HUMAN AND CLINICAL NUTRITION
Acute effects of raisin consumption on glucose and insulin reponses
in healthy individuals
, Joanne Lam
and Cyril W. C. Kendall
School of Medicine, New York Medical College, Valhalla, NY, USA
Clinical Nutrition and Risk Factor Modiﬁcation Center, St Michael’s Hospital, Toronto, ON, Canada
Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, ON, Canada
College of Pharmacy and Nutrition, University of Saskatchewan, Saskatoon, SK, Canada
(Received 11 July 2013 –Final revision received 8 September 2013 –Accepted 4 October 2013)
Journal of Nutritional Science (2014), vol. 3, e1, page 1 of 6 doi:10.1017/jns.2013.33
Raisins are popular snacks with a favourable nutrient proﬁle, being high in dietary ﬁbre, polyphenols and a number of vitamins and minerals, in addition to
being rich in fructose. In light of evidence demonstrating improvements in glycaemic control with moderate fructose intake and low-glycaemic index (GI)
fruits, our aim was to determine the GI, insulin index (II) and postprandial responses to raisins in an acute feeding setting. A total of ten healthy participants
(four male and six female) consumed breakfast study meals on four occasions over a 2- to 8-week period: meal 1: white bread (WB) (108 g WB; 50 g
available carbohydrate) served as the control and was consumed on two separate occasions; meal 2: raisins (R50) (69 g raisins; 50 g available carbohydrate);
and meal 3: raisins (R20) (one serving, 28 g raisins; 20 g available carbohydrate). Postprandial glucose and insulin were measured over a 2 h period for the
determination of GI, glycaemic load (GL) and II. The raisin meals, R50 and R20, resulted in signiﬁcantly reduced postprandial glucose and insulin
responses when compared with WB (P<0·05). Furthermore, raisins were determined to be low-GI, -GL and -II foods. The favourable effect of raisins
on postprandial glycaemic response, their insulin-sparing effect and low GI combined with their other metabolic beneﬁts may indicate that raisins are a
healthy choice not only for the general population but also for individuals with diabetes or insulin resistance.
Key words: Raisins: Dried fruit: Glycaemic index: Glycaemic load
Raisins are one of the most commonly consumed dried fruits,
are eaten across the globe, and have a unique nutrient proﬁle
that may confer distinctive health beneﬁts when compared
with other fruit. Raisins are a rich source of polyphenols
and phenolic acids, which may serve as antioxidants and pro-
mote an anti-inﬂammatory environment with potential health
. Raisins are also high in dietary ﬁbre and prebio-
tics, such as inulin, which have been shown to produce a heal-
thier colonic microﬂora proﬁle in addition to possibly aiding
weight management and reducing the risk of CVD
. A clini-
cal study found that raisins as part of a healthy diet improved
blood lipids and reduced other risk factors for CVD
Raisins are also high in fructose, which has a low glycaemic
index (GI). While concerns have been raised that fructose may
have adverse metabolic effects and promote weight gain, a
demonstrated that moderate intakes of
fructose may improve glycaemic control, without harming car-
diometabolic risk factors
. This is especially important in light
of recent evidence demonstrating that low-GI fruits may
improve glycaemic and cardiovascular markers, including
HbA1c and blood pressure
Given that raisins are the most commonly consumed dried
fruit, are high in fructose and the controversy surrounding the
cardiometabolic effects of fructose, we investigated the effect
Abbreviations: GI, glycaemic index; GL, glycaemic load; iAUC, incremental AUC; R20, raisins (20 g available carbohydrate); R50, raisins (50 g available carbohydrate); WB,
*Corresponding author: Dr Cyril W. C. Kendall, fax +1 416 978 5310, email email@example.com
© The Author(s) 2014. The online version of this article is published within an Open Access environment subject to the conditions of the Creative
Commons Attribution license <http://creativecommons.org/licenses/by/3.0/>.
JOURNAL OF NUTRITIONAL SCIENCE
of raisins on postprandial glycaemia and insulinaemia in an
acute feeding study.
Inclusion criteria included men or non-pregnant women aged
18–75 years who were in good health. Individuals with a
known history of AIDS, hepatitis, diabetes or a heart con-
dition, or individuals taking medication or with any condition
that might make participation dangerous to the individual or
affect the results were excluded.
A total of ten participants were studied. Using the tdistri-
bution and assuming an average CV of within-individual vari-
ation of incremental AUC (iAUC) values of 25 %, n10
participants has 80 % power to detect a 33 % difference in
iAUC with two-tailed P<0·05.
The study was open-label with a partial randomised, cross-
over design using standard GI methodology (ISO
26642:2010; International Organization for Standardization).
Eligible participants were studied on four separate days over
a period of 2–8 weeks with an interval of no less than 40 h
and no more than 2 weeks between tests. On each test day,
participants came to the clinic in the morning after a 10–14
h overnight fast. Participants were asked to maintain stable
dietary and activity habits throughout their participation in
the study. If any participant was not feeling well or had not
complied with the preceding experimental conditions, the
test was not carried out and was rescheduled for another
day. On each test occasion participants were weighed, and
two fasting blood samples were obtained by ﬁnger-stick at
5-min intervals. Finger-stick blood samples were collected
from hands warmed with an electric heating pad for 3–5
min before each sample. Blood samples were collected into
two separate vials: one (two or three drops of blood) for glu-
cose analysis and the other (between six and eight drops of
blood) for insulin. After the second fasting sample was col-
lected the participant was provided with the test meal. At
the ﬁrst bite, a timer was started and additional blood samples
were taken at 15, 30, 45, 60, 90 and 120 min. Before and
during the test, a blood glucose test record was ﬁlled out
with the participant’s initials, identiﬁcation number, date,
body weight, test meal, beverage, time of starting to eat,
time it took to eat, time and composition of last meal, and
any unusual activities. During the 2 h test, participants
remained seated quietly. After the last blood sample had
been obtained participants were offered a snack and then
allowed to leave.
The present study was conducted according to the guide-
lines laid down in the Declaration of Helsinki and all pro-
cedures involving human subjects/patients were approved by
the Western Institutional Review Board
. Written informed
consent was obtained from all participants before the start
of the study.
Each participant participated in a total of four breakfast study
meals. Two test meals were consumed: meal 1: R50, consisting
of 50 g available carbohydrate from raisins; and meal 2: R20,
consisting of 20 g available carbohydrate from raisins, which
is one standard serving (28 g) of raisins. The control white
bread (WB) meal, which provided 50 g available carbohydrate,
was consumed twice. The macronutrient proﬁles of the study
meals are provided in Table 1. The order of the test meals was
After consuming a meal, participants rated its palatability using
a visual analogue scale anchored at very ‘unpalatable’at one
end (0) and ‘very palatable’at the other (100). Therefore, the
higher the number, the higher was the perceived palatability
of the product.
The ﬁnger-stick samples for glucose analysis were placed in
a refrigerator and at the end of the test transferred to a
–20°C freezer until analysed, which was performed within
5 d. A YSI model 2300 STAT analyser (YSI Life Sciences)
was used for glucose analysis. For insulin analysis, the micro-
vette tubes were centrifuged and the serum transferred to
labelled polypropylene tubes and stored at –20°C before analy-
sis. Insulin levels were measured using a Human Insulin ELISA
Kit (Alpco Diagnostics).
Data were entered into a spreadsheet by two different individ-
uals and the values compared with assure accurate transcrip-
tion. Incremental areas under the glucose and insulin
response curves (AUC), ignoring area below fasting, were cal-
culated. For the purposes of the AUC calculation, fasting
Table 1. Nutrient content of test meals
Test meal Abbreviation Amount (g) Protein (g) Fat (g) Total CHO (g) Dietary fibre (g) Available CHO (g)
White bread WB 108·09·30·852·02·050·0
Raisins (50 g CHO) R50 69·01·70 53·43·450·0
Raisins (one serving) R20 28·00·70 21·71·420·3
glucose and fasting insulin were taken to be the mean of the
ﬁrst measurement of the blood glucose concentrations and
serum insulin concentrations at times –5 min and 0 min.
The GI and insulin index were calculated by expressing each
participant’s AUC for the test food as a percentage of the
same participant’s mean AUC for the two white bread con-
trols. Values >2 SD above the mean were excluded. The
blood glucose and serum insulin concentrations at each time,
AUC, GI and insulin index values were subjected to repeated-
measures ANOVA examining for the main effects of test meal
and the meal × participant interaction. After demonstration of
signiﬁcant heterogeneity, the signiﬁcance of the differences
between individual means was assessed using Tukey’s test to
adjust for multiple comparisons. Means differing by more
than the LSD (least signiﬁcant difference) were statistically sig-
niﬁcant, two-tailed P<0·05.
Glycaemic load (GL) was calculated using the formula:
GL = GI × g of available carbohydrate in the portion.
Glycaemic index classification
Using the classiﬁcation of Brand-Miller for the glucose scale,
products with a GI of 55 or lower are classiﬁed as being
low GI; those with a GI of 56 to 69 are classiﬁed as medium,
while those with a GI of 70 or greater are classiﬁed as high GI.
A total of ten participants (four male and six female) with a
mean age of 39 (SD 11) years and an average BMI of 26·4
(SD 6·2) kg/m
completed the study.
Within-subject variation of reference food
The mean within-subject CV of the iAUC values after the two
repeated WB tests was 17·0±3·6 % and was thus considered
technically satisfactory (average intra-subject variation of less
than 30 %).
Palatability scores are presented in Table 2. The subjective
palatability of the R50 and R20 meals was higher than that
of the WB control. However, this difference did not reach stat-
Postprandial glucose response and glycaemic index
Postprandial incremental glucose levels after the R50 meal
were signiﬁcantly higher than those after the WB meal at 15
and 30 min. At 60, 90 and 120 min, however, the postprandial
incremental glucose levels after R50 were signiﬁcantly lower
than after WB (Fig. 1). iAUC were signiﬁcantly lower after
both raisin meals than after WB (Fig. 2). The ﬁnal GI and
GL values are presented in Table 2.
Fig. 2. Incremental AUC (iAUC) for glucose after consumption of three meals
containing 50, 50 and 20 g of available carbohydrates from white bread (WB),
raisins (R50) and raisins (R20), respectively. Values are means, with standard
errors represented by vertical bars.
Mean values with unlike letters were
significantly different (P<0·05).
Fig. 1. Postprandial glucose responses to three meals containing 50, 50 and
20 g of available carbohydrates from white bread (○), raisins (•) and raisins
(Δ), respectively. Values are means, with standard errors represented by ver-
Mean values at a specific time point with unlike letters were sig-
nificantly different (P<0·05).
Table 2. Palatability, glycaemic index (GI), GI category, glycaemic load (GL), GL category and insulin index
(Mean values with their standard errors)
(mm) GI Insulin index
Test meal Abbreviation Mean SEM Mean SEM GI category* GL GL category Mean SEM
White bread WB 63·0
Raisins (50 g CHO) R50 75·0
Raisins (one serving) R20 72·0
6·0 N/A N/A 9·9
CHO, carbohydrate; N/A, not applicable.
Mean values within a column with unlike superscript letters were significantly different (P<0·05).
* Category from GI Factor (Atkinson et al.
Postprandial insulin response and insulin index
There was no signiﬁcant difference between the WB and
R50 meals in incremental postprandial insulin levels at 15
and 30 min. However, insulin levels were signiﬁcantly lower
at 45, 60 90 and 120 min with the R50 meal compared with
WB (Fig. 3). iAUC were also signiﬁcantly lower with raisins
compared with the WB control (Fig. 4). The ﬁnal insulin
index values are presented in Table 2.
The present study demonstrates that raisins are a low-GI and
-insulin index fruit that provides a favourable postprandial glu-
cose and insulin response. In terms of postprandial glucose
response, raisins elicited a swifter response compared with
WB for the ﬁrst 30 min. This, however, was followed by a
sharp decline and an overall lower AUC for glucose when
compared with WB (P<0·05), which is commonly observed
with other fruits. This postprandial glucose response pattern
may be explained by the high sucrose content of raisins. The
sucrose would be rapidly digested and the glucose rapidly
absorbed relative to starch. However, the fructose, which is
responsible for 50 % of the available carbohydrate content
of raisins, would not contribute to the rise in blood glucose.
Evidence from other studies suggests that the beneﬁts of fruc-
tose on glycaemic control may extend beyond simple replace-
ment of glucose. Moore et al.
demonstrated that the addition
of only 7·5 g of fructose, levels which are slightly lower than
the fructose content of one serving of raisins, to 75 g of glu-
cose as part of an oral glucose tolerance test signiﬁcantly low-
ered the glucose response when compared with 75 g glucose
with no added fructose
. A potential mechanism of action
for this improved glycaemic response with fructose ingestion
may be enhanced hepatic glucose uptake. Fructose ingestion
increases the hepatic concentrations of fructose-1-phosphate
(ﬁrst product of hepatic fructose metabolism), which in turn
competes with fructose-6-phosphate for binding to glucoki-
nase regulatory protein (GKRP). This leads to the release of
glucokinase (rate-limiting enzyme in the hepatic metabolism
of glucose) from GKRP, causing hepatic metabolism and
further uptake of glucose and thus lower postprandial glucose
. This glycaemic advantage with moderate
intakes of fructose over glucose is not a novel ﬁnding, and
has been reported in both healthy individuals and patients
with diabetes in the 1970s and 1980s
. A recent
meta-analysis put this link into perspective by demonstrating
that small doses of fructose < 10 g/meal or < 36 g/d can sig-
niﬁcantly improve serum levels of HbA1c and fasting glucose
. Furthermore, this daily intake level was not associated
with any adverse metabolic effects that have been linked to
high intake of fructose such as dyslipidaemia
Also of interest is the low GI of raisins as determined by the
present study (49 based on the glucose scale). A previous study
by Jenkins et al.
reported the GI of raisins to be 64.
However, this study was conducted on only six subjects.
More recently a study by Kim et al.
reported GI values of
49 in sedentary individuals, 49 in individuals with prediabetes
and 55 in aerobically trained adults. These results are very
similar to the GI value determined for raisins in the present
study. The health beneﬁts of low-GI fruit were demonstrated
in a recent secondary analysis of a clinical intervention that
showed that low-GI fruit consumption as part of a low-GI
diet was associated with statistically signiﬁcant reductions in
HbA1c, systolic blood pressure and overall CHD risk
original randomised clinical trial assessed the effects of a
low-GI v. a high-ﬁbre diet on glycaemic control in patients
with type 2 diabetes and included fruit intake advice as part
of the dietary intervention
. The secondary analysis included
152 patients and demonstrated that the GI of fruit was an
independent predictor of HbA1c reduction and that the lowest
quartile of GI intake led to the greatest reduction in HbA1c
It is important to note that in this study grapes were con-
sidered high-GI foods (GI > 90 based on the bread scale).
However, the present study suggests that raisins have a low
GI (GI < 70 based on the bread scale). The present study
also demonstrated that both serving sizes of raisins studied
(69 and 28 g) are low-GL foods. The beneﬁcial effects of
low-GI and -GL foods on diabetes and risk of CVD have
Fig. 4. Incremental AUC (iAUC) for insulin after consumption of three meals
containing 50, 50 and 20 g of available carbohydrates from white bread
(WB), raisins (R50) and raisins (R20), respectively. Values are means, with
standard errors represented by vertical bars.
Mean values with unlike
letters were significantly different (P<0·05).
Fig. 3. Postprandial insulin responses to three meals containing 50, 50 and
20 g of available carbohydrates from white bread (♦), raisins ( ) and raisins
(▪), respectively. Values are means, with standard errors represented by ver-
Mean values at a specific time point with unlike letters were sig-
nificantly different (P<0·05).
been demonstrated by a number of large cohort studies
Lastly, the type and amount of ﬁbre present in raisins should
not be overlooked as another component that may account for
the lowered glycaemic response. Overall, the present ﬁndings
support the notion that incorporation of raisins as part of a
healthy, low-GI diet in patients with diabetes or impaired glu-
cose tolerance can potentially improve glycaemic management
and provide additional cardiovascular beneﬁts.
The present study also demonstrated that raisins lead to a
lower postprandial insulin response when compared with
WB. This insulin-sparing effect may also be in part due to
the fructose content of raisins. Fructose is not an insulin secre-
tagogue and, unlike glucose, does not require insulin for cell
. The insulin-sparing effects of fructose have been
demonstrated in a number of other studies
. While long-
term impacts of raisins on insulin control require further inves-
tigation, the present study suggests that raisins, through acute
postprandial insulin-sparing effects, may be a healthy food
choice in patients with insulin resistance or diabetes.
The major limitation of the present study, as with all acute
feeding studies, is the inability to translate these acute ﬁndings
to long-term beneﬁts. However, at least in terms of the ben-
eﬁcial effect of fructose on glycaemic management, previous
studies have shown that these effects are sustainable over a
longer period of time
. Another shortcoming is the sample
size. While the use of ten subjects has been validated by a
number of studies, nevertheless this sample size reduces the
study precision and may lead to exaggerated associations.
While the potential beneﬁts of moderate consumption of
fructose on glucose control have been overshadowed by the
adverse outcomes, especially on serum lipids
ciated with overconsumption and over-utilisation of high-
fructose corn syrup in the everyday diet, the beneﬁts of
fructose as a component of whole fruits should not be over-
looked. Raisins are popular snacks that are readily accessible
at a reasonable price. Their nutrient proﬁle, being high in anti-
oxidants, dietary ﬁbre, prebiotics, vitamins and minerals,
indicate that they could contribute to overall health. While
long-term studies are needed, the present study demonstrates
that in addition to the aforementioned beneﬁts, raisins can
acutely improve postprandial glycaemic control and, as a
low-GI food, may serve as a healthy snack, when used in mod-
eration, in the diets of healthy individuals and for those with
diabetes or impaired glucose tolerance.
The present study was supported by Sun-Maid Growers of
California, Kingsburg, CA, USA. The authors wish to thank
Dr Arianna Carughi, Health & Nutrition Research Coordinator,
Sun-Maid Growers of California, for assistance with the study.
C. W. C. K. provided the establishment of funding, study
design, data gathering and manuscript preparation. A. E. and
J. L. were involved with data gathering and manuscript
C. W. C. K. has received research grants, travel funding,
consultant fees, honoraria or has served on the scientiﬁc advi-
sory board for Abbott, Advanced Food Materials Network,
Almond Board of California, American Peanut Council,
American Pistachio Growers, Barilla, California Strawberry
Commission, Canadian Institutes of Health Research, Canola
Council of Canada, Danone, General Mills, Hain Celestial,
International Tree Nut Council, Kellogg, Loblaw Brands
Ltd, Nutrition Impact, Oldways, Orafti, Paramount Farms,
Pulse Canada, Saskatchewan Pulse Growers, Solae,
Sun-Maid Growers of California and Unilever. A. E. and
J. L. have no conﬂicts of interest.
1. Lambert JD, Hong J, Yang GY, et al. (2005) Inhibition of carcino-
genesis by polyphenols: evidence from laboratory investigations.
Am J Clin Nutr 81, Suppl. 1, 284S–291S.
2. Erdman JW, Balentine D, Arab L, et al. (2007) Flavonoids and heart
health: Proceedings of the ILSI North America ﬂavonoids work-
shop, May 31–June 1, 2005, Washington, DC. J Nutr 137, Suppl.,
3. Dubick MA & Omaye ST (2001) Grape wine and tea polyphenols
in the modulation of atherosclerosis and heart disease. In Handbook
of Nutraceuticals and Functional Foods, 2nd ed., pp. 101–130
[REC Wildman, editor]. Boca Raton, FL: CRC Press.
4. Todd S, Woodward M, Tunstall-Pedoe H, et al. (1999) Dietary anti-
oxidants and ﬁber in the etiology of cardiovascular disease and all-
cause mortality: results from the Scottish Heart Health Study. Am J
Epidemiol 150, 1073–1080.
5. Bruce B, Spiller GA & Farquhar JW (1997) Effects of a plant-based
diet rich in whole grains, sun-dried raisins and nuts on serum lipo-
proteins. Veg Nutr Int J 1,58–63.
6. Sievenpiper JL, Chiavaroli L, de Souza RJ, et al. (2012) ‘Catalytic’
doses of fructose may beneﬁt glycaemic control without harming
cardiometabolic risk factors: a small meta-analysis of randomised
controlled feeding trials. Br J Nutr 108, 418–423.
7. Jenkins DJA, Srichaikul K, Kendall CWC, et al. (2011) The relation
of low glycaemic index fruit consumption to glycaemic control and
risk factors for CHD in type 2 diabetes. Diabetologia 54, 271–279.
8. Moore MC, Cherrington AD, Mann SL, et al. (2000) Acute fructose
administration decreases the glycemic response to an oral glucose tol-
erance test in normal adults. J Clin Endocrinol Metab 85,4515–4519.
9. Hawkins M, Gabriely H, Wozniak R, et al. (2002) Fructose
improves the ability of hyperglycemia per se to regulate glucose pro-
duction in type 2 diabetes. Diabetes 51, 606–614.
10. Akerblom HK, Siltanen I & Kallio AK (1972) Does dietary fruc-
tose affect the control of diabetes in children? Acta Med Scand
Suppl 542, 195–202.
11. Crapo PA, Kolterman OG & Olefsky JM (1980) Effects of oral
fructose in normal, diabetic, and impaired glucose tolerance sub-
jects. Diabetes Care 3, 575–581.
12. Akgün S & Ertel NH (1980) A comparison of carbohydrate metab-
olism after sucrose, sorbitol, and fructose meals in normal and dia-
betic subjects. Diabetes Care 3, 582–585.
13. Jenkins DJ, Wolever TM, Taylor RH, et al. (1981) Glycemic index
of foods: a physiological basis for carbohydrate exchange. Am J Clin
Nutr 34, 362–366.
14. Kim Y, Hertzler SR, Byrne HK, et al. (2008) Raisins are a low to
moderate glycemic index food with a correspondingly low insulin
index. Nutr Res 28, 304–308.
15. Jenkins DJ, Kendall CW, McKeown-Eyssen G, et al. (2008) Effect
of a low-glycemic index or a high-cereal ﬁber diet on type 2 dia-
betes: a randomized trial. JAMA 300, 2742–2753.
16. Liu S, Willett WC, Stampfer MJ, et al. (2000) A prospective study of
dietary glycemic load, carbohydrate intake, and risk of coronary
heart disease in US women. Am J Clin Nutr 71, 1455–1461.
17. Salmeron J, Ascherio A, Rimm EB, et al. (1997) Dietary ﬁber,
glycemic load, and risk of NIDDM in men. Diabetes Care 20,
18. Salmeron J, Manson JE, Stampfer MJ, et al. (1997) Dietary ﬁber,
glycemic load, and risk of non-insulin-dependent diabetes mellitus
in women. JAMA 277, 472–477.
19. Bantle JP (2009) Dietary fructose and metabolic syndrome and dia-
betes. J Nutr 139, 1263S–1268S.
20. Crapo PA, Scarlett JA & Kolterman OG (1982) Comparison of the
metabolic responses to fructose and sucrose sweetened foods. Am J
Clin Nutr 36, 256–261.
21. Teff KL, Elliott SS, Tschop M, et al. (2004) Dietary fructose
reduces circulating insulin and leptin, attenuates postprandial sup-
pression of ghrelin, and increases triglycerides in women. J Clin
Endocrinol Metab 89, 2963–2972.
22. Chong MFF, Fielding BA & Frayn KN (2007) Mechanisms for the
acute effect of fructose on postprandial lipemia. Am J Clin Nutr 85,
23. Bantle JP, Swanson JE, Thomas W, et al. (1992) Metabolic effects
of dietary fructose in diabetic subjects. Diabetes Care 15, 1468–1476.
24. Osei K, Falko J, Bossetti BM, et al. (1987) Metabolic effects of fruc-
tose as a natural sweetener in the physiologic meals of ambulatory
obese patients with type 2 diabetes. Am J Med 83, 249–255.
25. Stanhope KL, Schwarz JM, Keim NL, et al. (2009) Consuming
fructose-sweetened, not glucose-sweetened, beverages increases
visceral adiposity and lipids and decreases insulin sensitivity in over-
weight/obese humans. J Clin Invest 119, 1322–1334.
26. Swanson JE, Laine DC, Thomas W, et al. (1992) Metabolic effects
of dietary fructose in healthy subjects. Am J Clin Nutr 55, 851–856.
27. Atkinson FS, Foster-Powell K & Brand-Miller JC (2008)
International tables of glycemic index and glycemic load values:
2008. Diabetes Care 31, 2281–2283.