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Relationships between insulin release and taste

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Abstract

Tasting sweet food elicits insulin release prior to increasing plasma glucose levels, known as cephalic phase insulin release (CPIR). The characteristic of CPIR is that plasma insulin secretion occurs before the rise of the plasma glucose level. In this experiment, we examined whether taste stimuli placed on the tongue could induce CPIR. We used female Wistar rats and five basic taste stimuli: sucrose (sweet), sodium chloride (salty), HCl (sour), quinine (bitter) or monosodium glutamate (umami). Rats reliably exhibited CPIR to sucrose. Sodium chloride, HCl, quinine, or monosodium glutamate did not elicit CPIR. The non-nutritive sweetener saccharine elicited CPIR. However, starch, which is nutritive but non-sweet, did not elicit CPIR although rats showed a strong preference for starch which is a source of glucose. In addition, we studied whether CPIR was related to taste receptor cell activity. We carried out the experiment in rats with bilaterally cut chorda tympani nerves, one of the gustatory nerves. After sectioning, CPIR was not observed for sweet stimulation. From these results, we conclude that sweetness information conducted by thistaste nerve provides essential information for eliciting CPIR.
Biomedical Research 28 (2) 79-83, 2007
Relationships
between
insulin release
and
taste
Kazuyuki
Tonosaki1,
Yasunori
How1,
Yasutake
Shimizu2
and
Keiichi
Tonosaki1
1
Department
of
Oral
Physiology,
School
of
Dentistry,
Meikai
University,
Saitama
350-0283
and
2
Department
of
Veterinary
Physiology,
Facultyof Agriculture,Gifu University, Gifu, Japan
(Received
13
December
2006; andaccepted26
January
2007)
ABSTRACT
Tasting sweet food elicits insulin release prior to increasing plasma glucose levels, known as ce
phalic phase insulin release (CPIR). The characteristic
of
CPIR is that plasma insulin secretion oc
curs before the rise of the plasma glucose level. In this experiment, we examined whether taste
stimuli placed on the tongue could induce CPIR. We used female Wistar rats and five basic taste
stimuli: sucrose (sweet), sodium chloride (salty),
HC1
(sour), quinine (bitter) or monosodium glu-
tamate (umami). Rats reliably exhibited CPIR to sucrose. Sodium chloride,
HC1,
quinine, or
monosodium glutamate did not elicit CPIR. The non-nutritive sweetener saccharine elicited CPIR.
However, starch, which is nutritive but non-sweet, did not elicit CPIR although rats showed a
strong preference for starch which is a source
of
glucose. In addition, we studied whether CPIR
was related to taste receptor cell activity. We carried out the experiment in rats with bilaterally cut
chorda tympani nerves, one
of
the gustatory nerves. After sectioning, CPIR was not observed for
sweet stimulation. From these results, we conclude that sweetness information conducted by this
taste nerve provides essential information for eliciting CPIR.
Taste
sensations
have
been
classified
into
five
sub-
modalities: sweet, salty, sour, bitter, and umami,
which typically represent particular categories
of
stimuli. Sweetness is represented by carbohydrates,
sourness by spoilage materials, salt by minerals, bit
terness by toxic substances, and the umami by ami
no acids. On the basis
of
these signals, animals
discriminate
between
nutrient
and
toxic
substances.
The sense
of
taste involves not only responding to
foods and transmitting the chemical information
of
the food to the central nervous system but also set
ting up appropriate caloric intake action and taste
related reflexes (3, 4). For example, strong sourness
increases secretional saliva (4, 6, 9) which helps to
Address correspondence to: Dr. Keiichi Tonosaki
Department
of
Oral Physiology, School
of
Dentistry,
Meikai University, 1-1 Keyakidai, Sakatoshi, Saitama-
ken, Japan 350-0283
Tel (Fax): +81-49-279-2770
E-mail: tonosaki@dent.meikai.ac.jp
prepare for smooth digestion and absorption of food
before
it
reaches
the
stomach.
It is
also
known
that
taste stimuli can produce insulin secretion via the p
cell of the pancreas (1-3, 6). The characteristic of
cephalic phase insulin release (CPIR) is that plasma
insulin secretion occurs before the rise
of
the plas
ma glucose level. The typical characteristic of CPIR
is that plasma insulin is secreted within 2 min after
oral sensory stimulation, peaks at 4 min, and returns
to baseline within
8-10
min after stimulation (4, 6,
14-18). Although many CPIR related experiments
have been conducted using multiple animal species,
including human, the functional role
of
CPIR is not
clearly known (1, 3, 6-10). In CPIR research, food
substances are typically placed in the oral cavity. In
many cases, more attention is paid to "food compo
sition"
than to
"food
taste" (6, 7, 13).
There
is no
report that examines the effect
of
the 5 submodali-
ties
of
taste on CPIR systematically. It is important
to clarify this relationship between qualities
of
tastes
and CPIR. The purpose of this study is to clarify the
80
characteristics of taste specificity of CPIR using the
rat.
MATERIALS
AND
METHODS
Animals.
Male
Wistar
rats
weighting
120-220
g
were housed in plastic cages at
22±1°C
with a
12: 12h
light:
darkcycle(lighton 07 : 00-19 : 00 h).
They were given free access to laboratory chow
(LABO MR Sttock, Nihon-Nosan, Yokohama, Ja
pan) and water.
Taste solutions. Taste stimuli were sucrose (1.0 M,
sweetness), acetic acid (CH3COOH, 0.1 M, sour
ness),
salt
(NaCl, 0.5 M,
salty
taste),
quinine
hydrochloride (QHCl, 0.01 M, bitterness), sodium
glutamate (MSG, 0.2 M, umami), saccharin
(0.01
M),
and starch (5%, Merck KgaA, Germany). Each
chemical
was
dissolved
in
distilled
water.
Neural recordingprocedure. After the rat was suffi
ciently anesthetized with pentobarbital administra
tion (40 mg/kg, i.p.), the trachea was cannulated.
The rat was fixed in a supine position in a head
folder, and the chorda tympani (CT) nerve was ex
posed and cut near its entry into the tympanic bulla.
For
whole nerve recording, the entire nerve was
placed on a bipolar silver wire electrode. The elec
trophysiological recording method as well as the
methods
for
chemical
stimulation
of
the
taste
cells
have been previously described (12). Each chemical
solution was applied to the tongue for 20 s. Solu
tions
were
delivered
at
a
flow
rate
of
0.5
mL/s.
In-
terstimulus intervals were at least 1 min, during
which time the tongue was rinsed with distilled wa
ter.
Behavioral analysis (two bottle preference tests).
Rats were first trained to drink at equal rates from
two bottles
of
distilled water. After training, distilled
water was kept in one bottle while a test solution
was placed in the other. The position
of
the bottle
was switched every 24 h, and the intake volume was
measured every 24 h for 3 days. During the experi
ment, each rat was kept in an individual plastic cage
and
fed
solid
food
ad
lib.
The bilateral sectioning
of
chorda
tympani
nerve
(CT).
Six rats were subjected to surgery for bilateral
sectioning
of
the CT. Rats were anesthetized by i.p.
injection
of
pentobarbital (40 mg/kg). Each animal
was secured with a head holder in a prone position
and an incision was made along the mandible tip.
K.
Tonosaki
et
al.
Then both CT nerves were exposed and bilateral CT
nerves were sectioned. After each operation, the
wound was closed with autoclips and the animal
was returned to its cage for recovery.
Cardiac and oral catheter surgeries. After rats
reached a surgical level
of
anesthesia (pentobarbital,
40 mg/kg, i.p.), cardiac catheterization (0.5mm in
side diameter, 1.0 mm outer diameter) for blood col
lection was inserted from the right external jugular
vein to the right atrium. The catheter exited and ex
posed about 3.0 cm from the parietal region through
a hypodermic. Simultaneously, the catheter for the
taste stimulation (0.5 mm inside diameter, 1.0 mm
outer diameter) was implanted into the oral cavity
through the right cheek and exited and exposed
about 3.0 cm from the parietal region through a hy
podermic. After each operation, the animal was re
turned to its cage for recovery.
Samples and
measurements.
Taste stimulation and
blood collection were performed under non-anesthe
sia and non-restraint using customary methods. Taste
solutions (1.0 mL) were given for 45 s into the oral
cavity via the oral catheter. After a 12-h fast, blood
samples were obtained from the cardiac catheter at
-5, -1,
1, 3, 5, 7, 9, 11
and
15
min
after taste
stim
ulation. Plasma glucose levels were determined by
the glucose oxidase method (Glucose B-test, Wako
Pure Pharmaceutical, Osaka, Japan). Plasma insulin
concentrations were
determined
by ELISA kits
(Morinaga, Yokohama, Japan).
Statistical analysis. All values are presented as
means ± SE. Statistical significance
was
examined
by an
ANOVA,
with post hoc testing by means of
Duncan's multiple range test. Comparisons between
groups were made by Student's t-test. In all tests,
p < 0.05 was accepted as significant.
RESULTS
Chorda
tympani
(CT)
nerve responsesand water in
take
for
five fundamental taste solutions
The tongue was rinsed with distilled water. Gustato
ry CT nerve responses for various taste stimulations
are shown in Fig. 1. 1.0 M sucrose, 0.1 M acetic
acid, 0.5 M NaCl, 0.01 M QHCl and 0.2 M MSG
elicited robust CT responses (12).
In Fig. 2, rats distinguished each taste solution
from distilled water. Rats preferred sucrose solutions
(27.8 ± 5.5 mL/day, n = 4) but avoided other solu
tions (acetic acid: 1.1
±0.7
mL/day, n = 4; NaCl:
Insulin
release
and
taste
JX
sucrose
1 M
QHCl
0.01
M
81
Fig. 1 Typical
examples
of integrated
chorda
tympani
nerve
responses
to
sucrose,
acetic acid (CH,COOH). sodium chlo
ride (NaCl), quinine hydrochloride (QHCl)
and
monosodium
glutamate
(MSG).
o
I
i
+>
c
H
a
o
•H
-p
H
O
w
40
30
20
10
I
J
§L
IJ
Distilled
water
fH test solution
ita.
i.
sucrose
CH,COOH
NaCl
QHCl
MSG
1 M
0.1
M
0.5
M
0.01
M
0.2
M
Fig. 2 Oral intake of taste solutions and
distilled
water during 24 h preference tests (n =4). The open columns are the dis
tilled water intake ratios,
and
the
hatched
columns
are
the
taste
stimulus solution intake ratios
(mean
± SD).
2.2
±0.8
mL/day. n = 4: QHCl: 0.7 ± 0.7 mL/day,
n = 4; MSG: 7.5 ± 2.5 mL/day, n = 4). The water in
take
of
a rat was 25.1 ± 1.7 mL/day.
Fivefundamental taste solutions and
CPIR
In Fig. 3A, 3 min after the sucrose stimulation, there
was a 3 to 4 times increase in plasma insulin con
centration compared to levels prior to stimulation
(before stimulation 3.0
±0.7
ng/mL and after 3 min
12.4
±4.5
ng/mL, n = 5). The rise
of
the plasma in
sulin
concentration
was
transient,
and
declined
with
in 7 min. In Fig. 3B. the change
of
the plasma
glucose level after sucrose stimulation is plotted.
The
transient
increase
in
insulin
secretion
was
ob
served before the rise
of
the glucose level (before
stimulation 88.5 ± 8.5 mg/dL. 3 min after stimula
tion 99.3 ± 8.5 mg/dL, n = 6, 5 min after stimulation
112.2±
6.5
mg/dL.
n = 6.
11
min
after
stimulation
142.8 + 12.5 mg/dL. n = 6). Thus CPIR was induced
by the sucrose stimulation of the tongue. Table 1
presents the results of plasma insulin concentrations
and plasma glucose concentrations for acetic acid.
NaCl, QHCl and MSG. No significant changes were
observed.
Sweetness
and
CPIR
In presenting the 5 fundamental tastes, only sucrose
elicited
CPIR.
However,
sucrose
has
two
character
istics:
sweet
and
nutritive.
Next,
we
tested
whether
'sweet' or 'nutritive' could elicit CPIR. Testing with
the
non-nutritive
sweetener
saccharine
did
elicit
CPIR (Fig. 4A and B). However, the non-sweetener
nutritive starch did not elicit CPIR (Fig. 5A and B).
The
effect
of
bilateral sectioning CT nerve
Finally,
we
studied
whether
CPIR
was
related
to
82
Table
1
Plasma insulin and glucose levels in
rats
K.
Tonosaki
et
at.
before
3
minutes
5
minutes
7
minutes
11
minutes
n
Acetic
acid
sour
Insulin (ng/mL)
Glucose (mg/dL)
Insulin
Glucose
2.5
±0.2
98.5
±
6.0
2.4
±
0.5
93.5
±
0.2
2.3
±
0.2
92.5
±
7.5
2.5
±
0.5
92.5
±
7.0
2.5
±
0.5
92.5
±
7.0
6
5
NaCl
salty
3.9
±1.5
111.3
±4.5
3.4
±1.1
110.5
±4.0
3.4
± 1.1
111.3
±4.5
3.4
±1.5
110.5
±4.0
3.4
±1.5
110.5
±4.0
5
5
QHCl
bitter
Insulin
Glucose
3.5
±1.2
98.6
±4.5
2.9
±1.0
98.0
±4.5
3.5
±
1.0
101.0
±2.0
3.5
±1.0
101.0
±2.0
3.5
±1.0
105.0
±3.0
5
5
MSG
umami
Insulin
Glucose
2.5
±0.8
103.5
±4.5
2.5
±
0.8
103.5
±4.5
2.5
±1.0
105.5
±5.0
2.5
±1.0
105.5
±5.0
2.5
±1.5
108.5
±7.0
5
5
The values are indicated at I min before and 3, 5, 7,
11
min after taste stimulation, n: sample numbers. Data are means ± SE.
B
sucrose
Fig. 3 Effect of administration of
sucrose
on
plasma
insu
lin levels (n = 5) (A)
and
plasma
glucose
levels (n = 6) (B)
(mean±SD).
Arrows indicate
the
beginning of
the
taste
stimulation.
Significant
difference
between
conditions:
"P
<
0.01
and
*P
<
0.05.
j/Hfrrrf+M
B
a
I
J*
>•
»»
fi
-4
i
o
Jm
ta
5 0 5 10 IS
Time
(min)
starch
-5 0 5 [0 15
Time
(min)
Fig. 5 Effect of administration of starch on plasma insulin
levels (n = 5) (A)
and
plasma
glucose
levels (n = 5) (B)
(mean ± SD). Arrows indicate the beginning of the
taste
stimulation.
Significant
difference
between
conditions:
"P<0.01.
taste receptor cell activity. Experiments were carried
out in rats with bilaterally cut CT nerves, one
of
the
gustatory nerves. After sectioning, CPIR was not
observed
for
sweet
stimulation.
The
results
are
shown in Fig. 6A and B.
DISCUSSION
Five fundamental tastes, sweet, sour, salty, bitter and
umami, were examined in order to clarify the rela
20
.5 10
^fH
-i—*
B
ISO.
8 «o
5
saccharin
-t-*-«-t^«
0 5 10 IS
Time
(min)
Fig. 4 Effect of administration of
saccharine
on
plasma
in
sulin levels (n = 5) (A)
and
plasma
glucose
levels (n = 5) (B)
(mean±SD).
Arrows indicate
the
beginning of
the
taste
stimulation.
Significant
difference
between
conditions:
*P
<
0.05.
B
ISO
J 0 J 10 IS 5 0 5 10 IS
Time
(min)
Time
(min)
sucrose
(CT:CUT)
Fig. 6 Effect of administration of
sucrose
on
plasma
insu
lin levels (n = 6) (A)
and
plasma glucose levels (n = 6) (B)
with bilaterality sectioned the chorda tympani (CT)
nerves
(mean ± SD). An arrow indicates the beginning of the
taste
stimulation.
Significant
difference
between
conditions:
"P
<
0.01
and
*P
<
0.05.
tionship between cephalic phase insulin release
(CPIR) and taste quality since there are no previous
reports examining the relationships between CPIR
and these stimuli. In our experiments, the tongue
was
rinsed
with
distilled
water
and
the
taste
cells
were adapted to distilled water. Sucrose, acetic acid,
NaCl,
QHCl,
MSG
and
saccharin elicited robust CT
responses
(12).
The
characteristic
of
CPIR
is that
plasma insulin secretion (plasma insulin release) oc-
Insulin
release
and
taste
curs within 2 min after oral sensory stimulation, that
is, the transient increase in insulin secretion
was
ob
served before the rise
of
the plasma glucose level.
From
our
results, it is
clear
that
CPIR
was
elicited
only by sucrose stimulation, a sweet stimulus (2, 3,
16). Since sucrose has two characteristics, sweet and
nutritive, it is important to clarify which characteris
tic
is
related
to
CPIR.
We
tested
both
saccharin
and
starch:
the
artificial
sweetener
saccharin
is
sweet
but
not
nutritive
and
starch
is
nutritive
but
not
sweet.
The
non-nutritive
sweetener
saccharine
did
elicit
CPIR
whereas
the
non-sweetener
nutritive
starch
did
not. It has been reported that the rats show a strong
preference for starch which is a source
of
glucose,
but starch did not elicit CT responses (8, 10, 11).
From the results, it became clear that
CPIR
pecu
liarly appeared for sucrose, and it was proven that it
is important that CPIR is elicited by sweet, not by
nutritive
stimuli.
Next
we
studied
whether
CPIR
was related to taste receptor cell activity. We carried
out the experiment in rats with bilaterally cut CT
nerves, one
of
the gustatory nerves. After section
ing, CPIR was not observed for sucrose stimulation.
From
these
results,
we
conclude
that
sweetness
in
formation conducted by this taste nerve provides es
sential information for eliciting CPIR.
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... Via unknown mechanisms (VDCC, VR1, NCX, and others not depicted), this may result in Ca 2+ entry and GLP-1 release. Abbreviations: VR1, vanilloid receptor-1; NCX, Na + -Ca 2+ exchanger; AMY2, amylase 2; AQP, aquaporin; CALHM, calcium homeostasis modulator ion channel; ΔMP, change in membrane potential rodents, also the chorda-tympani nerve is involved [101,321]. Roles for the glossopharyngeal nerve or other gustatory nerves were not investigated. CPIR is induced by oral exposure to sweet substances but not to umami, salty, or bitter compounds [77, 134,321]. ...
... Roles for the glossopharyngeal nerve or other gustatory nerves were not investigated. CPIR is induced by oral exposure to sweet substances but not to umami, salty, or bitter compounds [77, 134,321]. During CPIR, blood insulin rises before blood glucose [134,171]. ...
... Oral glucose intake leads to higher insulin release than intravenous application, both in humans [83,227] and animals [213]. CPIR needs the oral component and is independent of digestion in humans [2,3] and animals [100,101,321]. Warm sweet solutions are perceived sweeter than cold ones [37,306] , which is due to TRPM5 regulation by temperature [306]; similarly, CPIR is temperature dependent in rats [275], which supports the involvement of oral sweet signals in the generation of CPIR. ...
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... Quinine treatment appeared to affect the elevated glycemia level of C. irritans naturally infected fish, especially on days 3 and 5 after the commencement of the treatment, suggesting that quinine increases tissue glucose utilization. However, the hypoglycemic effect of quinine because of its bitter taste can be mediated through stimulating synthesis and/or release of insulin from the insulin producing cells (Ashley, 2007;Rojas et al., 2009;Tonosaki et al., 2007). Glycemic homeostasis was achieved rapidly after the fish rejected quinine uptake that can be explained by gilthead sea bream resistance to glucose fluctuation due to starvation (Peres et al., 2013;Sitja-Bobadilla et al., 2005). ...
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Nutrient detection through the taste system triggers various physiological changes in the body. In this issue of Neuron, Yao and Scott (2022) identify two distinct classes of serotonergic neurons in Drosophila that transform sweet and bitter taste signals into endocrine and digestive responses.
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Cephalic phase insulin release (CPIR) is a transient pulse of insulin that occurs within minutes of stimulation from foods or food-related stimuli. Despite decades of research on CPIR in humans, the body of literature surrounding this phenomenon is controversial due in part to contradictory findings between studies. This has slowed progress towards understanding the sensory and neural basis of the response, as well as its overall relevance to health. This review aims to examine up-to-date knowledge in CPIR research and identify sources of CPIR variability in humans in an effort to guide future research. The review starts by defining CPIR and discussing its presumed functional roles in glucose homeostasis and feeding behavior. Next, the types of stimuli that have been reported to elicit CPIR, as well as the sensory and neural mechanisms underlying the response in rodents and humans are discussed, and areas where knowledge is limited are identified. Finally, factors that may contribute to the observed variability of CPIR in humans are examined, including experimental design, test procedure, and individual characteristics. Overall, oral stimulation appears to be important for eliciting CPIR, especially when combined with other sensory modalities (vision, olfaction, somatosensation). While differences in experimental design and testing procedure likely explain some of the observed inter- and intra-study variability, individual differences also appear to play an important role. Understanding sources of these individual differences in CPIR will be key for establishing its health relevance.
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Sweetness is the preferred taste of humans and many animals, likely because sugars are a primary source of energy. In many mammals, sweet compounds are sensed in the tongue by the gustatory organ, the taste buds. Here, a group of taste bud cells expresses a canonical sweet taste receptor, whose activation induces Ca ²⁺ rise, cell depolarization and ATP release to communicate with afferent gustatory nerves. The discovery of the sweet taste receptor, 20 years ago, was a milestone in the understanding of sweet signal transduction and is described here from a historical perspective. Our review briefly summarizes the major findings of the canonical sweet taste pathway, and then focuses on molecular details, about the related downstream signaling, that are still elusive or have been neglected. In this context, we discuss evidence supporting the existence of an alternative pathway, independent of the sweet taste receptor, to sense sugars and its proposed role in glucose homeostasis. Further, given that sweet taste receptor expression has been reported in many other organs, the physiological role of these extraoral receptors is addressed. Finally, and along these lines, we expand on the multiple direct and indirect effects of sugars on the brain. In summary, the review tries to stimulate a comprehensive understanding of how sweet compounds signal to the brain upon taste bud cells activation, and how this gustatory process is integrated with gastro-intestinal sugar sensing to create a hedonic and metabolic representation of sugars, which finally drives our behavior. Understanding of this is indeed a crucial step in developing new strategies to prevent obesity and associated diseases.
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Food anticipatory hormonal responses (cephalic responses) are proactive physiological processes, that allow animals to prepare for food ingestion by modulating their hormonal levels in response to food cues. This process is important for digesting food, metabolizing nutrients and maintaining glucose levels within homeostasis. In this systematic review, we summarize the evidence from animal and human research on cephalic responses. Thirty-six animal and fifty-three human studies were included. The majority (88%) of studies demonstrated that hormonal levels are changed in response to cues previously associated with food intake, such as feeding time, smell, and sight of food. Most evidence comes from studies on insulin, ghrelin, pancreatic polypeptide, glucagon, and c-peptide. Moreover, impaired cephalic responses were found in disorders related to metabolism and food intake such as diabetes, pancreatic insufficiency, obesity, and eating disorders, which opens discussions about the etiological mechanisms of these disorders as well as on potential therapeutic opportunities.
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Suppression of oral sweet sensation (OSS) acutely reduces intake of sweet-tasting food due to lower liking. However, little is known about other physiological responses during both the prandial and postprandial phase. Here, we explored the effects of Gymnema sylvestre (GS)-based suppression of OSS of several types of sweet-tasting food (muffin, sweet yogurt, banana) on gastric emptying, blood glucose (BG), plasma insulin (PI), appetite indices (hunger, fullness and prospective consumption), satisfaction and desire for tastes. Fifteen healthy subjects (22 ± 3 years, 9 women) took part in the study. Subjects rinsed their mouth with either GS solution or distilled water before eating the sweet-tasting food. Subjects felt decreased sweet taste intensity and reduced taste liking associated with GS rinsing after consuming each food, compared with rinsing with distilled water (p < 0.05). Gastric emptying, BG, PI and appetite indices during and after the prandial phase did not significantly change with GS rinsing compared to rinsing with distilled water (p > 0.05). Higher desire for sweet taste as well as lower satisfaction (p < 0.05) in the postprandial phase were observed with GS rinsing. These results suggest that the suppression of OSS does not affect gastric emptying, glycemic response and appetite during and after consumption of sweet-tasting food.
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Cigarette smoking can cause taste receptors to increase the taste threshold value. Consequently, the consumption of sugar and salt will not be controlled, therefore causing systemic diseases such as hypertension and diabetes. Nicotine and tobacco in cigarettes can stimulate MMP-9 which plays vital physiological roles in normal tissue growth and repair processes. This study aimed to find the correlation between taste threshold sensitivity and MMP-9, salivary secretion, blood pressure, and blood glucose levels in smoking and nonsmoking women. This was a cross-sectional study consisting of young adult women aged 18–24 years. Subjects were divided into two groups: the nonsmoking and smoking groups. In the combined data of both groups, the sweet taste threshold was correlated with age (r = 0.308, p=0.008), blood glucose levels (r = 0.238, p=0.043), and MMP-9 (r = –0.297, p=0.011). The salt taste threshold was only correlated with systolic blood pressure in the smoking (r = 0.440, p=0.032) and combined data groups (r = 0.260, p=0.026). By using partial correlation, it was shown that the relationship between the salt taste threshold and systolic blood pressure was influenced by smoking habits. The sweet taste threshold in women was found to correlate with age, blood glucose levels, and MMP-9 levels. On the other hand, there was a significant relationship between the salt taste threshold in women with systolic blood pressure, which was the only correlation analyzed in sthis study that was found to be influenced by smoking. However, both sweet and salt taste thresholds were not statistically correlated with salivary secretion.
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The past decade has witnessed a consolidation and refinement of the extraordinary progress made in taste research. This Review describes recent advances in our understanding of taste receptors, taste buds, and the connections between taste buds and sensory afferent fibres. The article discusses new findings regarding the cellular mechanisms for detecting tastes, new data on the transmitters involved in taste processing and new studies that address longstanding arguments about taste coding.
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A conditioned taste aversion paradigm was used to assess the qualitative similarities between the tastes of a polysaccharide (Polycose) solution and sugar solutions (sucrose, maltose, glucose, fructose). In Experiment 1, three groups of female rats were water deprived and conditioned to avoid a 0.025 M Polycose, a 0.1 M sucrose, or a 0.1 M maltose solution by pairing solution consumption with a lithium chloride (LiCl) injection; in a control group water consumption was paired with the LiCl injection. The extent to which the experimental groups generalized their conditioned aversion to the other three solutions was then assessed. The Polycose-conditioned group avoided the maltose solution more than the sucrose solution, and the maltose-conditioned group avoided the Polycose solution more than the sucrose solution. The sucrose-conditioned group avoided the maltose and Polycose solutions to the same relatively low degree. In additional tests the three experimental groups showed similar aversions to a glucose solution, but only the sucrose-conditioned rats avoided a fructose solution. Rats in a second experiment also displayed relatively little cross-generalization between Polycose and sucrose aversions even though they were tested with different solution concentrations. Additional tests confirmed the results obtained in Experiment 1 with maltose, glucose, and fructose solutions, and also revealed that the sucrose-conditioned group, but not the Polycose-conditioned group avoided saccharin solutions. Neither Polycose-nor sucrose-conditioned groups avoided quinine, sodium chloride, or hydrochloric acid solutions. These results, along with other recent findings, suggest that rats have two types of “carbohydrate” taste receptors, one for polysaccharides and one for sucrose, which produce qualitatively distinct gustatory sensations.
Article
The pancreatic secretory responses of dogs to various taste stimuli were examined in this study. Additionally, taste preferences were examined in 24-hour exposure tests to taste stimulus solutions as well as in short exposure tests to taste solutions mixed with commercial stock diet. The liquid and solid food preference tests produced quite different results. In dogs with cannulated gastric and duodenal fistulas, gustatory receptors were stimulated orally with 100 ml of taste stimulus solution (water 0.05 M monosodium glutamate (MSG), 0.05 M citric acid or 0.3 M sucrose) mixed with 25 g of a carrier (commercial stock diet, purified diet or cellulose). Pancreatic secretory responses to the taste stimuli varied with the type of carrier. Stock diet carrier was a better stimulant than the purified diet for both protein output and volume flow. Taste stimuli with a cellulose carrier did not produce any pancreatic response at all. The differences in responses to the different carriers were greater than the differences between taste stimuli when the same carrier was used. This experiment indicates that gustatory stimulation does influence the function of pancreatic secretion depending on the carriers used.
Article
Blood glucose and insulin levels were measured in undisturbed and free-moving rats. The insulin level rose in the 1st min after the start of food intake; the glucose level began to increase only in the 3rd min if a fluid carbohydrate-rich food was eaten. The insulin release followed a biphasic pattern. If the same quantity of food ingested orally was injected into the stomach in the same time as the animals needed to complete oral ingestion, delayed insulin release could be seen and the second phase of insulin release was exaggerated. The glucose level, which started to rise in the 3rd min, increased much more than during oral ingestion. With respect to insulin release the same phenomena could be observed if carbohydrate-free fluid food was used instead of carbohydrate-rich fluid food. It is argued that the oral cavity plays a major role in the first phase of insulin release, which in its turn seems to be important in the homeostasis of the blood glucose and insulin levels.
Article
The taste preference thresholds of adult female rats for polysaccharide (Polycose), maltose, and sucrose were compared. The nondeprived animals were given 24-hr two-bottle preference tests (saccharide solution vs. water) and, starting at 0.008%, the saccharide concentration was increased daily. The rats first preferred the Polycose solution to water at 0.01% (0.0001 M), the maltose solution to water at 0.09% (0.0025 M), and the sucrose solution to water at 0.09% (0.0026 M). Thus, on a molar basis the rats' Polycose threshold was 25 to 26 times lower than their maltose and sucrose threshold. It was postulated that the low taste threshold for polysaccharides allows the rat to detect starch which, unlike sugar, is very low in solubility.
Article
The taste preferences of adult female rats for solutions of five different carbohydrates were evaluated using brief (3-min) two-bottle preference tests. At the lowest concentration tested (0.03 molar) the order of preference was Polycose greater than maltose greater than sucrose greater than glucose = fructose. Whereas at the highest concentrations tested (0.5 or 1.0 molar) the preference order was sucrose greater than maltose greater than or equal to Polycose greater than glucose greater than fructose. Thus, at low concentrations starch-derived polysaccharides (Polycose) are more palatable to rats than are sugars. These findings are consistent with the hypothesis that rats have separate taste receptors for sugars and for starch-derived polysaccharides. The fact that maltose is the most preferred sugar at low concentrations is attributed to its stimulation of "polysaccharide" taste receptors.
Article
After sham-feeding of glucose, conscious trained dogs bearing double-barrelled fistulas of the oesophagus or of the stomach do not show any blood sugar increase. Nevertheless their IRI-levels in the peripheral venous blood increased considerably. This increase consists of two peaks of short duration between the 5th and the 10th as well as the 15th and the 25th min. Such IRI-peaks oceured also after sham-feeding of tap water, but to a smaller extent. Their temporal order corresponds to the early IRI-peaks after oral glucose administration in intact animals, but before the blood glucose increase which was observed by us previously. After the application of glucose into the oral opening of the oesophageal fistula the first IRI-peak does not occur, the second and the third peaks appeared to the same extent. A feed-forward of insulin secretion induced by oral ingestion is suggested. It may be interpreted within the scope of the "entero-insular axis" of the mechanism of insulin secretion.
Article
The occurrence of a reflex insulin discharge at the beginning of a meal, and its possible influence on intake were studied in 7 normal weight humans. Each subject was tested twice under three standard meal conditions. The evolutions of insulinemia and glycemia were recorded over an 84 min observation period, starting 2 min before food presentation. Blood was drawn continuously from an antecubital vein, and collected in 1-min samples for the first 30 min, and then in 3-min samples. The average glycemia curve was stable until some 18-20 min after meal onset. By contrast, a significant rise in plasma insulin appeared as early as the 4th min after meal onset and it is hypothesized to be preabsorptive, of cephalic and/or gastric origin. However, inter-test variations were large even in the same person. Schematically, three types of early insulin responses were observed: high and/or sustained rise, moderate and/or short increase, moderate decrease in plasma insulin. The shape of the early insulin response was not related to any meal characteristic. The potential biological and behavioral significance of the early insulin release is discussed.
Article
The ability of saccharin, in comparison with glucose and tap water, to elicit glycemia-independent neurally mediated insulin secretion was investigated in chronically catheterized, freely moving rats. Plasma glucose and insulin concentrations were measured continuously from venous blood with a sampling resolution of one per minute. In normal rats, 1 ml of 0.15% saccharin caused a significant rapid rise in peripheral plasma insulin levels lasting up to 5 min, without significant changes in glycemia. Tap water alone also induced a transient elevation in insulinemia but was much smaller than the saccharin-induced response. In streptozotocin diabetic rats bearing intrahepatic, presumably denervated islet isografts, these rapid insulin responses to oral saccharin and tap water stimulation were completely abolished, whereas the early insulin response to intravenous glucose was decreased by only about 30%. These results are consistent with the concept of gustatory and other oral sensory signals acting as triggers for neurally mediated insulin release.