Acute and second-meal effects of peanuts on glycaemic response and
appetite in obese women with high type 2 diabetes risk: a randomised
cross-over clinical trial
Caio E. G. Reis1*, Daniela N. Ribeiro1, Neuza M. B. Costa2, Josefina Bressan1, Rita C. G. Alfenas1
and Richard D. Mattes3
1Department of Nutrition and Health, Federal University of Vic ¸osa, Avenida PH Rolfs, s/n, Vic ¸osa, Minas Gerais 36570-000,
2CCA, Federal University of Espı ´rito Santo, Minas Gerais, Brazil
3Department of Foods and Nutrition, Purdue University, West Lafayette, IN, USA
(Submitted 13 April 2012 – Final revision received 10 August 2012 – Accepted 13 August 2012 – First published online 5 November 2012)
Nut consumption is associated with a reduced risk of type 2 diabetes mellitus (T2DM). The aim of the present study was to assess the
effects of adding peanuts (whole or peanut butter) on first (0–240min)- and second (240–490min)-meal glucose metabolism and selected
gut satiety hormone responses, appetite ratings and food intake in obese women with high T2DM risk. A group of fifteen women partici-
pated in a randomised cross-over clinical trial in which 42·5g of whole peanuts without skins (WP), peanut butter (PB) or no peanuts
(control) were added to a 75g available carbohydrate-matched breakfast meal. Postprandial concentrations (0–490min) of glucose, insu-
lin, NEFA, glucagon-like peptide-1 (GLP-1), peptide YY (PYY), cholecystokinin (CCK), appetitive sensations and food intake were assessed
after breakfast treatments and a standard lunch. Postprandial NEFA incremental AUC (IAUC) (0–240min) and glucose IAUC (240–490min)
responses were lower for the PB breakfast compared with the control breakfast. Insulin concentrations were higher at 120 and 370min
after the PB consumption than after the control consumption. Desire-to-eat ratings were lower, while PYY, GLP-1 and CCK concentrations
were higher after the PB intake compared with the control intake. WP led to similar but non-significant effects. The addition of PB to break-
fast moderated postprandial glucose and NEFA concentrations, enhanced gut satiety hormone secretion and reduced the desire to eat. The
greater bioaccessibility of the lipid component in PB is probably responsible for the observed incremental post-ingestive responses
between the nut forms. Inclusion of PB, and probably WP, to breakfast may help to moderate glucose concentrations and appetite in
Key words: Peanuts: Glucose: Appetite: Type 2 diabetes mellitus: Glucagon-like peptide 1: Glycaemic index
The incidence and prevalence of type 2 diabetes mellitus
(T2DM) have increased markedly worldwide, and its compli-
cations are the leading causes of morbidity and premature
mortality(1). The importance of diet in the prevention,
treatment and control of T2DM has been recommended(2).
It has been reported that nut consumption may improve
Peanut consumption may moderate appetite, food intake
and glycaemic control, and has been negatively associated
with type 2 diabetes risk(4). These beneficial effects may be
due to their nutritional components. Besides being a
low-glycaemic-index food, peanuts are energy dense, and a
good source of fibre, protein, niacin, folate, Mg, Se and Mn.
antioxidant and anti-inflammatory effects(5). However, the
mechanisms responsible for their health benefits have not
been completely elucidated(6).
Processing whole nuts to butter form results in cell-wall rup-
ture and greater fat and fat-soluble nutrient bioaccessibility(7).
The higher availability of fat in the intestinal lumen may
decrease the rate of carbohydrate absorption (by delaying gas-
tric emptying), favouring a reduced glycaemic response, and
stimulate the secretion of intestinal hormones that may curb
appetite and food intake as well as stimulate insulin release(8).
Therefore, the form in which peanuts are consumed (whole or
butter) may lead to different metabolic responses(9).
also contain bioactivecompounds that exert
*Corresponding author: Caio E. G. Reis, fax þ55 31 38992541, email email@example.com
Abbreviations: CCK, cholecystokinin; GLP-1, glucagon-like peptide-1; IAAC, incremental area above the curve; IAUC, incremental AUC; PB, peanut butter;
PYY, peptide YY; T2DM, type 2 diabetes mellitus; WP, whole peanuts without skins.
British Journal of Nutrition (2013), 109, 2015–2023
q The Authors 2012
British Journal of Nutrition
The aim of the present study was to assess the effects of
peanut consumption (whole peanuts or peanut butter) on
first- and second-meal glucose metabolism (blood glucose,
insulin and NEFA) and selected gut satiety hormone responses
(glucagon-like peptide-1 (GLP-1), cholecystokinin (CCK) and
peptide YY (PYY)), subjective appetite ratings (visual ana-
logue scale) and food intake in obese women with high
Study participants were recruited through public advertise-
ments. Eligibility criteria included the following: age 18–50
years; BMI 30–35kg/m2; not taking medications known to
affect glycaemia, fat metabolism or appetite; regular breakfast
consumer ($420kJ ingested within 2h of waking on $4d/
week); limited body weight fluctuation (,5kg in the past
3 months); willingness to eat all test foods; no self-reported
allergy to the foods provided in the study; no self-reported
sleep disorders. In addition to the aforementioned criteria,
participants had to meet one of the following conditions:
waist circumference $88cm; reported family history of
T2DM in first-degree relatives; fasting capillary blood glucose
5·5–7·0mmol/l; and/or 2h blood glucose 7·8–11·1mmol/l
(impaired glucose tolerance). Participants presenting with
T2DM, dyslipidaemia or high blood pressure were excluded.
A total of 141 individuals completed the first screening visit,
of which sixty-eight were eligible for and completed the
second screening visit. Finally, fifteen participants met all
screening criteria and completed the full study protocol.
The protocol was approved by the Human Research Ethics
Committee of the Federal University of Vic ¸osa, Brazil (no. 004/
2009). The present trial was registered at ClinicalTrials.gov
(registration no. NCT01413126). All volunteers were informed
about the objectives of the study and provided written
informed consent. Power calculations indicated that thirteen
individuals were necessary to detect a change in blood
glucose of 0·35mmol/l (a ¼ 0·05; power ¼ 0·80, SD 0·3)(10).
The present randomised cross-over clinical trial required
participants to complete three experimental sessions where
whole peanuts without skins (WP), peanut butter (PB) or no
peanuts (control) were consumed with a breakfast meal
separated by a washout period of at least 8d. Participants
were instructed not to consume alcohol or conduct any
non-habitual physical activity 24h before the sessions, and
to consume a low-carbohydrate meal the night before the
test sessions. Postprandial concentrations of blood glucose,
insulin, NEFA, GLP-1, CCK, PYY, appetite sensations and
food intake were assessed before and after breakfast treat-
ments and a standard lunch (Fig. 1).
For screening, participants arrived
between 07.30 and 08.00 hours after a 12h overnight fluid
and feed deprivation for the 2h oral glucose tolerance test,
and for measurement of height, waist circumference, body
weight, body composition, resting energy expenditure and
blood pressure. Participants were also asked to answer ques-
tionnaires regarding stress, physical activity and eating and
At each experimental session, body weight, capillary
glucose level, the number of hours of sleep the night
before and the time and composition of the last meal were
assessed. Finger stick blood glucose was measured using a
glucometer One Touch Ultra 2 (Johnson & Johnson Company)
to ensure that the participants were feed-deprived (glucose
An indwelling catheter was placed in the participant’s fore-
arm and blood samples were drawn and appetite was rated at
baseline (210) and at 15, 45, 60, 90, 120, 180 and 240min
after test breakfast completion (first-meal responses). At
240min, participants consumed a standard lunch. Afternoon
blood sampling and appetite scoring occurred at 265, 295,
310, 340, 370, 430 and 490min after consumption of the test
breakfast (second-meal responses), resulting in a total of 8h
of biochemical assessment. After leaving the laboratory,
participants recorded all food consumed and filled out the
appetite ratings(11)at 550, 610, 670 and 730min.
Participants were not allowed to eat or drink anything
(except water) besides the foods that were provided during
the study sessions. They were also not allowed to watch
any television show or talk about anything related to food,
or anything that could affect the assessed parameters. They
were allowed to read, listen to music, watch TV, use the
computer and walk inside the laboratory.
in the laboratory
Anthropometric and body composition measurements
Body weight was assessed using an electronic platform scale
(Model 2096 PP, Toledo Brazil), with a capacity for 150kg
and precision of 50g. Height was measured using a stadi-
ometer (SECA model 206; Seca) fixed to the wall. BMI was
computed based on weight (kg) and height (m2) (kg/m2),
–10 0 15 45 60 90 120 180 240 250 265 295 310 340 370 430 490 550 610 670 730 min
Fig. 1. Experimental study protocol. B, breakfast; L, lunch; LL, leave the laboratory; A, appetite; P, palatability;
(GLP-1), cholecystokinin and peptide YY analyses; , glucose, insulin, NEFA and GLP-1 analyses.
, glucose, insulin, NEFA, glucagon-like peptide-1
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Peanuts and glycaemic response2023
British Journal of Nutrition