ArticlePDF Available

The Effect of Coffee Consumption on Blood Glucose: A Review

Authors:





OPEN ACCESS Pakistan Journal of Nutrition
ISSN 1680-5194
DOI: 10.3923/pjn.2020.420.429
Review Article
The Effect of Coffee Consumption on Blood Glucose: A Review
Amal Hassan Alshawi
Department of Nutrition and Food Science, Princess Nourah Bint Abdulrahman University, Riyadh, Kingdom of Saudi Arabia
Abstract
This review describes the impact of drinking coffee on glycemic profile parameters (glycemic index [GI], glycemic load [GL], glucose
tolerance and insulin sensitivity) and diabetes mellitus. Coffee is very popular in Arab communities including Saudi Arabia. Clinical research
has revealed the negative effect of caffeine including a reduction in insulin sensitivity that impairs glucose tolerance. Epidemiological
studies also show that drinking coffee has positive effects on both glucose tolerance and sensitivity to insulin, which might assist in
reducing the risk of type 2 diabetes especially over long periods of consumption. More studies are thus needed to gain a deeper
understanding of how coffee drinking is linked to type 2 diabetes.
Key words: Caffeine, diabetes mellitus, insulin sensitivity, glucose tolerance, chlorogenic acid, coffee consumption
Citation: Amal Hassan Alshawi, 2020. The effect of coffee consumption on blood glucose: A review. Pak. J. Nutr., 19: 420-429.
Corresponding Author: Amal Hassan Alshawi, Department of Nutrition and Food Science, Princess Nourah Bint Abdulrahman University,
Riyadh, Kingdom of Saudi Arabia
Copyright: © 2020 Amal Hassan Alshawi. This is an open access article distributed under the terms of the creative commons attribution License, which
permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.
Competing Interest: The author has declared that no competing interest exists.
Data Availability: All relevant data are within the paper and its supporting information files.
Pak. J. Nutr., 19 (9): 420-429, 2020
INTRODUCTION
The word coffee derives from the Arabic word
quahweh
, leading to the Latin botanical genus
coffea
. Of the
coffee which is actually drunk, 99% comes from just two of the
103 kinds of coffee that have been discovered:
Coffea arabica
(Arabica) and
Coffea canephora
(Robusta). Coffee growing
occurs in sixty tropical and subtropical nations. Around 60% of
the coffee produced globally is grown on the American
continent. Here, Arabica coffee with its low caffeine content
and bitterness predominates1. Golden coffee, which comprises
around 95% of all coffee exports, is produced through minimal
processing of the green coffee beans2. Coffee is very common
in many countries with the highest per capita consumption
being in Europe where the average consumption is between
2.4 and 12 kg per person per year3.
Coffee contains caffeine, which is a bioactive compound.
It stimulates the central nervous system and positively affects
long-term memory. Drinking coffee has historically been
associated with negative health effects, more recent studies
show that it may be beneficial1. Consuming approximately
#400 mg of caffeine daily (3-4 cups) of brewed coffee or
having five cups of tea or five caffeinated soft drinks regard as
moderate seems to affect health in a neutral to positive way.
Adolescents can safely consume 100-175 mg of caffeine per
day while the safe level for children aged 6-12 is 45-85 mg4. In
Saudi Arabia, the term Arabic coffee is usually applied to a
green coffee bean extract that is very popular. Spices such as
saffron and cardamom are added to the roasted green coffee
beans to enhance the color and taste of the resulting coffee
product. In Saudi Arabia, as in other Arab Gulf countries, coffee
is usually drunk with snacks especially soft dates.
The efficiency of consuming brewed coffee on human
health has been the focus of many studies5. This review aims
to evaluate how drinking coffee affects blood glucose and the
implications for insulin sensitivity and glucose tolerance as
well as its impact on diabetes.
Search strategy: Databases were searched for a randomized
controlled trial that examined the effects of coffee
consumption on blood glucose in healthy humans. The
following keywords in the title/abstract were used: caffeine,
diabetes mellitus, insulin sensitivity, glucose tolerance,
chlorogenic acid and coffee consumption. The reference lists
from selected reports were reviewed for further relevant
studies. Studies that investigated the effect of different coffee
drinks are included because coffee consumption occurs more
frequently than pure caffeine intake in daily life.
A review of the literature was conducted utilizing
databases such as PubMed, Google Scholar, LWW Health
Library and Science Direct. Furthermore, studies cited in the
selected articles were verified. Studies on association of
caffeine, coffee consumption and diabetes were included.
General properties of coffee: When coffee beans are ripe,
they can be processed by the wet method or by drying in the
sun for 3-9 days (the dry method). A temperature of 200EC is
required for the necessary transformation to take place during
roasting. When this occurs, the coffee beans become dry,
brittle and brown; they increase in size and develop their
characteristic aroma and flavor. Regardless of whether coffee
is prepared on an industrial scale or brewed at home, hydrous
extraction of the dissolved roast and ground coffee is
involved6.
The coffee quality is determined by the chemical
composition of the roasted beans, which is also affected by
drying, storing, roasting and grinding after the harvest. The
coffee bean quality relies on color, shape and size of the bean,
the crop year, the processing methods, the roast potential and
the processing method as well as the flavour7. Roasting is vital
because the chemical compounds that are generated by the
changes that happen during the roasting process are what
gives coffee its characteristic flavour8.
Recent research has demonstrated that coffee and its
by-products are rich in antioxidants. They contain trigonelline
and chlorogenic acids as well as caffeine, which are all
bioactive compounds9. These compounds have a positive
effect on health and this means that coffee is potentially a
functional food product2.
The coffee plant has a secondary metabolite which is
caffeine, (1, 3, 7-trimethylxanthine)-a purine alkaloid. The
caffeine content in the green coffee beans varies. If calculated
by dry weight, it represents up to 2.3% of Robusta beans
and up to 1.3% of Arabica beans. Coffee beans also contain
fairly large amounts of chlorogenic acids, which are widely
distributed secondary metabolites in plants with 5-O-
caffeoylquinic acid being the most common6. After
investigating the effects of various methods of brewing on the
polyphenol, methylxanthine and antioxidant capacities of 13
different brews of coffee, Baeza
et al
.10 concluded that their
antioxidant capacities complied with the total phenol and
chlorogenic acid derivate contents. Wachamo
et al
.11
suggested that the high phenolic content of green coffee
probably accounted for its association with the reduced threat
of diseases of oxidative etiology. The impact of drinking coffee
on various health consequences was reviewed by Bordenave
et al
.12 who concluded that it benefitted carbohydrate and
lipid metabolism as well as the cardiovascular system.
421
Pak. J. Nutr., 19 (9): 420-429, 2020
The blood glucose response to foods: Currently, the focus in
the glycemic response (GR) to foods is of considerable interest
because it is thought to have a relationship with chronic
diseases including obesity, diabetes and cardiovascular
disease13. GR to a food or meal for a person is specified by the
amount and quality of the carbohydrates14 and this can be
ascertained by the GI, GL, or glycemic impact15. The concept of
the GI was first coined in 1981 by Augustin
et al
.13 in their
research with patients who had type 2 diabetes mellitus. The
carbohydrate content of specific foods is evaluated by the GI
by measuring their glycemic effects after they have been
ingested16,17. The GI could be demonstrated as the incremental
area beneath the curve of the blood glucose response to a
50 g portion of available carbohydrate of a tested sample. It is
expressed as a percentage of the same person reaction after
eating an identical carbohydrate portion from standard food.
The variability and/or value of the GI results can be influenced
by a number of methodological factors; however, variation can
be minimized and reproducible findings obtained by careful
use of appropriate methods18.
The Food and Agriculture Organization of the United
Nations (FAO)/World Health Organization (WHO) outlines the
most appropriate method for calculating the GI19. The FAO, in
its consultation report on dietary carbohydrates in human
nutrition, suggests using GI values as well as other data on
food composition19. Low GI foods like legumes and low-fat
animal products are recommended as part of many
weight-loss diets20. All published data on the GI values of
600 particular foods was compiled and listed in a single table
by Fiona
et al
.20.
To assist in the creation of a local food exchange list for
diabetics, Al-Mssallem21 identified the GI value of popular
Saudi foods. Fohl, gareesh, korsan, kelija eneazaa and kelija
malkee are five common Saudi foods with high carbohydrate
content and were evaluated for their GI values (45, 89, 61, 58
and 51%, respectively). Alkaabi
et al
.22 assessed the GI values
of five popular types of dates in both diabetic and healthy
individuals. Their findings demonstrated a low GI value for all
five types of dates and the authors concluded that the dates
would not cause a significant rise in the concentration of
postprandial glucose if eaten by diabetics. Farhat
et al
.23
investigated the GI values of Lebanese mixed meals and
desserts and found that they ranged from intermediate
(50-70%) to low (#50%). A study on the GI values of breakfast
cereals in the diet of United Kingdom (UK) citizens showed
that these ranged from high ($70%) to low (#55%); most had
a moderate GI of between 60 and 65%24.
To measure GL, the entire amount of ingested
carbohydrates (in grams) is multiplied by the GI value of each
food and then divided by 10025. Wh en t he e ffe ct of GI/ GL o n
appetite and GR were identified, there were no significant
differences in appetitive rating, plasma glucose, insulin
response, or food consumption26. The GR is modulated by
several aspects of the meal including the nutrient
composition, the duration, volume/weight, energy density,
rheology and palatability27,28.
The GR is a food's capacity to raise blood sugar29. The way
that food has been processed or cooked affects GR30. Because
dietary fats slow the absorption of glucose, they may delay the
blood glucose and insulin responses31,32. Bataineh investigated
the glycemic and insulinemic indices of some popular Arabic
sweets when ingested by healthy individuals and found that
substituting olive oil for ghee in maa'moul, ghuraybah and
hareesah lowered GRs without a significant effect on the
insulinemic responses33. The blood glucose response of foods
containing differing amounts of carbohydrates can be
compared directly with the glycemic glucose equivalent
(GGE); the glucose quantity in grams would result in a GR
equal to a particular weight of a food34,35. Observing the
glucose continuously might be used to record the GR with
levels of interstitial glucose reported every 5 to 10 minutes
continuously for 3-7 days for a comprehensive observation of
the GR of a single meal or food36.
Due to lack and/or resistance of insulin, type 2 diabetes
mellitus is linked with the target tissues impaired insulin
response. Although increased insulin secretion overcomes
insulin resistance at first, this compensation ultimately fails
and results in progressively raised blood glucose levels. Before
people develop type 2 diabetes, they go across a stage of
impaired glucose tolerance (IGT) and increased plasma
glucose levels during fasting; thus, this stage is an
intermediate dysglycemia state between diabetes and
normal glucose tolerance37. The American Diabetes
Association proposed a new diagnostic criterion in 199738
whereby diabetes screening was carried out by testing plasma
glucose levels during fasting39. The importance of measuring
insulin sensitivity is frequently highlighted due to its
important role in diabetes, cardiovascular and hypertension
disease40; tools to measure insulin sensitivity and resistance is
a key goal of many studies41-43. Song
et al
.44 studied the
relationship between insulin resistance and dietary behavior
among healthy people in Korea: They found that a pattern
based on beans and whole grains was linked with a lower
prevalence of insulin resistance.
The effect of coffee consumption on the glycemic profile: If
people are to make informed choices about drinking coffee
and public health initiatives are to be prioritized appropriately,
then it is important to know the benefits and adverse effects
422
Pak. J. Nutr., 19 (9): 420-429, 2020
on health45. The relationship between coffee components like
antioxidant phenolic compounds, c af fe i ne , m i cronutrients and
fiber suggests beneficial effects3. According to Van Dam
et al
.45
coffee contains a number of substances that may impact
glucose metabolism.
The Hoorn45 study was a cross-sectional and prospective
study that was population-based and involved Dutch male
and female adults with a range of age 50-74 years. Initially, an
oral glucose tolerance test (OGTT) was conducted and a
follow-up was performed during an average period of six years
and four months. Some variables such as cigarette smoking,
alcohol intake, body mass index (BMI), physical activity and
dietary factors were adjusted. The results showed that habitual
coffee-drinking can lower the threat of IGT and impact post-
load rather than fasting glucose metabolism45. A link between
habitual coffee-drinking and the incidence of increased
plasma glucose levels during fasting, IGT and type 2 diabetes
was assessed.
Caffeine is one of the substances other than
macronutrients that can affect insulin sensitivity and blood
glucose concentrations in individuals with diabetes46. Despite
research carried out on short terms with people in good
health that continue to indicate that ingesting caffeine
cause acute transient insulin resistance and IGT47,48, these
conclusions appear to be contradicted by epidemiological
studies46. For an individual with existing diabetes, blood
glucose concentrations may be affected by caffeine in various
ways. Glucose transportation from blood to the muscles may
be hindered by caffeine as it acts as an adenosine receptor
antagonist to inhibit the uptake of glucose into muscle cells
even when insulin is present49. Moreover, elevated blood
glucose concentrations due to caffeine intake could be a
consequence of high epinephrine (adrenaline), which in turn
induces insulin resistance50,51. Other studies have also shown
how caffeine might impact glucose metabolism. Luiz
et al
.52
found that caffeine intake led to a significant increase
in blood glucose concentrations. Robinson
et al
.53 and
Lee
et al
.54 c on fi r me d t h at i ng es t in g ca f fe i ne i nc r ea s ed g lu co s e
concentration and loaded when compared to a placebo. Both
studies noted that caffeine caused a reduction in the insulin
sensitivity index compared to placebo.
Several studies have addressed the short-term and
long-term effects of coffee or caffeine consumption on
glucose tolerance55; they concluded that coffee consumption
and/or caffeine impaired glucose tolerance in the short-
term56,57. IGT is a state of hyperglycemia where resistance to
insulin sensitivity happens in peripheral tissues as a response
to glucose58. Insulin resistance and glucose tolerance can be
impaired by short-term administration of coffee, which
blocks the impact of the adenosine AI receptor that regulates
the uptake of glucose in skeletal muscles59. However, the
findings from some epidemiological studies demonstrate
that long-term and habitual coffee drinking might support
standard glucose tolerance and enhance insulin sensitivity60-63.
Thus, coffee may suppress insulin sensitivity in the short-term
but drinking coffee regularly can stimulate glucose tolerance
and insulin sensitivity64-66. In other words, ingesting caffeine
habitually changes the negative impact of caffeine on glucose
tolerance and insulin sensitivity to a positive one55.
Consuming coffee and caffeine were linked to lower
serum levels of leptin and plasminogen activator
inhibitor-167. In elderly individuals, low coffee consumption
for short periods predicts impairment of normal glucose
tolerance68 while also lowering glucose tolerance in healthy
men69. However, other studies report different results:
Feinberg
et al
.70 demonstrated that subjects showed a marked
reduction in blood glucose concentration after drinking coffee
although insulin levels were not affected. Shengxi
et al
.71
noted that just the intake of coffee polyphenols enhances
peripheral endothelial function after glucose loading among
adults in good health. Thom72 reported that instant coffee
enriched with chlorogenic acid lowered glucose absorption by
6.9% versus a control.
A lowered insulin sensitivity after short-term ingestion of
coffee72-74 may be due to the caffeine-induced antagonism
of adenosine receptors accompanied by a rise in levels of
epinephrine75. For individuals with type 2 diabetes mellitus,
the impact of drinking black espresso coffee does not seem to
be mediated by alterations in insulin sensitivity76. For the study
of insulin secretion and sensitivity, long-term trials on the
impact of caffeine and some components of coffee could be
more related. A cross-sectional study of 936 male senior
citizens without type 2 diabetes revealed that drinking coffee
was linked to higher insulin sensitivity but not a reduced
secretion of insulin61; however, a cross-sectional study of 2112
healthy women found a potential decrease of insulin secretion
as the result of consuming coffee. It is possible that this
decrease could be relevant to a constituent in coffee other
than caffeine62.
Recent research reported no alteration in postprandial
glycemic response to Lebanese mankoucheh when
accompanied by Turkish coffee77. Post-exercise insulin
concentrations and blood glucose were significantly changed
by caffeine and extract from green beans of coffee versus
placebo78.
Type 2 diabetes and consuming coffee: The global increase
in diabetes seems to be due to population ageing and
urbanization wi th ass oc iat ed alt er ati on s in ph ysi ca l a cti vi ty
423
Pak. J. Nutr., 19 (9): 420-429, 2020
and diet79. Specific criteria and diagnostic tests were used to
identify people who are pre-diabetic and thus at risk of
developing diabetes as well as those who have diabetes80.
Diabetes is classified into type 1, type 2, gestational and
secondary diabetes80. The vast majority of diabetics (90-95%)
have type 2, which used to be called non-insulin-dependent
or adult-onset diabetes81. Preventing type 2 diabetes is now a
significant public health issue. Type 2 diabetes can largely be
avoided by a healthy life style and a sound dietary pattern82.
Treatment of diabetes is focused on normalizing metabolism
with an emphasis on blood glucose and lipids especially
low-density lipoprotein (LDL), cholesterol and blood pressure
to prevent complications that are diabetes-related81.
Coffee contains a significant amount of caffeine and
chlorogenic acid and is a complex mix of chemicals. Over the
last few decades, studies have identified the benefit or
harm to health from drinking coffee83. Coffee may impact
postprandial hyperglycemic excursion, although there
have been conflicting results. Drinking coffee raises energy
expenditure and thermogenesis to induce insulin sensitivity84.
Coffee can produce an acute impairment of glucose tolerance
or insulin resistance in healthy, non-diabetic adults and has
been consistently demonstrated by a minimum of 17
short-term studies. We concluded that this effect contributes
to the progression of type 2 diabetes in susceptible people85.
Conversely, long-term coffee intake is possibly linked
with a lowered threat of type 2 diabetes86,87. Alkaabi
et al
.88
suggested that eating dates with coffee was common among
Arabs and that this might affect hyperglycemic excursion after
meals. They studied the effect of coffee on the GI tract of type
2 diabetic and healthy subjects when eating a common variety
of dates. They found that coffee did not adversely impact
capillary glucose levels after the consumption of dates either
in diabetic or healthy subjects at least in the short-term
88.
Information about the daily coffee consumption of a sample
of 1141 American Indian males and females with a range of
age 45-74 years was collected in a prospective cohort study.
The sample was within the normal average of glucose
tolerance at the baseline examination and was monitored with
a mean of 7.6 years. The findings indicated that subjects who
consumed more than 11 cups of coffee per day had a 67%
lower threat of developing diabetes through the follow-up
period compared to non-coffee consumers89. Another
prospective study followed 910 adults aged $50 years with a
mean of 8 years after their coffee consumption had been
assessed. These findings indicated that both former and
current coffee consumers had a reduced risk of diabetes
incident versus people who never ingest coffee. The subjects
with impaired baseline glucose who were former and current
coffee consumers also had a lower risk of diabetes. This
research strikingly demonstrates how caffeinated drinking
coffee can protect against the incidence of diabetes63.
Furthermore, according to Hamer
et al
.90, more than
fourteen cohort studies have revealed a reverse association
between drinking coffee beverages and the threat of
type 2 diabetes. Hamer
et al
.90 investigated the prospective
association between consuming coffee and tea beverages
and the threat of type 2 diabetes mellitus. The study was
conducted for 11.7 years of follow-up with a sample of
4055 males and 1768 females from the Whitehall cohort in the
UK; they concluded that drinking a moderate amount of
coffee and tea (more than 3 cups a day) was not prospectively
linked with the incidence of type 2 diabetes90. A cross-
sectional study of 954 non-diabetic adults who drink
caffeinated coffee on a regular basis based on a food
frequency questionnaire found a positive link to insulin
sensitivity that was inversely related to 2 h post-load glucose
levels91. Dutch male and female adults were followed for
a mean duration of 6.4 years in another prospective
cross-sectional study. They found that drinking coffee favored
post-load rather than fasting glucose45. Research conducted
with 2434 Finnish men and women reported that drinking
coffee had a significant and inverse link with both fasting
glucose and insulin and also with the response to a 2 h
glucose tolerance test55,92.
A review of these epidemiologic studies showed that
drinking coffee can significantly decrease the threat of type 2
diabetes93-96. Akash
et al
.55 found a number of mechanisms
that might be involved. Ryanodine receptors are activated by
caffeine and this improves the insulin secretion of $-cells of
the pancreatic islets. Glucose metabolism and homeostasis are
regulated by chlorogenic acid and magnesium55. Chu
et al
.97.
reported numerous compounds in coffee that may produce a
matrix effect by working together and providing bioactivities
that lower the threat of evolving type 2 diabetes. Finally,
coffee consumption is linked with the threat of diabetes
mellitus, the occurrence of stroke, heart failure and some
cancers in an inverse dose-dependent fashion; however, there
may be harmful effects related to high anxiety, insomnia and
acute myocardial infarction97,98. However, until the association
between the threat of type 2 diabetes and long-term coffee
consumption is more thoroughly understood, it would be
premature to suggest coffee intake consumption as a way of
preventing type 2 diabetes mellitus55,99,100.
424
Pak. J. Nutr., 19 (9): 420-429, 2020
CONCLUSIONS AND RECOMMENDATIONS
Generally, the literature on short-term clinical trials that
addressed the link between consuming coffee and type 2
diabetes mellitus shows that caffeine decreases insulin
sensitivity and negatively affects glucose tolerance.
Nevertheless, several prospective cohort studies in various
countries have demonstrated that drinking coffee is linked
with a significant decrease in the threat of developing type 2
diabetes mellitus. More studies are required to clearly
understand how the main components of coffee affect
glucose metabolism. Moreover, epidemiologic research needs
to be carried out in Arab populations and specifically in the
Saudi community to accurately identify how drinking coffee
affects blood glucose and other aspects of health. Effective
strategies in clinical research and related epidemiological
studies are needed to clarify the effect of coffee consumption
for people with type-diabetes especially in the local contest.
The use of coffee drinks could be a practical, effective and
environmentally friendly method to enhance insulin
sensitivity.
REFERENCES
1. Mejia, E.G.d. and M.V. Ramirez-Mares, 2014. Impact of
caffeine and coffee on our health. Trends Endocrinol.,
Metabo., 25: 489-492.
2. Ribeiro, V.S., A.E. Leitão, J.C. Ramalho and F.C. Lidon, 2014.
Chemical characterization and antioxidant properties of a
new coffee blend with cocoa, coffee silverskin and green
coffee minimally processed. Food Res. Int., 61: 39-47.
3. Pimentel, G.D., T.O. Micheletti, R.C. Fernandes and A. Nehlig,
2019. Coffee Intake and Obesity. In: Nutrition in the
Prevention and Treatment of Abdominal Obesity. Watson,
R.R. (Ed.). Elsevier, UK, pp: 329-351.
4. Mitchell, D.C., C.A. Knight, J. Hockenberry, R. Teplansky,
T.J. Hartmand, 2014. Beverage caffeine intakes in the U.S.
Food and Chem. Toxicol., 63: 136-142.
5. Ochiai, R., Y. Sugiura, Y. Shioya, K. Otsuka, Y. Katsuragi and
T. Hashiguchi, 2014. Coffee polyphenols improve peripheral
endothelial function after glucose loading in healthy male
adults. Nutr. Res., 34: 155-159.
6. Pimpley, V., S. Patil, K. Srinivasan, N. Desai and P.S. Murthy,
2020. The chemistry of chlorogenic acid from green coffee
and its role in attenuation of obesity and diabetes. Prep.
Biochem. Biotechnol., 10.1080/10826068.2020.1786699
7. Lee, L.W., M.W. Cheong, P. Curran, B. Yu and S.Q. Liu, 2015.
Coffee fermentation and flavor An intricate and delicate
relationship. Food Chem., 185: 182-191.
8. Giacalone, D., T.K. Degn, N. Yang, C. Liu, I. Fisk and
M. Münchow, 2019. Common roasting defects in coffee:
Aroma composition, sensory characterization and consumer
perception. Food Qual. Preference, 71: 463-474.
9. Muñoz, A.E., S.S. Hernández, A.R. Tolosa, S.P. Burillo and
M.O. Herrera, 2020. Evaluation of differences in the
antioxidant capacity and phenolic compounds of green and
roasted coffee and their relationship with sensory properties.
Food Sci. Technol., Vol. 128 10.1016/j.lwt.2020.109457
10. Baeza, G., M. Amigo-Benavent, B. Sarriá, L. Goya, R. Mateos
and L. Bravo, 2014. Green coffee hydroxycinnamic acids but
not caffeine protect human HepG2 cells against oxidative
stress. Food Res. Int., 62: 1038-1046.
11. Wachamo, H.L., Vol. 6, No. 4 2017. Review on Health Benefit
and Risk of Coffee Consumption. Med. Aromat. Plants,
10.4172/2167-0412.1000301
12. Bordenave, N., L.B. Kock, M. Abernathy, J.C. Parcon,
A.A. Gulvady, B.J.W.v, Klinken and P. Kasturi 2015. Toward a
more standardised and accurate evaluation of glycemic
response to foods: Recommendations for portion size
calculation. Food Chem., 167: 229-235.
13. Augustin, L.S., C.W. Kendall, D.J. Jenkins, W.C. Willett and
A. Astrup
et al
., 2015. Glycemic index, glycemic load and
glycemic response: An International Scientific Consensus
Summit from the International Carbohydrate Quality
Consortium (ICQC). Nutr. Metab. Cardiovasc. Dis., 25: 795-815.
14. Hardy, D.S., J.T. Garvin and H. Xu, 2020. Carbohydrate quality,
glycemic index, glycemic load and cardiometabolic risks in
the US, Europe and Asia: A dose‒response meta-analysis.
Nutr. Metab. Cardiovasc. Dis., 30: 853-871.
15. Salari-Moghaddam, A., A.H. Keshteli, F. Haghighatdoost,
A. Esmaillzadeh and P. Adibi, 2019. Dietary glycemic index
and glycemic load in relation to general obesity and central
adiposity among adults. Clin. Nutr., 38: 2936-2942.
16. Schwingshackl, L. and G. Hoffmann, 2013. Long-term effects
of low glycemic index/load vs. high glycemic index/load diets
on parameters of obesity and obesity-associated risks: A
systematic review and meta-analysis. Nutr. Metab.
Cardiovasc. Dis., 23: 699-706.
17. Singh, A., P. Raigond, M.K. Lal, B. Singh and N. Thakur, 2020.
Effect of cooking methods on glycemic index and
in vitro
bioaccessibility of potato (
Solanum tuberosum
L.)
carbohydrates. LWT-Food Sci. Technol., Vol. 127
10.1016/j.lwt.2020.109363
18. Mann, J., J.H. Cummings, H.N. Englyst, T. Key and S. Lui
et al
.,
2007. FAO/WHO scientific update on carbohydrates in human
nutrition: Conclusions. Eur. J. Clin. Nutr., 61: S132-S137.
19. Gibson, N., H.C. Schönfeldt and B. Pretorius, 2011.
Development of a rapid assessment method for the
prediction of the glycemic index. J. Food Compos. Anal.,
24: 750-754.
425
Pak. J. Nutr., 19 (9): 420-429, 2020
20. Atkinson, F.S., K. Foster-Powell and J.C. Brand-Miller, 2008.
International tables of glycemic index and glycemic load
values: 2008. Diabetes Care, 31: 2281-2283.
21. Al-Mssallem, M.Q., 2014. The association between the
glycaemic index of some traditional saudi foods and the
prevalence of diabetes in Saudi Arabia: A review article.
J. Diabetes Metab., Vol. 5. 10.4172/2155-6156.1000452
22. Alkaabi, J.M., B. Al-Dabbagh, S. Ahmad, H.F. Saadi, S. Gariballa
and M. Al Ghazali, 2011. Glycemic indices of five varieties
of dates in healthy and diabetic subjects. Nutr. J., Vol. 10.
10.1186/1475-2891-10-59
23. Farhat, A.G., S.R. Moukarzel, R.J. El-Said and C.F. Daher, 2010.
Glycemic index of commonly consumed lebanese mixed
meals and desserts. Asian J. Clin. Nutr., 2: 48-57.
24. Aston, L.M., J.M. Gambell, D.M. Lee, S.P. Bryant and S.A. Jebb,
2008. Determination of the glycaemic index of various
staple carbohydrate-rich foods in the UK diet. Eur. J. Clin.
Nutr., 62: 279-285.
25. AlGeffari, M.A., E.S. Almogbel, T.A. Homaidan, R. El-Mergawi
and I.A. Barrimaha, 2016. Glycemic indices, glycemic load and
glycemic response for seventeen varieties of dates grown in
Saudi Arabia. Ann. Saudi Med., 36: 397-403.
26. Brouns, F., I. Bjorck, K.N. Frayn, A.L. Gibbs, V. Lang, G. Slama
and T.M.S. Wolever, 2005. Glycaemic index methodology.
Nutr. Res. Rev., 18: 145-171.
27. Camps, G., M. Mars, C.d. Graaf and P.A. Smeets, 2016. Empty
calories and phantom fullness: a randomized trial studying
the relative effects of energy density and viscosity on gastric
emptying determined by MRI and satiety. Am. J. Clin. Nutr.,
104: 73-80.
28. Pribic, T., L. Hernandez, A. Nieto, C. Malagelada, A. Accarino
and F. Azpiroz, 2018. Effects of meal palatability on
postprandial sensations. Neurogastroenterology Motil.,
Vol. 30, No. 2 10.1111/nmo.13248
29. Farvid, M.S., F. Homayouni, M. Shokoohi, A. Fallah and
M.S. Farvid, 2014. Glycemic index, glycemic load and their
association with glycemic control among patients with type
2 diabetes. Eur. J. Clin. Nutr., 68: 459-463.
30. Marques, A.M., B.S. Linhares, R.D. Novaes, M.B. Freitas,
M.M. Sarandy and R.V. Gonçalves, 2020. Effects of the amount
and type of carbohydrates used in type 2 diabetes diets in
animal models: A systematic review. PLos ONE, Vol. 15, No. 6
10.1371/journal.pone.0233364
31. Fernandez, M.A. and A. Marette, 2020. Dairy Products and
Diabetes: Role of Protein on Glycaemic Control. In: Milk and
Dairy Foods: Their Functionality in Human Health and
Disease. Givens, D.I. (Ed.). Academic Press, United States
pp: 173-203.
32. Korat, A.V.A., Y. Li, F. Sacks, B. Rosner, W.C. Willett, F.B. Hu
and Q. Sun, 2019. Dairy fat intake and risk of type 2
diabetes in 3 cohorts of US men and women. Am. J. Clin.
Nutr., 110: 1192-1200.
33. Bataineh, M.F., 2002. Glycemic and Insulinemic Indices of
Certain Popular Arabic Sweets with Modified Fat Content.
Master Thesis, University of Jordan
34. Wallace, A.J., Eady, S.L. J.A. Willis, Scott, R.S., J.A. Monro and
C.M. Frampton, 2009. Variability in measurements of blood
glucose response to foods in human subjects is not reduced
after a standard breakfast. Nutr. Res., 29: 238-243.
35. Wallace, A.J., J.A. Monro, R.C. Brown, C.M. Framptond, 2008.
A glucose reference curve is the optimum method to
determine the glycemic glucose equivalent values of foods in
humans. Nutr. Res., 28: 753-759.
36. Powers, M.A., R.M. Cuddihy, D. Wesley and B. Morgan,
2010. continuous glucose monitoring reveals different
glycemic responses of moderate- vs high-carbohydrate lunch
meals in people with type 2 diabetes. J. Am. Diabet. Assoc.,
10: 1912-1915.
37. Cai, X., L. Xia, Y. Pan, D. He, H. Zhu, T. Wei and Y. He, 2019.
Differential role of insulin resistance and $-cell function in the
development of prediabetes and diabetes in middle-aged
and elderly Chinese population. Diabetology Metab.
Syndrome, Vol. 11, No. 24 10.1186/s13098-019-0418-x
38. The Expert Committee on the Diagnosis and Classification of
Diabetes Mellitus, 2003. Report of the expert committee on
the diagnosis and classification of diabetes mellitus. Diabetes
Care, 26: S5-S20.
39. Chia, C.W., J.M. Egan and L. Ferrucci, 2018. Age-related
changes in glucose metabolism, hyperglycemia and
cardiovascular risk. Circ. Res., 123: 886-904.
40. Jia, T., X. Huang, A.R. Qureshi, H. Xu and J. Ärnlöv
et al
., 2014.
Validation of insulin sensitivity surrogate indices and
prediction of clinical outcomes in individuals with and
without impaired renal function. Kidney Int., 86: 383-391.
41. Antuna-Puente, B., E. Disse, R. Rabasa-Lhoret, M. Laville,
J. Capeau and J.P. Bastard, 2011. How can we measure
insulin sensitivity/resistance? [Comment mesurer la
sensibilité/résistance à linsuline?]. Diabetes Metab.,
37: 179-188.
42. Kim, S.H., A. Silvers, J. Viren and G.M. Reaven, 2016.
Relationship between insulin sensitivity and insulin
secretion rate: not necessarily hyperbolic. Pathophysiology,
33: 961-967.
43. Tohidi, M., A. Ghasemi, F. Hadaegh, A. Derakhshan, A. Chary
and F. Azizi, 2014. Age- and sex-specific reference values for
fasting serum insulin levels and insulin resistance/sensitivity
indices in healthy Iranian adults: Tehran lipid and glucose
study. Clin. Biochem., 47: 432-438.
44. Song, S., H.Y. Paik and Y. Song, 2012. High intake of whole
grains and beans pattern is inversely associated with insulin
resistance in healthy Korean adult population. Diabetes Res.
Clin. Pract., 98: E28-E31.
426
Pak. J. Nutr., 19 (9): 420-429, 2020
45. Dam, R.M.v., J.M. Dekker, G. Nijpels, C.D.A. Stehouwer,
L.M. Bouter and R.J. Heine, 2004. Coffee consumption and
incidence of impaired fasting glucose, impaired glucose
tolerance and type 2 diabetes: the Hoorn study. Diabetologia,
47: 2152-2159.
46. Whitehead, N. and H. White, 2013. Systematic review of
randomised controlled trials of the effects of caffeine or
caffeinated drinks on blood glucose concentrations and
insulin sensitivity in people with diabetes mellitus. J. Hum.
Nutr. Diet., 26: 111-125.
47. Louie, J.C.Y., F. Atkinson, P. Petocz and J.C.B rand-Miller, 2008.
Delayed effects of coffee, tea and sucrose on postprandial
glycemia in lean, young, healthy adults. Asia Pac. J. Clin. Nutr.,
17: 657-662.
48. Moisey, L.L., S. Kacker, A.C. Bickerton, L.E. Robinson and
T.E. Graham, 2008. Caffeinated coffee consumption impairs
blood glucose homeostasis in response to high and low
glycemic index meals in healthy men. Am. J. Clin. Nutr.,
87: 1254-1261.
49. Sacramento, J.F., F.O. Martins, T. Rodrigues, P. Matafome,
M.J. Ribeiro, E. Olea and S.V. Conde, 2020. A2 adenosine
receptors mediate whole-body insulin sensitivity in a
prediabetes animal model: primary effects on skeletal muscle.
Front. Endocrinol., 10.3389/fendo.2020.00262
50. Shi, X., W. Xue, S. Liang, J. Zhao and X. Zhang, 2016. Acute
caffeine ingestion reduces insulin sensitivity in healthy
subjects: a systematic review and meta-analysis. Nutr. J.,
Vol. 15 10.1186/s12937-016-0220-7
51. Guarino, M.P., M.J. Ribeiro, J.F. Sacramento and S.V. Conde,
2013. Chronic caffeine intake reverses age-induced insulin
resistance in the rat: effect on skeletal muscle Glut4
transporters and AMPK activity. AGE, 35: 1755-1765.
52. Silva, L.A.d., J. Wouk, V.M.R. Weber, C.d.L. Eltchechem and
P.d. Almeida
et al
., 2017. Mechanisms and biological effects
of Caffeine on substrate metabolism homeostasis: A
systematic review. J. Applied Pharm. Sci., 7: 215-221.
53. Robinson, L.E., S. Savani, D.S. Battram, D.H. McLaren,
P. Sathasivam and T.E. Graham, 2004. Caffeine ingestion
before an oral glucose tolerance test impairs blood glucose
management in men with type 2 diabetes. J. Nutr.,
134: 2528-2533.
54. Lee, S.J., R. Hudson, K. Kilpatrick, T.E. Graham and R. Ross,
2005. Caffeine ingestion is associated with reductions in
glucose uptake independent of obesity and type 2 diabetes
before and after exercise training. J. Diabetes Care,
28: 566-572.
55. Akash, M.S.H., K. Rehman and S. Chen, 2014. Effects of coffee
on type 2 diabetes mellitus. Nutrition, 30: 755-763.
56. Campbell, B., C. Wilborn, P.L. Bounty, L. Taylor and
M.T. Nelson
et al
, 2013. International society of sports
nutrition position stand: energy drinks. J. Int. Soc. Sports
Nutr., 10.1186/1550-2783-10-1
57. Reis, C.E.G., J.G. Dórea and T.H.M.da Costa, 2019. Effects of
coffee consumption on glucose metabolism: A systematic
review of clinical trials. J. Traditional Complementary Med.,
9: 184-191.
58. Akash, M.S.H., K. Rehman, H. Sun and S. Chen, 2013.
Interleukin-1 receptor antagonist improves normoglycemia
and insulin sensitivity in diabetic Goto-Kakizaki-rats.
Eur. J. Pharmacol., 701: 87-95.
59. Alagbonsi, A.I., T.M. Salman, H.M. Salahdeen and A.A. Alada,
2016. Effects of adenosine and caffeine on blood glucose
levels in rats. Niger. J. Exp. Clin. Biosci., 4: 35-41.
60. Ohnaka, K., M. Ikeda, T. Maki, T. Okada and T. Shimazoe
et al
.,
2012. Effects of 16-week consumption of caffeinated and
decaffeinated instant coffee on glucose metabolism in a
randomized controlled trial. J. Nutr. Metab., Vol. 2012
10.1155/2012/207426
61. Ärnlöv, J., B. Vessby and U. Risérus, 2004. Coffee consumption
and insulin sensitivity. JAMA, 291: 1199-1201.
62. Wu, T., W.C. Willett, S.E. Hankinson and E. Giovannucci, 2005.
Caffeinated coffee, decaffeinated coffee and caffeine in
relation to plasma C-peptide levels, a marker of insulin
secretion, in U.S. women. Diabetes Care, 28: 1390-1396.
63. Smith, B., D.L. Wingard, T.C. Smith, D. Kritz-Silverstein and
E. Barrett-Connor, 2006. Does coffee consumption reduce the
risk of type 2 diabetes in individuals with impaired glucose?
Diabetes Care, 29: 2385-2390.
64. Kempf, K., C. Herder, I. Erlund, H. Kolb and S. Martin
et al
.,
2010. Effects of coffee consumption on subclinical
inflammation and other risk factors for type 2 diabetes: A
clinical trial. Am. J. Clin. Nut., 91: 950-957.
65. Cherniack, E.P., N. Buslach and H.F. Lee, 2018. The potential
effects of caffeinated beverages on insulin sensitivity.
J. Am. Coll. Nutr., 37: 161-167.
66. Williamson, G., 2020. Protection against developing type 2
diabetes by coffee consumption: assessment of the role of
chlorogenic acid and metabolites on glycaemic responses.
Food and Funct., 11: 4826-4833.
67. Pham, N.M., A. Nanri, K. Yasuda, K. Kurotani and Keisuke
Kuwahara
et al
., 2015. Habitual consumption of coffee and
green tea in relation to serum adipokines: a cross-sectional
study. Eur. J. Nutr., 54: 205-214.
68. Hiltunen, L.A., 2006. Are there associations between coffee
consumption and glucose tolerance in elderly subjects?
Eur. J. Clin. Nutr., 60: 1222-1225.
69. Beaudoin, M.S., L.E. Robinson and T.E. Graham, 2011. An oral
lipid challenge and acute intake of caffeinated coffee
additively decrease glucose tolerance in healthy men. J. Nutr.,
141: 574-581.
70. Feinberg, L.J., H. Sandberg, O.D. Castro and S. Bellet, 1968.
Effects of coffee ingestion on oral glucose tolerance curves in
normal human subjects. Metabolism, 17: 916-922.
427
Pak. J. Nutr., 19 (9): 420-429, 2020
71. Meng, S., J. Cao, Q. Feng, J. Peng and Y. Hu, 2013. Biological
values of acupuncture and chinese herbal medicine: impact
on the life science Evidence-Based Complementary Altern.
Med., Vol. 2013 10.1155/2013/801457
72. Thom, E., 2007. The effect of chlorogenic acid enriched coffee
on glucose absorption in healthy volunteers and its effect on
body mass when used long-term in overweight and obese
people. J. Int. Med. Res., 35: 900-908.
73. Gavrieli, A., E. Fragopoulou, C.S. Mantzoros and
M. Yannakoulia, 2013. Gender and body mass index
modify the effect of increasing amounts of caffeinated
coffee on postprandial glucose and insulin concentrations;
a randomized, controlled, clinical trial. Metabolism,
62: 1099-1106.
74. Pham, N.M., A. Nanri, T. Kochi, K. Kuwahara and
H. Tsuruoka
et al
., 2014. Coffee and green tea consumption is
associated with insulin resistance in Japanese adults.
Metabolism, 63: 400-408.
75. Battram, D.S., T.E. Graham, E.A. Richter and F. Dela, 2005. The
effect of caffeine on glucose kinetics in humans ‒ influence of
adrenaline. J. Physiol., 569: 347-355.
76. Krebs, J.D., A. Parry-Strong, M. Weatherall, R.W. Carroll and
M. Downie, 2012. A cross-over study of the acute effects
of espresso coffee on glucose tolerance and insulin sensitivity
in people with type 2 diabetes mellitus. Metabolism,
61: 1231-1237.
77. Kahale, K.H., C. Tranchant, S. Pakzad and A.G. Farhat, 2015.
Effect of sumac spice, Turkish coffee and yerba mate tea
on the postprandial glycemic response to Lebanese
mankoucheh. Nutr. Food Sci., 45 : 433 -447.
78. Beam, J.R., A.L. Gibson, C.M. Kerksick, C.A. Conn, A.C. White
and C.M. Mermier, 2015. Effect of post-exercise caffeine and
green coffee bean extract consumption on blood glucose
and insulin concentrations. Nutrition, 31: 292-297.
79. Wylie-Rosett, J. and L.M. Delahanty, 2017. The Role of Diet in
the Prevention and Treatment of Diabetes. In: Nutrition in
the Prevention and Treatment of Disease. Coulston, A.M.,
C.J. Boushey and L.M. Delahanty (Eds.). Academic Press,
United States pp: 691-707.
80. American Diabetes Association, 2012. Diagnosis and
classification of diabetes mellitus. Diabetes Care, 35: S64-S71.
81. American Diabetes Association, 2012. Standards of Medical
Care in Diabetes. Diabetes Care, 35: S11-S63.
82. Ley, S.H., O. Hamdy, V. Mohan and F.B. Hu, 2014. Prevention
and management of type 2 diabetes: Dietary components
and nutritional strategies. Lancet, 383: 1999-2007.
83. Kwok, M.K., G.M. Leung and C.M. Schooling, 2016.
Habitual coffee consumption and risk of type 2 diabetes,
ischemic heart disease, depression and Alzheimers
disease: a Mendelian randomization study. Sci. Rep., Vol. 6,
10.1038/srep36500
84. Sarriá, B., S. Martínez-López, R. Mateos and L. Bravo-Clemente,
2016. Long-term consumption of a green/roasted coffee
blend positively affects glucose metabolism and insulin
resistance in humans. Food Res. Int., 89: 1023-1028.
85. Lane, J.D., 2011. Caffeine, glucose metabolism and type 2
diabetes. J. Caffeine Res., 1: 23-28.
86. Ding, M., S.N. Bhupathiraju, M. Chen, R.M. van Dam and
F.B. Hu, 2014. Caffeinated and decaffeinated coffee
consumption and risk of type 2 diabetes: A systematic
review and a dose-response meta-analysis. Diabetes Care,
37: 569-586.
87. Dam, R.M.V., W.C. Willett, J.E. Manson and F.B. Hu, 2006.
Coffee, caffeine and risk of type 2 diabetes: A prospective
cohort study in younger and middle-aged U.S. women.
Diabetes Care, 29: 398-403.
88. Alkaabi, J., B. Al-Dabbagh, H. Saadi, S. Gariballa and J. Yasin,
2013. Effect of traditional arabic coffee consumption on the
glycemic index of khalas dates tested in healthy and diabetic
subjects. Asia Pac. J. Clin. Nutr., 22: 565-573.
89. Zhang, Y., E.T. Lee, L.D. Cowan, R.R. Fabsitz and B.V. Howard,
2011. Coffee consumption and the incidence of type 2
diabetes in men and women with normal glucose
tolerance: The strong heart study. Nutr. Metab. Cardiovasc.
Dis., 21: 418-423.
90. Hamer, M., D.R. Witte, A. Mosdøl, M.G. Marmot and
E.J. Brunner, 2008. Prospective study of coffee and tea
consumption in relation to risk of type 2 diabetes mellitus
among men and women: The Whitehall II study. Br. J. Nutr.,
100: 1046-1053.
91. Loopstra-Masters, R.C., A.D. Liese, S.M. Haffner,
L.E. Wagenknecht and A.J. Hanley, 2011. Associations
between the intake of caffeinated and decaffeinated coffee
and measures of insulin sensitivity and beta cell function.
Diabetologia, 54: 320-328.
92. Alperet, D.J., S.A. Rebello, E.Y.H. Khoo, Z. Tay and S.S.Y. Seah,
2020. The effect of coffee consumption on insulin
sensitivity and other biological risk factors for type 2 diabetes:
a randomized placebo-controlled trial. Am. J. Clin. Nutr.,
111: 448-458.
93. Natella, F. and C. Scaccini, 2012. Role of coffee in modulation
of diabetes risk. Nutr. Rev., 70: 207-217.
94. Zaharieva, D.P. and M.C. Riddell, 2013. Caffeine and glucose
homeostasis during rest and exercise in diabetes mellitus.
Applied Physiol. Nutr. and Metab., 38: 813-822.
95. Bidel, S., G.Hu, J. Sundvall, J. Kaprio, J. Tuomilehto, 2006.
Effects of coffee consumption on glucose tolerance, serum
glucose and insulin levels - A cross-sectional analysis. Horm.
Metab. Res., 38: 38-43.
96. Bhatti, K. Salman, OKeefe, H. James, Lavie and J. Carl, 2013.
Coffee and tea: perks for health and longevity? Curr. Opin.
Clin. Nutr. Metab. Care, 16: 688-697.
428
Pak. J. Nutr., 19 (9): 420-429, 2020
97. Chu, Y.F., Y. Chen, R.M. Black, P.H. Brown, B.J. Lyle, R.H. Liu and
B. Ou, 2011. Type 2 diabetes-related bioactivities of coffee:
Assessment of antioxidant activity, NF-6B inhibition and
stimulation of glucose uptake. Food Chem., 124: 914-920.
98. Asfaw, G. and M. Tefera, 2020. Total polyphenol content of
green, roasted and cooked Harar and Yirgacheffee Coffee,
Ethiopia. J. Applied Sci. Environ. Manage., 24: 187-192.
99. Higdon, J.V. and B. Frei, 2006. Coffee and health: A review
of recent human research. Crit. Rev. Food Sci. Nutr.,
46: 101-123.
100. Gao, F., Y. Zhang, S. Ge, H. Lu and R. Chen
et al
., 2018. Coffee
consumption is positively related to insulin secretion in the
shanghai high-risk diabetic screen (SHiDS) study. Nutr.
Metab., Vol. 84 10.1186/s12986-018-0321-8
429
... Today, however, medical-sports researchers benefit from combining physical activity with some pharmacological interventions to control obesity and the symptoms of T2D (Alshawi, 2020). As the most popular and common beverage globally, coffee indicates weight loss and improvement of T2D symptoms (Farajpour et al., 2017). ...
... As the most popular and common beverage globally, coffee indicates weight loss and improvement of T2D symptoms (Farajpour et al., 2017). Thus, some existing literature claims that the beneficial effects of coffee are caused by caffeine which is the most crucial and active compound of it (Alshawi, 2020). Caffeine (1, 3, 7-Trimethylxanthine) is a methylated purine alkaloid derived from the methyl-xanthine family (with the chemical formula C8H10N4O2). ...
... Caffeine (1, 3, 7-Trimethylxanthine) is a methylated purine alkaloid derived from the methyl-xanthine family (with the chemical formula C8H10N4O2). Since caffeine has full potential for altering energy metabolism and affects glucose homeostasis in individuals with diabetes and obesity, it has been investigated in both epidemiological and experimental studies (Alshawi, 2020;Farajpour et al., 2017;Jafari, et al., 2014). Chronic consumption of caffeinated compounds, such as coffee, has also been associated with a significant reduction in the risks of T2D in cohort studies (Alshawi, 2020). ...
Article
Full-text available
The study aimed to examine the combined effects of caffeine and aerobic exercise on leptin levels and some indices of insulin resistance in diabetics Thirty-two males with type 2 diabetes participated in a quasi-experimental and double-blind design. All participants were divided into four homogeneous groups of 8 individuals, including placebo (P), caffeine supplementation (C), aerobic training (AT), and aerobic training and caffeine (AT + C). The design protocol included eight weeks of aerobic exercise and caffeine consumption. Blood samples were taken to measure serum levels of leptin, glucose, insulin, HbA1c, HOMA-IR, and insulin sensitivity (QUICKI) indices at two phases. Data were analyzed by repeated measure ANOVA, Bonferroni posthoc, and independent T-test at a significant level of a s 0.05. The results showed that the levels of leptin, glucose, insulin, HbA1c, and HOMA-IR in the three intervention groups significantly decreased compared to the placebo group (P = 0.001). In addition, QUICKI was significantly increased in the three groups of caffeine (C), aerobic training (AT), and aerobic training + caffeine (AT + C) compared to the placebo group (P = 0.001). Also, the AT+C group has double effects on the investigated indices compared to the caffeine (C) group (P = 0.001). Regular aerobic exercise and caffeine supplementation may be more effective treatments for improving insulin resistance indicators associated with type 2 diabetes.
... Consequently, they are exposed to caffeine for extended periods [19]. Coffee consumption and insulin act as inducers of CYP1A2 enzyme activity [20]; it is also known that regular coffee consumption reduces the risk of prediabetes and T2DM in connection with genetic polymorphisms [21,22]. However, the relationships among CYP1A2, coffee consumption, and T2DM are still unclear. ...
Article
Full-text available
Cytochrome P450 1A2 (CYP1A2) is known to be the main enzyme directly responsible for caffeine metabolism. Rs762551 (NC_000015.10:g.74749576C>A) is a single nucleotide polymorphism of the CYP1A2 gene, and it is known mainly for metabolizing caffeine. A significant worldwide health issue, type 2 diabetes (T2DM), has been reported to be negatively associated with coffee consumption. Yet, some studies have proven that high intakes of coffee can lead to a late onset of T2DM. Objectives: This study aims to find any significant correlations among CYP1A2 polymorphism, coffee consumption, and T2DM. Methods: A total of 358 people were enrolled in this study—218 diagnosed with T2DM, and 140 representing the control sample. The qPCR technique was performed, analyzing rs762551 (assay C_8881221) on the LightCycler 480 (Roche, Basel, Switzerland) with Gene Scanning software version 1.5.1 (Roche). Results: Our first observation was that the diabetic patients were likely to consume more coffee than the non-diabetic subjects. People with the AA genotype, or the fast metabolizers, are the least common, yet they are the highest coffee consumers and present the highest glucose and cholesterol levels. Another important finding is the correlation between coffee intake and glucose level, which showed statistically significant differences between the diabetic group (p = 0.0002) and the control group (p = 0.029). Conclusions: The main conclusion of this study is that according to genotype, caffeine levels, glucose, and cholesterol are interconnected and proportionally related, regardless of type 2 diabetes.
... [16][17][18] Caffeine has a negative effect in the form of decreasing insulin sensitivity which interferes with glucose tolerance and increases blood glucose. 6,16 Therefore, the low caffeine in green coffee extract increases its activity in lowering blood sugar. 7 Chlorogenic acid prevents insulin resistance so that it triggers a faster decrease in blood sugar. ...
Article
Introduction: Diabetes mellitus is a disease characterized by an increase in blood sugar levels due to abnormalities in the insulin hormone system. The number of people with this disease is expected to increase every year. Therefore, it is necessary to develop diabetes mellitus drugs that have effective performance in reducing blood glucose level. Coffee contain chlorogenic acid and caffeine. Chlorogenic acid play a role in increasing insulin sensitivity. However, the caffeine causes a decrease in glucose tolerance. The removal of caffeine or the decaffeination process is expected to improve the quality of coffee as an anti-diabetic drug. The aim of this study was to investigate the effectiveness of decaffeinated coffee extract in reducing blood sugar. Materials and methods: Green or roasted coffee extract was decaffeinated using activated charcoal. Decaffeinated coffee extract with the lowest caffeine and the highest chlorogenic acid based on HPLC measurement was used for antidiabetic test. The anti-diabetic test was conducted with 52 DM type 2 patient selected by purposive sample. The test were divided into two groups: intervention (26 respondents) and control group (26 respondents). The data were analysed by Paired and Independent t test. Results: Decaffeinated green coffee extract is very suitable for use as a drug to lower blood sugar in DM type 2 patients than decaffeinated roasted coffee extract because of higher in chlorogenic acid and lower in caffeine (Figure 2). Treatment by decaffeinated green coffee extract for 3 weeks showed a significant decrease in average fasting blood glucose level from 144.7 g/dl to 92.23 g/dl. All statistical tests showed a p value = 0.001 (below the significant value), this value proves the success of reducing blood glucose by decaffeinated green coffee extract. Conclusion: The decaffeinated green coffee extract decreases fasting blood sugar significantly.
... Information regarding the spread of coffee and caffeinated products consumed by the Saudi population, particularly individuals with type II diabetes, remains unclear [28,29]. An exploration of the effect of habitual caffeine intake among adults with diabetes in the Saudi context is needed [30]. The prevalence of type II diabetes is high among the Saudi adults and considered a major public health problem. ...
Article
Full-text available
Information regarding the spread and effect of coffee and caffeine intake by individuals with type II diabetes remains unclear. This study aims to identify the amount and sources of habitual caffeine intake by individuals with type II diabetes and to investigate its association with other health outcomes, especially HbA1c. This is a cross-sectional survey involving 100 people medically defined as having type II diabetes comprising both genders, recruited from a care centre. All participants completed a caffeine semi-quantitative food frequency questionnaire (C-FFQ) to estimate their caffeine consumption, a two day 24-h recall, and a detailed questionnaire. The average caffeine intake was calculated from all sources and the differences in mean by gender were tested using a regression model (adjusted to important confounders). Regression models were used to verify the association between average caffeine intake on HbA1c and other health outcomes with adjustment for important confounders. A p value < 0.05 represented statistical significance. Arabic coffee (gahwa) and tea were the most common sources of caffeine among Saudi adults living with diabetes. Average caffeine intake for the whole sample was 194 ± 165 mg/day, which is 2.3 ± 2 mg/kg. There was an inverse association between caffeine intake and age: difference in mean −3.26 mg/year (95%CI: −5.34, −1.18; p = 0.003). Males had significantly higher consumption of caffeine compared to females: difference in mean 90.7 mg/day (95%CI: 13.8, 167.6; p = 0.021). No association was found between average caffeine intake and HbA1C or any other cardiovascular risk factors. This information can help public health practitioners and policy makers when assessing the risk of caffeine consumption among this vulnerable group.
Article
Full-text available
Background. Type 2 diabetes, as the most common metabolic disease, is a chronic and progressive disorder that causes permanent complications and increases cardiovascular diseases, brain vessels, peripheral vessels, and mortality in affected people. This study, therefore, aimed to investigate the effect of eight weeks of interval training and caffeine supplementation on glycemic indices in men with type 2 diabetes. Methods. The current research was a semi-experimental study. As a pilot research, 50 people were selected trough an available and targeted manner, among men with type 2 diabetes (with a history of more than one year) referring to Salamat and Sheikh Al-Rais Specialist clinics, Tabriz, Iran In the period of 2020-2021. 32 people met the inclusion criteria and entered into the study. Participants in the study were simple randomly divided into four homogenous groups of 8 including; Placebo, caffeine, exercise and exercise + caffeine were divided. Drug interventions and intermittent exercises were performed for 8 weeks. Blood samples were collected during two stages (pre-test and post-test) to measure serum levels of glucose, insulin, HbA1c and HOMA-IR index. The data were analyzed using repeated analysis of variance, Bonferroni post hoc and independent t tests at a significance level of 0.05. Results. The results showed that the levels of the glucose, insulin, HbA1c, and HOMA-IR in the three intervention groups significantly decreased compared to those in the placebo group (P=0.001). Furthermore, the results of post hoc test showed that the combined group of interval training + caffeine, compared to the caffeine group, had double effects on the changes in studied indices (P=0.001). Conclusion. A combination of interval training and caffeine supplementation may have been adopted as an effective method to improve and treat symptoms associated with type 2 diabetes.
Article
Full-text available
Kopi merupakan minuman yang menjadi konsumsi bagi sebagian besar penduduk di Indonesia. Kopi memiliki manfaat kesehatan serta kemampuan untuk mencegah sejumlah penyakit, menurunkan angka kematian dan morbiditas, serta meningkatkan harapan hidup. Kopi terbukti mencegah dan mengurangi risiko beberapa penyakit kronis, antara lain hipertensi, penyakit jantung, aritmia, kanker hati, obesitas, dan diabetes tipe 2. Kopi mengandung lebih dari 1000 fitokimia, termasuk kafein, asam klorogenat (CGA), alkaloid, fenolik, lakton, diterpen, kafestol, kahweol, niasin, karbohidrat, lemak, vitamin B3, magnesium, dan kalium. Kafein mempunyai manfaat dalam menetralkan efek adenosin, dan meningkatkan kewaspadaan, serta mengurangi kelelahan. Polifenol pada kopi juga berperan sebagai agen anti penuaan dengan cara menghambat pembentukan radikal bebas pada kulit. Penelitian ini bertujuan untuk mengetahui kandungan senyawa kopi dan manfaat dari minum kopi untuk kesehatan. Metode penelitian yang dilakukan yaitu menggunakan studi literatur dengan mengumpulkan sejumlah artikel atau jurnal yang berkaitan dengan masalah dan tujuan penelitian. Kopi telah terbukti menurunkan kadar kortisol dalam darah, oleh karena itu kopi dapat membantu relaksasi. Kopi berkafein memiliki efek akut pada kadar kortisol serum tetapi tidak berpengaruh pada kadar glukosa darah. Banyak aspek karakterisasi dampak kafein pada otak masih belum dilakukan kajian lebih mendalam, namun karakterisasi efek kronis dari kebiasaan konsumsi kopi dan kafein pada arsitektur fungsional otak serta bagi kesehatan manusia.
Article
Full-text available
Background and aims: Despite the proven evidence of high glycemic index (GI) and glycemic load (GL) diets to increase cardiometabolic risks, knowledge about the meta-evidence for carbohydrate quality within world geographic regions is limited. We conducted a meta-analysis to synthesize the evidence of GI/GL studies and carbohydrate quality, gathering additional exposures for carbohydrate, high glycemic carbohydrate, total dietary fiber, and cereal fiber and risks for type 2 diabetes (T2DM), coronary heart disease (CHD), stroke, and mortality, grouped into the US, Europe, and Asia. Secondary aims examined cardiometabolic risks in overweight/obese individuals, by sex, and dose-response dietary variable trends. Methods and results: 40-prospective observational studies from 4-Medline bibliographical databases (Ovid, PubMed, EBSCOhost, CINAHL) were search up to November 2019. Random-effects hazard ratios (HR) and 95% confidence intervals (CI) for highest vs. lowest categories and continuous form combined were reported. Heterogeneity (I2>50%) was frequent in US GI/GL studies due to differing study characteristics. Increased risks ((HRGI,T2DM,US=1.14;CI:1.06,1.21), HRGL,T2DM,US=1.02 (1.01, 1.03)), HRGI,T2DM,Asia=1.25;1.02,1.53), and HRGL,T2DM,Asia=1.37 (1.17, 1.60)) were associated with cardiometabolic diseases. GI/GL in overweight/obese females had the strongest magnitude of risks in US-and Asian studies. Total dietary fiber (HRT2DM,US = 0.92;0.88,0.96) and cereal fiber (HRT2DM,US = 0.83;0.77,0.90) decreased risk of developing T2DM. Among females, we found protective dose-response risks for total dietary fiber (HR5g-total-dietary-fiber,T2DM,US = 0.94;0.92,0.97), but cereal fiber showed better ability to lower T2DM risk (HR5g-cereal-fiber,T2DM,US = 0.67;0.60,0.74). Total dietary-and cereal fibers' dose-response effects were nullified by GL, but not so for cereal fiber with GI. Conclusions: Overweight/obese females could shift their carbohydrate intake for higher cereal fiber to decrease T2DM risk, but higher GL may cancel-out this effect.
Article
Full-text available
Sugar types, sugar amounts, phenolic contents constituents were determined in fresh fruits of 17 Saudi date cultivars and the obtained values were correlated with the corresponding vales of glycemic index. Glucose and fructose were presented in all tested cultivars in the range 104–395 g kg⁻¹ and 82–361 g kg⁻¹, respectively. Glucose/fructose ratio constituted between 1.03–1.27. Sucrose was considered the main sugar in four date cultivars. Total phenolics presented in the range 2.15–3.86 g kg⁻¹. Antioxidant activities varied between tested cultivars and ranged from 2.46 to 9.80 µmol Trolox g⁻¹ as assayed by DPPH method and from 5.90 to 17.78 µmol Trolox g⁻¹ as assayed by FRAP method. No significant correlation was found between the levels of glucose, fructose, sucrose, total phenolics and antioxidant activity with the corresponding glycemic index values.
Article
Full-text available
Background: Reports from previous studies on the effects of adenosine and caffeine on blood glucose are controversial and inconclusive. The present study sought to investigate the effect of acute adenosine infusion and caffeine injection on blood glucose level in rats. Materials and Methods: Thirty-four male albino rats (300-400 g) were randomly divided in a blinded-fashion into six groups, namely, Group I (n = 6) received normal saline (0.1-0.2 ml), Group II (n = 6) received adenosine (347.8 µg/kg/min), Group III (n = 5) received caffeine (6 mg/kg), followed by adenosine (347.8 µg/kg/min), Group IV (n = 5) were diabetic rats that received adenosine (347.8 µg/kg/min), Group V (n = 6) received caffeine (6 mg/kg), and Group VI (n = 6) received nifedipine (300µg/kg), followed by caffeine (6 mg/kg). Administrations were done through the femoral vein, while blood samples were taken from the carotid artery for glucose measurement. Results: Adenosine caused a reduction in blood glucose level in normal and diabetic rats, though the reduction was more noticeable in diabetic rats. Pretreatment of rats with caffeine completely abolished the adenosine-induced reduction in blood glucose and produced an exaggerated increase in blood glucose comparable to the level seen in rats that received caffeine alone. Pretreatment of rats with nifedipine reduced the caffeine-induced hyperglycemia by two-third. Conclusion: This study suggests that adenosine receptors could be of therapeutic target in the treatment of Type 1 diabetes due to its blood glucose-lowering potential in both diabetic and normal rats. It also suggests that intracellular calcium mobilization is more implicated in caffeine-induced hyperglycemia than adenosine receptor antagonism, even though other unidentified mechanism(s) remain to be explored.
Article
Full-text available
Epidemiological studies indicate an inverse association of coffee consumption with risk of type 2 diabetes mellitus. However, studies to determine the clinical effects of coffee consumption on the glucose metabolism biomarkers remain uncertain. The aim of this systematic review was to evaluate the effects of coffee consumption on glucose metabolism. A search of electronic databases (PubMed and Web of Science) was performed identifying studies published until September 2017. Eight clinical trials (n = 247 subjects) were identified for analyses. Participants and studies characteristics, main findings, and study quality (Jadad Score) were reported. Short-term (1–3 h) and long-term (2–16 weeks) studies were summarized separately. Short-term studies showed that consumption of caffeinated coffee may increase the area under the curve for glucose response, while for long-term studies, caffeinated coffee may improve the glycaemic metabolism by reducing the glucose curve and increasing the insulin response. The findings suggest that consumption of caffeinated coffee may lead to unfavourable acute effects; however, an improvement on glucose metabolism was found on long-term follow-up. © 2018 Center for Food and Biomolecules, National Taiwan University
Article
Epidemiological studies show a convincing long-term and dose-dependent protection of coffee and decaffeinated coffee against developing type 2 diabetes. The mechanisms of this effect are still not understood even though several have been proposed, including a potential effect on blood glucose by chlorogenic acids. However, there is minimal effect of decaffeinated coffee on postprandial blood glucose and insulin when consumed with carbohydrates, although there may be effects on incretin hormones, but these have been measured in only a few studies. Although chlorogenic acids do not affect carbohydrate digestion directly, they may affect glucose absorption and subsequent utilisation, the latter through metabolites derived from endogenous pathways or action of the gut microbiota. To advance understanding of the protective effect of coffee chlorogenic acids, more chronic intervention studies are needed on decaffeinated coffee, coupled with mechanistic studies in vitro using more realistic concentrations of the relevant chlorogenic acid metabolites.
Article
Background: In observational studies, coffee consumption has been consistently associated with a lower risk of type 2 diabetes mellitus. Trials examining the effect of coffee consumption on glucose metabolism have been limited by the use of surrogate insulin sensitivity indices, small sample sizes, lack of blinding, and short follow-up duration. Objectives: We aimed to overcome limitations of previously conducted coffee trials in a randomized placebo-controlled trial of the effect of coffee consumption on insulin sensitivity. Methods: We conducted a 24-wk randomized placebo-controlled trial in 126 overweight, non-insulin sensitive (HOMA-IR ≥1.30), Chinese, Malay, and Asian-Indian males and females aged 35-69 y. Participants were randomly assigned to receive 4 cups of instant regular coffee (n = 62) or 4 cups of a coffee-like placebo beverage (n = 64) per day. The primary outcome was the amount of glucose metabolized per kilogram of body weight per minute (Mbw) assessed during steady-state conditions with a hyperinsulinemic euglycemic clamp. Secondary outcomes included other clamp-based insulin sensitivity measures, biological mediators of insulin sensitivity, and measures of fasting glucose metabolism. Results: Coffee consumption did not significantly change insulin sensitivity compared with placebo (percentage mean difference in Mbw = 4.0%; 95% CI: -8.3, 18.0%; P = 0.53). Furthermore, no significant differences in fasting plasma glucose (2.9%; 95% CI: -0.4, 6.3%; P = 0.09) or biological mediators of insulin resistance, such as plasma adiponectin (2.3%; 95% CI: -1.4, 6.2%; P = 0.22), were observed between coffee and placebo groups over 24 wk of intervention. Participants in the coffee arm experienced a loss of fat mass (FM) (-3.7%; 95% CI: -6.3, -1.1%; P = 0.006) and reduction in urinary creatinine concentrations (-21.2%; 95% CI: -31.4, -9.5%; P = 0.001) compared with participants in the placebo arm over 24 wk of intervention. Conclusions: Consuming 4 cups/d of caffeinated coffee for 24 wk had no significant effect on insulin sensitivity or biological mediators of insulin resistance but was associated with a modest loss of FM and reduction in urinary creatinine concentrations.This trial was registered at clinicaltrials.gov as NCT01738399. Registered on November 28, 2012. Trial sponsor: Nestlé Research, Lausanne, Switzerland. Trial site: National University of Singapore.
Article
Background: Previous studies have examined dairy products with various fat contents in relation to type 2 diabetes (T2D) risk, although data regarding dairy fat intake per se are sparse. Objectives: We aimed to evaluate the association between dairy fat intake and risk of T2D in 3 prospective cohorts. We also examined associations for isocalorically replacing dairy fat with other macronutrients. Methods: We prospectively followed 41,808 men in the Health Professionals Follow-Up Study (HPFS; 1986-2012), 65,929 women in the Nurses' Health Study (NHS; 1984-2012), and 89,565 women in the NHS II (1991-2013). Diet was assessed quadrennially using validated FFQs. Fat intake from dairy products and other relevant sources was expressed as percentage of total energy. Self-reported incident T2D cases were confirmed using validated supplementary questionnaires. Time-dependent Cox proportional hazards regression was used to estimate the HR for dairy fat intake and T2D risk. Results: During 4,219,457 person-years of follow-up, we documented 16,511 incident T2D cases. Dairy fat was not associated with risk of T2D when compared with calories from carbohydrates (HR for extreme quintiles: 0.98; 95% CI: 0.95, 1.02). Replacing 5% of calories from dairy fat with other sources of animal fat or carbohydrate from refined grains was associated with a 17% (HR: 1.17; 95% CI: 1.13, 1.21) and a 4% (HR: 1.04; 95% CI: 1.00, 1.08) higher risk of T2D, respectively. Conversely, a 5% calorie replacement with carbohydrate from whole grains was associated with a 7% lower risk of T2D (HR: 0.93; 95% CI: 0.88, 0.98). Conclusions: Dairy fat intake was not associated with T2D risk in these cohort studies of US men and women when compared with calories from carbohydrate. Replacing dairy fat with carbohydrates from whole grains was associated with lower risk of T2D. Replacement with other animal fats or refined carbohydrates was associated with higher risk.
Article
Background & aims: Although the association between dietary Glycemic Index (GI), Glycemic Load (GL) and general/abdominal obesity has extensively been examined, limited data are available in this regard in developing countries. The aim of this study was to examine the association between dietary GI and GL with general and abdominal obesity. Methods: This cross-sectional study was conducted among adults in Isfahan, Iran. Dietary GI and GL were assessed using a validated dish-based 106-item semi-quantitative food frequency questionnaire (DS-FFQ). Data regarding height, weight and waist circumference were collected using a self-reported questionnaire. Overweight or obesity was defined as body mass index ≥25 kg/m2, and abdominal obesity was defined as waist circumference ≥80 cm for women and ≥94 cm for men. Results: There was no significant association between dietary GI and GL and general obesity. After adjustment for potential confounders, participants in the highest quintile of dietary GI had a higher chance for abdominal obesity (OR: 1.29; 95% CI: 1.01-1.64), compared with those in the lowest quintile. No significant association was observed between dietary GL and abdominal obesity. After adjustment for potential confounders, women in the top quintile of dietary GI had higher chance for abdominal obesity compared with those in the bottom quintile (OR: 1.48, 95% CI: 1.02-2.15). No significant association was found between dietary GI and abdominal obesity among men. We failed to find any significant association between dietary GI and general obesity in either gender [Comparing top vs. bottom quintiles, for men: OR: 0.97; 95% CI: 0.74-1.29 and for women: OR: 1.01; 95% CI: 0.75-1.40]. No significant association was found between dietary GL and general [for men: OR: 1.13; 95% CI: 0.85-1.49 and for women: OR: 1.01; 95% CI: 0.76-1.35], as well as abdominal obesity [for men: OR: 1.21; 95% CI: 0.88-1.67 and for women: OR: 1.25; 95% CI: 0.88-1.77]. Conclusions: We found a significant positive association between dietary GI and abdominal obesity. When we conducted analyses stratified by gender, we also observed such association in women, but not in men. No other significant associations were observed between dietary GI and GL with general or abdominal obesity.
Article
Aging and diabetes mellitus are 2 well-known risk factors for cardiovascular disease (CVD). During the past 50 years, there has been an dramatic increase in life expectancy with a simultaneous increase in the prevalence of diabetes mellitus in the older population. This large number of older individuals with diabetes mellitus is problematic given that CVD risk associated with aging and diabetes mellitus. In this review, we summarize epidemiological data relating to diabetes mellitus and CVD, with an emphasis on the aging population. We then present data on hyperglycemia as a risk factor for CVD and review the current knowledge of age-related changes in glucose metabolism. Next, we review the role of obesity in the pathogenesis of age-related glucose dysregulation, followed by a summary of the results from major randomized controlled trials that focus on cardiovascular risk reduction through glycemic control, with a special emphasis on older adults. We then conclude with our proposed model of aging that body composition changes and insulin resistance link possible dysregulation of physiological pathways leading to obesity and diabetes mellitus-both forms of accelerated aging-and risks for CVD.