methods and study design: This randomized, double-blind, placebo-controlled
trial included 44 patients (26 male and 18 female) with T2D and overweight/obesity.
After blocked randomization, patients received either capsules containing 400  mg
GCE twice per day (n =  22) or a placebo (n =  22) and were followed for 10 weeks.
In this study, glycemic indices, lipid profiles, anthropometric examinations, blood
pressure, high-sensitivity C-reactive protein (hs-CRP), and malondialdehyde
(MDA) were measured twice; at baseline and at the end of the study.
Results: After 10  weeks of supplementation, GCE supplementation significantly
reduced body weight (p =  0.04) and body mass index (BMI) (p= 0.03) compared
to the placebo. The intention-to-treat (ITT) analysis indicated patients in the GCE
group had a lower fasting blood glucose (FBG) concentration compared to the
placebo group; however, this decreasing was marginally significant (8.48  ± 8.41 vs.
1.70  ±  5.82 mg/dL, p =  0.05). There was no significant dierence in insulin levels
and HOMA-IR between the groups. At the end of the study, significant changes
in systolic blood pressure (SBP) (p =  0.01), triglyceride (TG) level (p =  0.02), high-
density lipoprotein (HDL) (p =  0.001), and TG-to-HDL ratio (p =  0.001) were
found between the intervention and placebo groups. Our trial indicated GCE
supplementation had no eect on diastolic blood pressure (DBP), low-density
lipoprotein (LDL), or total cholesterol. During the supplementation period, the
hs-CRP level significantly decreased in the GCE group compared to the placebo
group (p =  0.02). No significant changes were observed in the MDA level between
the two groups at the end of the study (p =  0.54).
OPEN ACCESS
EDITED BY
Kenji Watanabe,
Yokohama College of Pharmacy, Japan
REVIEWED BY
Vali Musazadeh,
Tabriz University of Medical Sciences, Iran
Niloufar Rasaei,
Tehran University of Medical Sciences, Iran
Naheed Aryaeian,
Iran University of Medical Sciences, Iran
*CORRESPONDENCE
Mahdieh Golzarand
mahdieh_golzarand@yahoo.com
Parvin Mirmiran
mirmiran@endocrine.ac.ir
RECEIVED 17 June 2023
ACCEPTED 03 November 2023
PUBLISHED 16 November 2023
CITATION
Khalili-Moghadam S, Hedayati M,
Golzarand M and Mirmiran P (2023) Eects of
green coee aqueous extract supplementation
on glycemic indices, lipid profile, CRP, and
malondialdehyde in patients with type 2
diabetes: a randomized, double-blind,
placebo-controlled trial.
Front. Nutr. 10:1241844.
doi: 10.3389/fnut.2023.1241844
COPYRIGHT
© 2023 Khalili-Moghadam, Hedayati,
Golzarand and Mirmiran. This is an open-
access article distributed under the terms of
the Creative Commons Attribution License
(CC BY). The use, distribution or reproduction
in other forums is permitted, provided the
original author(s) and the copyright owner(s)
are credited and that the original publication in
this journal is cited, in accordance with
accepted academic practice. No use,
distribution or reproduction is permitted which
does not comply with these terms.
TYPE Clinical Trial
PUBLISHED 16 November 2023
DOI 10.3389/fnut.2023.1241844
Khalili-Moghadam et al. 10.3389/fnut.2023.1241844
Frontiers in Nutrition 02 frontiersin.org
Conclusion: Our findings showed beneficial eects of GCE on SBP, TG, hs-CRP,
and HDL levels in patients with T2D and overweight/obesity over a 10-week
period of supplementation.
Clinical trial registration: https://en.irct.ir/trial/48549, identifier
[IRCT20090203001640N18].
KEYWORDS
type 2 diabetes, Hs-CRP, Malondialdehyde, Insulin, lipid profile, green coee
Introduction
Generally, patients with type 2 diabetes mellitus (T2D) are at
increased risk for various cardiovascular and renal diseases. ese
patients have several comorbidities, such as fatty liver disease,
atherogenic dyslipidemia, and hypertension, which are associated
with an increased risk of disability and mortality (1). A total of 425
million adults suer from diabetes globally, which is anticipated to rise
to 629 million by 2040 (2). So, pharmacotherapy and lifestyle changes
are necessary to control T2D in the long term (3). Dietary modication
is also recommended to reduce the complications of T2D, and
currently, most studies have focused on the eects of nutraceuticals
on treating or preventing diabetes complications (4).
e green coee bean is an unroasted coee fruit that is rich in
bioactive phytochemical compounds (5). e main bioactive
ingredient of green coee is chlorogenic acid (CGA), which has
benecial eects on blood pressure, inammatory markers, oxidative
stress, and diabetes in experiments (6). Several mechanisms have
been proposed by which CGA exerts its eects, such as inhibiting the
cytochrome P450 1A enzymes that increase the pro-inammatory
response (7), increasing the expression of genes that reduce oxidative
stress (8), decreasing insulin resistance by activating the hepatic
proliferation-activated receptor α (PPAR-α) (9), or improving blood
glucose by activating AMP-activated protein kinase (AMPK) (10).
However, the health benets of green coee for humans are
inconsistent. Several randomized controlled trials (RCTs) have
evaluated the eects of green coee extract (GCE) supplementation
on cardiometabolic risk factors. Some studies have found that GCE
has favorable eects on cardiometabolic risk factors, while others
have not (1115). In addition, most studies have been conducted on
healthy adults or subjects with overweight or obesity, and there is a
lack of individual studies on patients with T2D (11, 16, 17). Results
of a recent meta-analysis on 27 RCTs showed an advantageous
inuence of GCE on glycemic markers, triglycerides (TG), and high-
density lipoprotein (HDL); however, due to the high heterogeneity
between studies, the results should beinterpreted with caution (18).
In regards to inammatory markers, there are also contradictory
results (19).
Despite the protective eects of GCE on chronic diseases (20),
research regarding the eects of GCE on T2D is scarce. Moreover,
most of the previous studies assessed the eects of CGA rather than
GCE in animal models. Besides, ndings concerning the eects of
GCE are rather inconsistence. us, wedesigned a clinical trial study
to assess the eects of GCE supplementation on glycemic indices, lipid
prole, hs-CRP, and malondialdehyde (MDA) in patients with T2D
and overweight/obesity.
Methods
Study design
e present study was a parallel randomized, double-blind,
placebo-controlled trial. e National Nutrition and Food Technology
Research Institute of Shahid Beheshti University of Medical Sciences’
ethics committee approved this study. It is also registered on the
Iranian Registry of Clinical Trials (registration number:
IRCT20090203001640N18). At the beginning, the participants signed
a “written informed consent form.
In this study, 44 patients with T2D and overweight/obesity who
were referred to the Taleghani Hospital, Tehran, between June 2022
and December 2022 participated. Inclusion criteria were as follows:
being aged 30–70 years old, suering from T2D [fasting blood glucose
(FBG) 126 mg/dL, measured twice, 2-h plasma glucose 200 mg/dL,
or HbA1C 6.5%, or taking oral hypoglycemic medicines] (21),
having a history of diabetes between 1 and 10 years, and having a body
mass index (BMI) of 25–35 kg/m2. Exclusion criteria were as follows:
receiving insulin therapy, pregnancy or lactation, going on diet during
the past 3 months, taking any dietary supplements at least once a week
in the past 3 months, and having severe hepatic, renal, and
inammatory diseases. Wealso removed patients who took less than
80% of their capsules or changed the type or dosage of medications
during the intervention. At baseline, patients were asked to complete
a questionnaire regarding socio-demographic characteristics, diet and
drug histories, and medical history through a comprehensive face-to-
face interview.
Intervention
In this study, the sample size was calculated based on the primary
outcome with a power of 80% and an alpha of 0.05. en, participants
were randomly assigned into two groups of 22 patients that received
either oral capsules of a GCE or a homologated placebo (starch). Both
GCE and placebo capsules were produced by Bonyan Salamat Kasra
Co., Tehran, Iran, and were similar in size, shape, and smell. GCE
contains 0–2% caeine and 45–50% CGA by weight. Randomization
was conducted using the permuted block method based on sex.
Blocked randomization was done with block sizes of four concealed
in a container by one of the researchers. e blocks were composed of
A and B characters, representing bottles of capsules coded with A or
B to ensure concealment. e other investigator randomly assigned
the participants to one of the two groups. Subjects were recommended
to consume two capsules (each capsule contains 400 mg GCE or
Khalili-Moghadam et al. 10.3389/fnut.2023.1241844
Frontiers in Nutrition 03 frontiersin.org
placebo) aer their main meals to reduce gastrointestinal
complications for 10 weeks. All participants were contacted every two
weeks to ensure that they complied with the supplementation protocol
(adherence of at least 80% was considered good) and to evaluate the
side eects. Subjects who reported severe side eects or consumed less
than 80% of the capsules were excluded from the study. e
participants and researchers were blinded by the intervention.
Nutritional recommendations (based on the food guide pyramid)
were given to the subjects during the study period, and they were
requested to maintain their usual physical activity.
Dietary assessment
In order to assess dietary changes during the trial period, all the
patients were asked to provide two three-day food records (1 weekend
day and 2 weekdays) at the beginning and end of the intervention.
Food records consisted of the serving size of consumed foods and
ingredients. Also, the subjects were interviewed to report their intake
based on household measures. e Household Measures and food
model booklet with pictures of household items was used to better
estimation of portion size of the food and beverages. ese measures
were used to obtain the grams of food consumed. Nutritionist IV
soware (First Databank, San Bruno, CA, UnitedStates), which is
adapted for the national composition food tables, was used to perform
nutrient analysis.
Outcomes assessment
At baseline and at the end of the study, all physical, clinical, and
biochemical factors were measured. Weight was measured using a
Seca digital scale (Germany) while the subjects were minimally
clothed and without shoes, with a precision of 100 g. Also, height was
measured using a tape meter attached to the wall to the nearest 0.5 cm.
In addition, BMI was calculated by dividing weight (kg) by the square
of height (m
2
) at baseline and 10 weeks later. Aer 10 min of rest,
systolic blood pressure (SBP) and diastolic blood pressure (DBP) were
measured twice using a digital sphygmomanometer (Citizen, Japan)
with a precision of 1 mmHg. Finally, the average of the two
measurements was considered the subject’s blood pressure. Physical
activity level was assessed using a short form of the International
Physical Activity Questionnaire (IPAQ) (22). e physical activity
data were reported as metabolic equivalent minutes per week
(MET-minutes/wk).
At the beginning and aer 10 weeks of intervention, 10 mL of
venous blood was drawn from participants aer a 12-h fasting period.
e blood serum was obtained by centrifugation at a rate of 3,500
rounds per minute. Aerwards, the serum samples were frozen and
stored at 70°C until the time of the experiments at the research
institute for endocrine sciences, Shaid Beheshti University of Medical
Sciences, Tehran, Iran. e serum concentrations of FBG, TG, total
cholesterol, and HDL were assessed using an enzymatic colorimetric
method (Delta Darman, Iran). Also, the serum insulin levels were
measured using the enzyme-linked immunosorbent assay (ELISA)
technique (Monobind, Austria). To estimate insulin resistance, the
homoeostasis model assessment of insulin resistance (HOMA-IR) was
calculated according to the equation by Matthews et al. (23):
HOMA-IR = [insulin (Mu/L) × glucose (mg/dL)]/405. e low-density
lipoprotein (LDL) levels were calculated using the Friedewald formula:
LDL = TC – HDL – (TG/5) (24). e serum hs-CRP levels were
assessed using turbidimetry (Delta Darman, Iran). e serum
concentration of MDA was measured using a colorimetric method
using a commercial kit (Karmania Pars Gene, Iran). e intra-assay
coecients of variation (CVs) for serum FBG, insulin, TG, cholesterol,
LDL, HDL, and CRP were 0.92, 6.1, 0.97, 2.8, 1.63, and 7.3,
respectively.
Statistical analysis
e statistical tests were performed using SPSS soware (version
20.0; Chicago, IL, UnitedStates). e Kolmogorov–Smirnov test was
used to test the normality of variable distributions. Quantitative
variables are expressed as the mean ± standard deviation (SD), and
categorized variables are reported as counts (percent). Baseline
characteristics and biochemical variables of the subjects were
compared using the student’s t-test and the chi-squared test for
quantitative and qualitative variables, respectively. A students paired
t-test was used to compare baseline and 10-week values of outcomes
within each group. To examine the eect of supplementation on
outcomes of interest, an analysis of covariance (ANCOVA) with
adjustment for the baseline value, age, sex, smoking, physical activity,
medications, and baseline BMI was used. All analyses were conducted
using the intention-to-treat (ITT) method. Missing values were
replaced by the single imputation method. Two-sided p values < 0.05
were considered statistically signicant.
Results
Participants flow
In this RCT, a total of 44 patients with T2D and overweight/
obesity were enrolled into two groups: the GCE supplementation
group (n = 22) and the placebo group (n = 22). During the 10-week
follow-up, four subjects in the placebo group and one subject in the
intervention group dropped out due to poor adherence to the
supplementation, side eects such as stomachaches, or being unwilling
to continue the study (Figure1). Finally, 39 subjects completed study,
but weanalyzed 44 patients using the ITT method. Patients had a
compliance rate of 88.6%. Wefound no major intervention-related
adverse eects in either groups during the study.
e baseline characteristics of the participants are shown in
Table1. e mean age of participants was 56.1 ± 6.20 years. Also, 41%
of participants were women. No signicant dierences were found
between the GCE and placebo groups in terms of age, BMI, smoking
status, or physical activity at baseline.
e dietary intake of participants is shown in Table 2. No
signicant dierences were observed in the dietary intake between the
GCE and placebo groups at the baseline of the trial. Also, no signicant
changes were observed in the dietary intakes between the two groups
aer 10 weeks, except for the percent of energy from saturated fatty
acid (SFA) consumption. Aer 10 weeks, subjects in the placebo group
consumed less SFA compared to the GCE group (8.22 ± 1.85 vs.
9.55 ± 1.54% of energ y).
Khalili-Moghadam et al. 10.3389/fnut.2023.1241844
Frontiers in Nutrition 04 frontiersin.org
Anthropometric and glycemic induces
Anthropometric and glycemic induces at baseline and aer
10 weeks of supplementation are reported in Table 3. Body weight
(p = 0.04) and BMI (p = 0.03) signicantly decreased in the GCE group
compared to the placebo group aer 10 weeks of supplementation. e
ITT analysis indicated patients in the GCE group had a lower FBG
concentration compared to the placebo group; however, this
decreasing was marginally signicant (8.48 ± 8.41 vs. 1.70 ± 5.82 mg/
dL, p = 0.05) than the placebo group. During the intervention, no
signicant dierence in insulin level (6.23 ± 13.2 vs. 3.59 ± 6.28
μIU/dL, p = 0.20) and HOMA-IR (2.84 ± 5.72 vs. 1.07 ± 2.46,
p = 0.08) was found between the two groups.
Blood pressure and lipid profile
Blood pressure and lipid prole at baseline and aer 10 weeks of
supplementation are reported in Table4. At the end of the study, GCE
signicantly reduced SBP (5.56 ± 3.41 vs. 0.90 ± 2.67 mmHg,
p = 0.01), TG level (49.7 ± 72.5 vs. 4.40 ± 98.6 mg/dL, p = 0.02), and
TG-to-HDL ratio (1.40 ± 1.83 vs. 0.13 ± 2.12, p = 0.001), and
increased HDL level (3.22 ± 5.10 vs. 1.73 ± 6.10 mg/dL, p = 0.001)
compared to the placebo. Our trial indicated no eect of GCE on DBP,
LDL, or total cholesterol aer 10 weeks of supplementation.
Hs-CRP and MDA levels
Table5 shows hs-CRP and MDA concentrations at baseline and
end of the study in the GCE and placebo groups. During the
supplementation period, the hs-CRP level signicantly decreased in
the GCE group compared to the placebo group (p = 0.02). No
signicant changes were observed in the MDA level between the two
groups at the end of the study.
Discussion
In this RCT among participants with T2D and overweight/
obesity, GCE supplementation with doses of 800 mg/d for 10 weeks
led to a significant decrease in weight, BMI, SBP, HOMA-IR,
serum TG, and CRP levels, and a significant increase in serum
HDL levels. Our results did not show beneficial effects of GCE
supplementation on SBP and serum concentrations of insulin,
FIGURE1
Flow chart of study.
TABLE1 Baseline characteristics of the participants.
Variables Green
coee
group
(n =  22)
Placebo
group
(n =  22)
p-value
Age (year) 55.4 ± 6.68 56.7 ± 5.74 0.47
Female (%) 10 (45.5) 8 (36.4) 0.54
Smoking (yes) 6 (27.3) 4 (18.2) 0.47
Education level (%)
Under diploma 16 (72.7) 14 (63.6) 0.51
Diploma and over 6 (27.3) 8 (36.4)
Oral drugs (%)
Metformin 16 (72.7) 19 (86.4) 0.26
Glybencelamid 6 (27.3) 7 (31.8) 0.74
Statins 6 (27.3) 5 (22.3) 0.72
Physical activity
(MET-h/wk)
34.3 ± 3.95 35.3 ± 3.64 0.41
Data are presented as percent and mean ± standard deviation. p value is reported based on
independent t-test for continuous variables and chi-square for non-continuous variable.
Khalili-Moghadam et al. 10.3389/fnut.2023.1241844
Frontiers in Nutrition 05 frontiersin.org
total cholesterol, LDL, and MDA. Evidence has verified the safety
of the dose and duration of the GCE intervention. According to
the previous studies, which used a dosage of 400–1,000 mg/d with
a duration of 8–12 weeks, wechose this dose and duration in the
current study (25).
Anthropometric and lipid profile
Our results regarding body weight and BMI were in line with
ndings from previous studies (12, 26). In a trial of the eect of GCE
on body composition in women with obesity, GCE supplementation
(400 mg/d for 8 weeks) reduced body weight and BMI (12). Also, a
meta-analysis has reported that consumption of GCE with a dosage of
180–200 mg/d can lead to a weight loss of 2.5 kg. However, there was
a high heterogeneity (I
2
= 97%) between studies that made conclusions
with diculty (26) Green coee is a rich source of a natural
antioxidant known as CGA. erefore, the weight-lowering eect of
green coee may bedue to the CGA (27). CGA can contribute to body
weight loss through its anti-hyperlipidemia eects. In an animal
model, CGA can reduce cholesterol synthesis and increase fatty acid
oxidation by inhibiting β-hydroxy-β-methyl glutaric acyl-coenzyme
A reductase (28). ese mechanisms can explain the reduced eects
of GCE supplementation on lipid prole in this trial. Also, CGA has a
reducing eect on the deposition of fatty acids in the adipose tissue by
decreasing the serum insulin level, which leads to body weight loss
(12). In the current trial, GCE consumption caused a signicant
reduction and increase in TG and HDL levels, respectively. A trial on
subjects with obesity who consumed 1,000 mg/d of green coee for 6
weeks reported a signicant improvement in their lipid prole (15).
Similar to our ndings, in a RCT on patients with nonalcoholic fatty
liver disease (NAFLD) who consumed 400 mg of GCE for 8 weeks,
they observed a signicant increase in HDL levels (16). But this trial
did not detect any signicant eect of GCE on TG, LDL, or total
cholesterol compared to the placebo. However, in another trial on
subjects with metabolic syndrome, consumption of 400 mg GCE for
8 weeks had no improvement eect on lipid prole parameters (11).
Several mechanisms were proposed for the anti-lipogenic eect of
CGA. is phytochemical component has an inhibitory eect on
pancreatic lipase activity, which decreases fat absorption. In addition,
CGA has an increasing and decreasing eect on fatty acid oxidation
and fatty acid biosynthesis, respectively (8, 29, 30).
Glycemic indices
Our trial showed that GCE could decrease FBG compared to
the placebo; however this reduction was marginally signicant. But
this study did not detect any signicant eect of GCE on insulin
and HOMA-IR. Some of previous studies have reported dierent
results (11, 31). Roshan etal. (11) found that the subjects in the
GCE group (dosage of 800 mg/d and duration of 8 weeks) had
signicantly greater decreases in blood glucose and insulin
resistance compared to the placebo. In an animal study, GCE
treatment eectively reduced the FBG (dosage of 100 mg/kg and
duration of 6 weeks) compared to the placebo group in high-fat
diet (HFD)-induced obese mice (31). Also, in another animal
study, GCE (80 mg/d) resulted in attenuation of HFD-induced
insulin resistance aer 14 weeks (32). But, in line with our ndings
an HFD diet plus 0.5% w/w GCE in mice with metabolic syndrome
did not improve insulin resistance aer 12 weeks (33). A meta-
analysis that summarized the results from six interventional
studies reported that GCE has a reducing eect on blood glucose
(34). Also, this meta-analysis concluded that GCE has no eect on
insulin or HOMA-IR (34). Some reason can explain these slight
TABLE2 Dietary intake of participants at the baseline and after 10  weeks
supplementation.
Dietary
factors
Time Green
coee
group
(n =  22)
Placebo
group
(n =  22)
p-
valuea
Energy (kcal/d) Baseline 2,266 ± 232 2,186 ± 174 0.20
10 weeks 2,123 ± 243 2,109 ± 220 0.19
Carbohydrate
(% of energy)
Baseline 61.3 ± 4.55 58.2 ± 7.52 0.11
10 weeks 58.1 ± 3.81 59.9 ± 5.74 0.28
Protein (% of
energy)
Baseline 15.3 ± 1.61 14.9 ± 1.71 0.38
10 weeks 15.1 ± 2.71 15.7 ± 1.68 0.65
Fat (% of
energy)
Baseline 26.8 ± 4.77 30.3 ± 6.90 0.07
10 weeks 29.6 ± 5.44 27.5 ± 5.45 0.21
SFA (% of
energy)
Baseline 8.99 ± 2.93 9.58 ± 2.85 0.50
10 weeks 9.55 ± 1.54 8.22 ± 1.85 0.009
MUFA (% of
energy)
Baseline 9.91 ± 2.08 9.45 ± 2.48 0.51
10 weeks 10.3 ± 2.67 9.42 ± 2.31 0.21
PUFA (% of
energy)
Baseline 6.25 ± 2.09 5.67 ± 1.60 0.30
10 weeks 6.06 ± 2.43 6.15 ± 2.21 0.99
Fiber (g/d) Baseline 41.3 ± 12.07 39.1 ± 6.01 0.44
10 weeks 40.5 ± 12.3 39.3 ± 8.23 0.65
Cholesterol
(mg/d)
Baseline 200 ± 84.7 188 ± 66.9 0.59
10 weeks 198 ± 72.8 182 ± 86.5 0.43
Sodium (mg/d) Baseline 3,256 ± 1,021 3,358 ± 1,113 0.75
10 weeks 3,342 ± 1,284 2,885 ± 633 0.09
Magnesium
(mg/d)
Baseline 483 ± 95.9 446 ± 75.9 0.16
10 weeks 434 ± 98.1 455 ± 77.6 0.41
Potassium
(mg/d)
Baseline 4,534 ± 1,045 4,373 ± 840 0.57
10 weeks 4,183 ± 1,120 795 ± 193 0.93
Calcium (mg/d) Baseline 1,395 ± 402 1,331 ± 284 0.54
10 weeks 1,318 ± 512 1,245 ± 279 0.60
Selenium
(μg/d)
Baseline 111 ± 24.2 121 ± 29.6 0.22
10 weeks 105 ± 6.1 117 ± 6.7 0.18
Vitamin C
(mg/d)
Baseline 173 ± 55.4 146 ± 66.3 0.15
10 weeks 134 ± 12.2 142 ± 13.5 0.67
Vitamin E
(mg/d)
Baseline 10.3 ± 2.9 12.6 ± 7.7 0.20
10 weeks 10.6 ± 0.8 10.1 ± 0.8 0.68
Data are presented as mean ± standard deviation.
ap value is reported based on independent t-test for baseline values and ANCOVA test for
nal values.MUFA, monounsaturated fatty acids; PUFA, polyunsaturated fatty acids; SFA,
saturated fatty acids.
Khalili-Moghadam et al. 10.3389/fnut.2023.1241844
Frontiers in Nutrition 06 frontiersin.org
TABLE3 Anthropometric and glycemic indices at baseline and after 10 weeks supplementation.
Variable Time Green coee group (n =  22) Placebo group (n =  22) p-valuea
Weight (kg) Baseline 75.8 ± 4.49 73.7 ± 4.40 0.04
10 weeks 73.3 ± 3.50c72.9 ± 3.75
Mean changes 2.62 ± 2.23 0.72 ± 2.13
BMI (kg/m2)Baseline 27.9 ± 1.39 27.4 ± 1.25 0.03
10 weeks 26.9 ± 1.37c27.0 ± 1.15
Mean changes 1.01 ± 0.94 0.3 ± 0.83
FBG (mg/dL) Baseline 141 ± 18.4 141 ± 12.9 0.05
10 weeks 132 ± 13.5c138 ± 11.8
Mean changes 8.48 ± 8.41 1.70 ± 5.82
Insulin (μIU/dL) Baseline 17.7 ± 18.9 16.2 ± 9.27 0.20
10 weeks 11.5 ± 8.2b12.6 ± 4.12b
Mean changes 6.23 ± 13.2 3.59 ± 6.28
HOMA-IR Baseline 6.76 ± 7.89 5.47 ± 3.98 0.08
10 weeks 3.92 ± 2.97b4.40 ± 1.80
Mean changes 2.84 ± 5.72 1.07 ± 2.46
Data are presented as mean ± standard deviation.
ap value is reported based on ANCOVA test with adjustment for baseline values, age, sex, smoking, physical activity, medications, and baseline BMI.
bp value is reported based on paired t-test (p < 0.05).
cp value is reported based on paired t-test (p < 0.01).BMI, body mass index; FBG, fasting blood glucose; HOMA-IR, homeostatic model assessment for insulin resistance.
TABLE4 Blood pressure and lipid profile at baseline and after 10 weeks supplementation.
Variable Time Green coee group (n =  22) Placebo group (n =  22) p-valuea
SBP (mmHg) Baseline 130 ± 6.27 124 ± 5.67b0.01
10 weeks 125 ± 4.31d123 ± 4.41
Mean changes 5.56 ± 3.41 0.90 ± 2.67
DBP (mmHg) Baseline 80.5 ± 6.37 78.4 ± 5.25 0.51
10 weeks 80.2 ± 5.13 77.8 ± 4.35
Mean changes 0.33 ± 2.77 0.61 ± 2.58
Triglyceride (mg/dL) Baseline 187 ± 86.4 172 ± 109 0.02
10 weeks 138 ± 45.9 d168 ± 47.4
Mean changes 49.7 ± 72.5 4.40 ± 98.6
Cholesterol (mg/dL) Baseline 176 ± 36.2 172 ± 40.9 0.34
10 weeks 173 ± 42.2 16 ± 45.5
Mean changes 3.93 ± 29.9 10.6 ± 28.0
LDL (mg/dL) Baseline 171 ± 34.4 172 ± 40.9 0.50
10 weeks 154 ± 35.1c163 ± 45.6
Mean changes 17.1 ± 28.2 9.78 ± 33.8
HDL (mg/dL) Baseline 42.5 ± 11.8 40.7 ± 7.83 0.001
10 weeks 45.7 ± 12.1d39.0 ± 5.39
Mean changes 3.22 ± 5.10 1.73 ± 6.10
TG/HDL ratio Baseline 4.64 ± 2.31 4.29 ± 2.32 0.001
10 weeks 3.23 ± 1.34d4.42 ± 1.44
Mean changes 1.40 ± 1.83 0.13 ± 2.12
Data are presented as mean ± standard deviation.
ap value is reported based on ANCOVA test with adjustment for baseline values, age, sex, smoking, physical activity, medications, and baseline BMI.
bp value is reported based on independent t-test (p < 0.05).
cp value is reported based on paired t-test (p < 0.05).
dp value is reported based on paired t-test (p < 0.01).BMI, body mass index; DBP, diastolic blood pressure; HDL, high density lipoprotein; LDL, low density lipoprotein; SBP, systolic blood
pressure.
Khalili-Moghadam et al. 10.3389/fnut.2023.1241844
Frontiers in Nutrition 07 frontiersin.org
contradictory results; the dierence in population study can beone
of the reasons for the inconsistency in the results. In current study,
weassessed the eects of GCE on diabetic patients, but previous
studies assessed the eects of GCE on dierent population. Also,
the dierence in the baseline FBG and insulin levels can beanother
reason for the inconsistency in the results. It is suggested that CGA
could improve FBG by activating AMP-activated protein kinase
(AMPK), and activation of this kinase consequently increased
glucose uptake in the cells by glucose transporter 4 (GLU4) fusion
with the plasma membrane (10). Also, CGA can inhibit the key
enzymes linked to the absorption of glucose (including pancreatic
amylase isoenzymes I and II, α-glucosidase, and α-amylase),
leading to postprandial blood glucose improvement (10).
Furthermore, CGA can decrease glucose production
(glycogenolysis and gluconeogenesis) by inhibiting the glucose-6-
phosphatase enzyme (35). It is thought that GCE lowers insulin
resistance by the activation of insulin receptor substrate-1 via
inhibiting c-Jun N-terminal kinase phosphorylation. is causes
GLUT4 translocation to the adipocyte membrane (36). Also, GCA
can decrease insulin resistance by activating the hepatic
proliferation-activated receptor α (PPAR-α), which facilitates the
clearing of lipids from the liver (9).
Hs-CRP and MDA levels
Our trial demonstrated that GCE administration for 10 weeks in
patients with T2D signicantly decreased CRP. Our results were in
agreement with a double-blind, placebo-controlled, randomized trial of
the eect of GCE on adult patients with non-alcoholic fatty liver disease
conducted by Shahmohammadi etal. (17). ey reported that GCE
supplementation has an improving eect on hs-CRP levels. But, in a
placebo-controlled double-blind pilot study on healthy men, GCE had
no eect on CRP compared to the placebo group (14). e inconsistent
results can bedue to dierences in the duration and dosage of the
intervention, sample size, and population. e main reason for this
inconsistency in the result can bedue to the dierence in population
study. In comparison with the previous study that has assessed the eects
Of GCE on healthy subjects, but weassessed the eects of GCE on
diabetic population, that these subjects have more inammation than
healthy subjects. is study was conducted only on men subjects, which
can beanother reason of inconsistency in the results. Also, all subjects in
the current study have higher BMI and age compared to the subjects of
previous study. A recent meta-analysis of eight trials found that GCE
supplementation (dosage 50–1,200 mg/d, duration of 8–12 weeks) has no
eect on CRP (19). However, based on the results of this meta-analysis,
GCE supplementation has a decreasing eect on tumor necrosis factor
alpha (TNF-α) as an inammatory biomarker (37). CGA, by increasing
the expression of genes encoding enzymes, including glutathione
peroxidase and superoxide dismutase, exerts reducing eects on
oxidative stress (8). Also, CGA has improved eects on inammation by
inhibiting the cytochrome P450 1A enzymes that increase the
pro-inammatory response in peripheral blood mononuclear cells (7).
Our ndings did not show a signicant eect of GCE on MDA levels
aer 10 weeks.
Study strengths and limitations
e randomized, placebo-controlled design was the main strength
of our study. However, using a xed dose of GCE and a short period
of intervention were the limitations of the current study. erefore,
additional studies with a large sample size, dierent dosages, and
longer durations are required to demonstrate the potential eects of
GCE in patients with T2D.
Conclusion
Based on the ndings of our study, GCE administration at a
dosage of 800 mg/d for 10 weeks in patients with T2D decreased SBP,
TG, and CRP and increased HDL compared to placebo. Moreover,
FBG reduction in GCE group was marginally signicant compared to
the placebo group. erefore, GCE may have a benecial eect on
lipid prole and inammation in patients with T2D.
Data availability statement
e original contributions presented in the study are included in
the article/supplementary material, further inquiries can bedirected
to the corresponding authors.
Ethics statement
e studies involving humans were approved by Faculty of
Nutrition and Food Technology, National Nutrition and Food
TABLE5 CRP and MDA at baseline and after 10 weeks supplementation.
Variable Green coee group (n =  22) Placebo group (n =  22) p-valuea
CRP (mg/L) Baseline 3.31 ± 2.41 2.69 ± 2.13 0.02
10 weeks 2.28 ± 1.46b2.88 ± 1.84
Mean changes 1.04 ± 1.21 0.18 ± 1.85
MDA (μmol/L) Baseline 1.44 ± 0.96 1.15 ± 0.59 0.18
10 weeks 1.19 ± 0.78 1.25 ± 0.59
Mean changes 0.25 ± 1.06 0.09 ± 0.67
Data are presented as mean ± standard deviation.
ap value is reported based on ANCOVA test with adjustment for baseline values, age, sex, smoking, physical activity, medications, and baseline BMI.
bp value is reported based on paired t-test (p < 0.01).BMI, body mass index; CRP, C-reactive protein; MDA, malondialdehyde.
Khalili-Moghadam et al. 10.3389/fnut.2023.1241844
Frontiers in Nutrition 08 frontiersin.org
Technology, Research Institute, Shahid Beheshti University of
Medical Sciences, Tehran, Iran. e studies were conducted in
accordance with the local legislation and institutional requirements.
e participants provided their written informed consent to
participate in this study.
Author contributions
SK-M and PM conceived and designed the study. SK-M, PM, and
MH contribute to data collection. SK-M and MG analyzed the data
and draed the initial manuscript. All authors contributed to the
article and approved the nal manuscript.
Acknowledgments
The authors gratefully wish to thank the National Nutrition
and Food Technology Research Institute, Shahid Beheshti
University of Medical Sciences, Tehran, Iran, for their study
funding and financial support. Wethank the laboratory section of
the Research Institute for Endocrine Science, Shahid Beheshti
University of Medical Sciences. Wealso thank all the patients who
participated in the study.
Conflict of interest
e authors declare that the research was conducted in the
absence of any commercial or nancial relationships that could
beconstrued as a potential conict of interest.
Publisher’s note
All claims expressed in this article are solely those of the authors
and do not necessarily represent those of their aliated organizations,
or those of the publisher, the editors and the reviewers. Any product
that may be evaluated in this article, or claim that may be made by its
manufacturer, is not guaranteed or endorsed by the publisher.
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d2fo00983h
... Green coffee bean extract (GC) is a supplement extracted from raw coffee beans prior to fermentation and roasting. It has antioxidant properties and reduces belly fat, body weight, incidence of cancer, diabetes and liver disease [12][13][14]. The bioactive compounds present in green coffee, not only chlorogenic acids and their derivatives, but also caffeine, theophylline, and theobromine, cafestol, kahweol, tocopherols and trigonelline [13,14]. ...
... It has antioxidant properties and reduces belly fat, body weight, incidence of cancer, diabetes and liver disease [12][13][14]. The bioactive compounds present in green coffee, not only chlorogenic acids and their derivatives, but also caffeine, theophylline, and theobromine, cafestol, kahweol, tocopherols and trigonelline [13,14]. However, the antioxidant activity of coffee beans mainly depends on the phenolic compound chlorogenic acid (CGA). ...
... However, the antioxidant activity of coffee beans mainly depends on the phenolic compound chlorogenic acid (CGA). Previous studies reported that CGA improves insulin sensitivity, increases glucose uptake in skeletal muscle and modulates several metabolic pathways [14,15]. ...
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Objectives Metabolic syndrome is a cluster of conditions that increases the risk of atherosclerotic cardiovascular diseases. The current study was a randomized, double blind, placebo-controlled study that aimed to determine the impact of green coffee (GC) in obese patients with metabolic syndrome through analysis of miRNA-155, miRNA-133a and the inflammatory biomarkers such as resistin, TNF-α, total sialic acid, homocysteine, high sensitivity C-reactive protein (hs-CRP), and the anti-inflammatory cytokine, adiponectin. Methods One hundred-sixty obese patients were randomly supplemented either with GC capsules (800 mg) or placebo daily for six months. Both groups were advised to take a balanced diet. Blood samples were collected at baseline and after six months of supplementation. Results GC supplementation for 6 months reduced BMI (p = 0.002), waist circumference (p = 0.038), blood glucose (p = 0.002), HbA1c% (p = 0.000), Insulin (p = 0.000), systolic blood pressure (p = 0.005), diastolic BP (p = 0.001) compared with placebo. GC significantly decreased total cholesterol (TC, p = 0.000), LDL-C (p = 0.001), triglycerides (TG, p = 0.002) and increased HDL-C (p = 0.008) compared with placebo group. In addition, GC significantly (p ≤ 0.005) reduced total sialic acid, homocysteine, resistin, TNF-α, hs-CRP and the oxidative stress marker malondialdehyde (MDA), but increased serum adiponectin (p = 0.000) compared to placebo group. There was a significant reduction in the gene expression of miR-133a (p = 0.000) in GC group as compared with baseline levels and with the control placebo group (p = 0.001) after 6 months. Conclusion GC administration modulated metabolic syndrome by decreasing BMI, high BP, blood glucose, dyslipidemia, miRNA-133a and inflammatory biomarkers that constitute risk factors for cardiovascular diseases. ClinicalTrials.gov registration No. is NCT05688917. Graphical Abstract
... Prior studies [13][14][15][16][17] have reported that coffee consumption is related to a lower risk of T2D, as observed by blood glucose levels or biomarkers in patients and animal models. Some studies indicate the ability of coffee extract, coffee components (chlorogenic acid, CGA; caffeine, CE; and caffeic acid, CA) [18][19][20][21], and green coffee bean extract (GCBE) to improve glucose and lipid metabolism [22][23][24]. However, the exact cellular mechanisms are not clearly understood, and prior researchers have suggested that the mechanism or pathway of these compounds' effects in T2D should be elucidated. ...
... Thus, inhibiting pancreatic lipase activity is one strategy to reduce lipid absorption and lipid blood levels. This result is consistent with a previous study that reported the lipid-preventing capacity of green coffee beans in humans [23,24]. Decreasing coffee's cholesterol solubility was attributed to its soluble fibers and lipid content, breaking bile salt down from micelle solution and forming a larger size [34]. ...
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Functional foods and nutrition have become increasingly popular in preventing and reducing the incidence of diabetes. Green coffee bean extract (GCBE) has received much interest because of the evidence that coffee consumption reduces the risk of diabetes and many inflammatory diseases. This study was designed to investigate the phytochemicals contained in GCBE and their antioxidant, anti-diabetic, and anti-inflammatory efficacies. GCBE phytochemicals were analyzed using high-performance liquid chromatography (HPLC). This analysis demonstrated that chlorogenic acid was the predominant component of GCBE, followed by caffeine and caffeic acid. The antioxidant capacity of GCBE was assessed using the 1,1-diphenyl-2-picrylhydrazyl (DPPH) and 2,2’-azinobis 3-ethylbenzothiazoline-6-sulfonic acid (ABTS) assays, demonstrating significant scavenging capacity with IC50 values of 2.96 ± 1.04 and 7.63 ± 1.03 µg/mL, respectively. The anti-hyperlipidemic efficacy of GCBE was observed through inhibiting cholesterol absorption (by increasing micelle sizes and decreasing cholesterol solubility), lipid digestion, and pancreatic lipase activity in vitro. The investigations revealed that GCBE possessed anti-hyperlipidemic properties by inhibiting cholesterol absorption, lipid digestion, and pancreatic lipase activity. Specifically, GCBE increased micelle particle sizes by ~6.5-fold, decreased cholesterol solubility by 2-fold, and reduced pancreatic lipase activity by 25%. Additionally, the in vitroanti-hyperglycemic activity of GCBE was evaluated by inhibition of α-amylase and α-glucosidase capacity. GCBE demonstrated anti-hyperglycemic activity by inhibiting α-amylase activity (32.80 ± 7.06% inhibition), while α-glucosidase activity remained unaffected. The anti-inflammatory potential of GCBE was evaluated by mRNA regulation using RT-PCR analysis. This analysis revealed that GCBE attenuated mRNA expression of COX-2, TNF-α, IL-1b, and IL-6 in LPS-induced RAW264.7 cells. GCBE’s antioxidant, anti-hyperlipidemic, and anti-hyperglycemic efficacies and its molecular mechanisms in modulating the inflammation pathway found in the present study highlight its potential as a supplement in functional foods or beverages. Doi: 10.28991/HEF-2024-05-01-08 Full Text: PDF
... 48 Therefore, consuming coffee at inappropriate times may worsen impaired glucose tolerance in diabetic patients, potentially heightening the adverse effects linked to CKD development. Also, consuming coffee during the above periods will lower insulin sensitivity and glucose tolerance in peripheral tissues, 49,50 potentially exacerbating the risk of CKD among diabetic individuals. ...
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Obesity has increasingly become a worldwide epidemic, as demonstrated by epidemiological and clinical studies. Obesity may lead to development of a broad spectrum of cardiovascular diseases (CVDs), such as coronary heart disease (CHD), hypertension, heart failure (HF), cerebrovascular disease, atrial fibrillation (AF), ventricular arrhythmias, and sudden cardiac death (SCD). In addition to hypertension, there are other cardiometabolic risk factors (CRFs) such as visceral adiposity, dyslipidemia, insulin resistance, diabetes, elevated levels of fibrinogen, and C-reactive protein and others, all of which increase the risk of CVD events. Mechanisms involved between obesity and CVD mainly include insulin resistance, oxidative stress, inflammation, and adipokines dysregulation, which cause maladaptive structural and functional alterations of the heart, particularly left ventricular (LV) remodeling and diastolic dysfunction. Natural products of plants, provide a diversity of nutrients and different bioactive compounds, including phenolics, flavonoids, terpenoids, carotenoids, anthocyanins, vitamins, minerals, fibers, and others, which possess a wide range of biological activities including antihypertensive, antilipidemic, antidiabetic, and other activities, thus conferring cardiometabolic benefits. In this review, we discussed the main therapeutic interventions using extracts from herbs and plants in preclinical and clinical trials with protective properties targeting CRFs. Molecular mechanisms and therapeutic targets of herbs and plants extracts for the prevention and treatment of CRFs are also reviewed.
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Obesity has increasingly become a worldwide epidemic, as demonstrated by epidemiological and clinical studies. Obesity may lead to the development of a broad spectrum of cardiovascular diseases (CVDs), such as coronary heart disease, hypertension, heart failure, cerebrovascular disease, atrial fibrillation, ventricular arrhythmias, and sudden cardiac death. In addition to hypertension, there are other cardiometabolic risk factors (CRFs) such as visceral adiposity, dyslipidemia, insulin resistance, diabetes, elevated levels of fibrinogen and C-reactive protein, and others, all of which increase the risk of CVD events. The mechanisms involved between obesity and CVD mainly include insulin resistance, oxidative stress, inflammation, and adipokine dysregulation, which cause maladaptive structural and functional alterations of the heart, particularly left-ventricular remodeling and diastolic dysfunction. Natural products of plants provide a diversity of nutrients and different bioactive compounds, including phenolics, flavonoids, terpenoids, carotenoids, anthocyanins, vitamins, minerals, fibers, and others, which possess a wide range of biological activities including antihypertensive, antilipidemic, antidiabetic, and other activities, thus conferring cardiometabolic benefits. In this review, we discuss the main therapeutic interventions using extracts from herbs and plants in preclinical and clinical trials with protective properties targeting CRFs. Molecular mechanisms and therapeutic targets of herb and plant extracts for the prevention and treatment of CRFs are also reviewed.
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Introduction Chronic and acute chlorogenic acid (CGA) can improve glucose tolerance (GT) and insulin sensitivity (IS). However, whether acute administration of CGA has beneficial effects on hepatic lipid metabolism and cecal microbiota composition remains unclear. Methods In the current study, diabetic db/db mice were administered CGA or metformin, and db/m mice were used as controls to explore the effects of CGA on hepatic lipid metabolism, including fatty acid oxidation and transportation and triglyceride (TG) lipolysis and synthesis. Moreover, alterations in the inflammatory response and oxidative stress in the liver and gut microbe composition were evaluated. Results The results showed that CGA decreased body weight and improved glucose tolerance and insulin resistance, and these effects were similar to those of metformin. CGA decreased hepatic lipid content by increasing the expression of CPT1a (carnitine palmitoyltransferase 1a), ACOX1 (Acyl-CoA oxidase 1), ATGL (adipose triglyceride lipase), and HSL (hormone-sensitive lipase) and decreasing that of MGAT1 (monoacylglycerol O-acyltransferase 1), DGAT1 (diacylglycerol O-acyltransferase), DGAT2, CD36, and FATP4 (fatty acid transport protein 4). Additionally, CGA restored the expression of inflammatory genes, including TNF-α (tumor necrosis factor-alpha), IL-1β (interleukin-1beta), IL-6, and IL-10, and genes encoding antioxidant enzymes, including SOD1 (superoxide dismutases 1), SOD2 (superoxide dismutases 2), and GPX1 (glutathione peroxidase 1). Furthermore, CGA improved the bacterial alpha and beta diversity in the cecum. Moreover, CGA recovered the abundance of the phylum Bacteroidetes and the genera Lactobacillus, Blautia, and Enterococcus. Discussion CGA can improve the antidiabetic effects, and microbes may critically mediate these beneficial effects.
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Abstract Many studies have investigated the relationship between coffee and diabetes. Evaluation of the current evidence on the effect of coffee intake on diabetes is critical. Therefore, we aimed to investigate the potential association between green coffee extract (GCE) and fasting blood glucose (FBG), insulin and homeostatic model assessment of insulin resistance (HOMA-IR) by pooling together the results from clinical trials. PubMed, Scopus and Google Scholar were searched for experimental studies which have been published up to December 2018. Randomized controlled trials (RCTs) that investigated the effect of GCE supplementation on FBG, insulin and HOMA-IR in adults were included for final analysis. A total of six articles were included in the meta-analysis. Results revealed that GCE supplementation reduced FBG level (SMD: −0.32, 95% CI − 0.59 to − 0.05, P = 0.02) but had no effect on insulin levels (SMD: −0.22, 95% CI −0.53 to 0.09, P = 0.159). Although analysis showed that GCE supplementation cannot change the HOMA-IR status (SMD: −0.30, 95% CI −0.73 to 0.13, P = 0.172), after stratified studies by GCE dosage ( 400 mg/day) there was a significant decrease in HOMA-IR status in a dose greater than 400 mg. These findings suggest that GCE intake might be associated with FBG improvement.
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Objective: This study aimed to evaluate the effects of decaffeinated green coffee extract (DGCE) supplementation on anthropometric indices, blood glucose, leptin, adiponectin, and neuropeptide Y (NPY) in breast cancer survivors with obesity. Method: A total of 44 breast cancer survivors with obesity aged between 18 and 70 years and with a mean body mass index (BMI) of 31.62 ± 4.97 kg m-2 participated in this double-blind randomized clinical trial. Eligible patients were randomized to the intervention (n = 22) and control (n = 22) groups. They received two 400 mg capsules of DGCE or two identical placebos daily for 12 weeks. Serum concentrations of leptin, adiponectin, NPY, fasting blood sugar, insulin, and homeostatic model assessment for insulin resistance (HOMA-IR) were measured at the baseline and after completion of the intervention. Also, weight, waist circumference, fat percentage, muscle percentage, and visceral fat were measured. Results: There were no significant differences in terms of changes of anthropometric indices and concentrations of leptin, adiponectin, NPY, and blood sugar between the two studied groups. Conclusion: Supplementation with DGCE in breast cancer survivors with obesity had no significant effect on anthropometric indices and blood glucose, leptin, adiponectin, and NPY levels.
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Chlorogenic acid (CGA), one of the most abundant polyphenols in the human diet, exhibits many biological properties, including antibacterial properties. Numerous studies have investigated the antibacterial effects of CGA, however, the molecular mechanisms governing its effects against Streptococcus pyogenes have not been fully elucidated. S. pyogenes is a gram-positive pathogen that causes a wide range of human infections and postinfectious immune-mediated disorders. In this study, we used an iTRAQ-based proteomic technique to investigate the underlying mode of action of CGA against S. pyogenes. KEGG and GO analyses indicated that CGA affected the expression of proteins alterations involved in multiple pathways, downregulating the expression of ribosomal proteins, and upregulating the expression of proteins associated with fatty acid metabolism, pyruvate metabolism and propanoate metabolism, while activating the expression of oxidation-reduction related proteins. Moreover, further cell-based experiments verified that CGA scavenges intracellular ROS in S. pyogenes. These results suggest that CGA may exert its antibacterial action through several actions, such as downregulating ribosomal subunits, affecting lipid metabolism and scavenging intracellular ROS. The results of this study may help to elucidate the molecular mechanisms by which CGA combats pathogens.
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Inflammation is considered a major contributor to non-alcoholic fatty liver disease (NAFLD) and several chronic diseases such as cardiovascular disease and type two diabetes. Green coffee bean extract (GCBE) supplementation has been suggested to enhancing antioxidant capacity in people with obesity but results across studies are mixed. We conducted a meta-analysis of randomized controlled trials of GCBE supplementation in overweight/obese with normal liver function and NAFLD adults with ALT, AST, γ-GTP, ALP, LDH, CRP, IL-6, and TNF-α as outcomes by searching PubMed and other databases. Eight studies were included, totaling 330 participants randomized to GCBE supplementation or placebo ranging from 50 mg/day to 1200mg/day for 8–12 weeks. GCBE supplementation resulted in lower levels of TNF-α (mean difference =1.37 pg/mL [95% CI =0.97–1.76]; p<0.00001). No significant difference was found in the remaining markers. In conclusion, GCBE supplementation attenuated TNF-α, a circulating inflammatory marker mediator which may be linked with lower systemic inflammation. However, potential cellular and molecular mechanisms by which GCBE exerts this positive effect warrants further investigations in human model studies.
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Background and aim Two meta-analyses summarized data on the effects of green coffee extract (GCE) supplementation on anthropometric measures. However, the accuracy of those meta-analyses is uncertain due to several methodological limitations. Therefore, we aimed to conduct a comprehensive systematic review and dose-response meta-analysis to summarize all available evidence on the effects of GCE supplementation on anthropometric measures by considering the main limitations in the previous meta-analyses. Methods We searched available online databases for relevant publications up to January 2020, using relevant keywords. All randomized clinical trials (RCTs) investigating the effects of GCE supplementation, compared with a control group, on anthropometric measures [including body weight, body mass index (BMI), body fat percentage, waist circumference (WC) and waist-to-hip ratio (WHR)] were included. Results After identifying 1871 studies from our initial search, 15 RCTs with a total sample size of 897 participants were included in the systematic review and meta-analysis. We found a significant reducing effect of GCE supplementation on body weight (weighted mean difference (WMD): -1.23, 95% CI: -1.64, -0.82 kg,P < 0.001), BMI (WMD: -0.48, 95% CI: -0.78, -0.18 kg/m², P = 0.001), and WC (WMD: -1.00, 95% CI: -1.70, -0.29 cm, P = 0.006). No significant effect of GCE supplementation on body fat percentage and WHR was seen. In the dose-response analyses, there was no significant association between chlorogenic acid (CGA) dosage, as the main polyphenol in green coffee, and changes in anthropometric measures. Conclusion We found that GCE supplementation had a beneficial effect on body weight, BMI and WC. It provides a cost-effective and safe alternative for the treatment of obesity. Additional well-designed studies are required to further confirm our findings.
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Objectives The current study evaluated the effects of green coffee extract (GCE) on serum lipid profile and adiponectin levels in patients with nonalcoholic fatty liver disease (NAFLD). Design This randomized, double-blind, placebo-controlled clinical trial was conducted on NAFLD patients aged 20–60 years and body mass index (BMI) of 25−35 kg/m². Setting Patients were recruited from the Bahman poly-clinic (Neyshabur, Iran) between January and June 2016. Interventions The study subjects were randomly assigned to receive a daily dose of 400 mg GCE (n = 24) or placebo (n = 24) for eight weeks. Main outcome measures Serum liver enzyme levels, lipid profile, adiponectin concentrations, and hepatic steatosis grade were measured for all patients at baseline and the end of the trial. Results GCE supplementation significantly reduced BMI [mean difference (MD): −0.57 and 95 % confidence interval (CI): −0.84 to −0.29, P < 0.001] and increased serum high-density lipoprotein cholesterol (MD: 7.06, 95 % CI: 0.25–13.87, P < 0.05) compared to the control group. Serum total cholesterol decreased significantly within the GCE group (MD: −13.33, 95 % CI: −26.04 to −0.61, P < 0.05). Triglyceride levels reduced significantly in GCE group compared to the placebo group (MD: -37.91; 95 % CI: −72.03 to −3.80; P = 0.03). However, this reduction was not significant when was further adjusted for mean changes in BMI and daily energy intake (MD: -23.43; 95 % CI: −70.92 to 24.06; P = 0.32). Hepatic steatosis grade, liver enzymes, and adiponectin levels did not show significant differences between the two groups after the intervention. Conclusions GCE supplementation improved serum lipid profile and BMI in individuals with NAFLD. GCE may be useful in controlling NAFLD risk factors.