Abstracts - Association for Chemoreception Sciences

#P169 POSTER SESSION IV:
CHEMICAL SIGNALING AND BEHAVIOR;
ANIMAL BEHAVIOR/PSYCHOPHYSICS;
CHEMOSENSATION AND METABOLISM;
VOMERONSASAL AND CHEMICAL
COMMUNICATION
#P170 POSTER SESSION IV:
CHEMICAL SIGNALING AND BEHAVIOR;
ANIMAL BEHAVIOR/PSYCHOPHYSICS;
CHEMOSENSATION AND METABOLISM;
VOMERONSASAL AND CHEMICAL
COMMUNICATION
Oral stimulation with sugar elicits cephalic phase insulin
release and improves glucose tolerance in C57BL/6 and
Tas1r3 knock-out mice
John I. Glendinning 1 , Sarah Stano 1 , Olivia Goldman 1 , Danica Yang 1 ,
Robert F. Margolskee 2 , Anthony Sclafani 3 , Joseph R. Vasselli 4
1
Barnard College, Columbia University/Biology Department New
York, NY, USA, 2 Monell Chemical Senses Center Philadelphia, PA,
USA, 3 Brooklyn College of CUNY/Psychology Department Brooklyn,
NY, USA, 4 New York Obesity Nutrition Research Center, St. Luke’s-
Roosevelt Hospital New York, NY, USA
In rats, oral stimulation by sugars elicits cephalic phase insulin
release (CPIR). This CPIR has been found to improve tolerance
to glucose challenges. Here, we asked whether oral stimulation
by glucose has similar effects in C57BL/6 wild-type (WT) mice.
To explore the role of the T1r3 subunit of the heterodimeric
sweet taste receptor (T1r2+T1r3) in this process, we also
examined Tas1r3 knock-out (KO) mice. We subjected all mice
to a 2 g/kg glucose challenge. To this end, we administered a
2.8 M glucose solution either orally (by allowing mice to take
a predetermined number of licks) or post-orally (by injecting
a specific volume into the esophagus by feeding tube). We
collected tail blood immediately prior to glucose administration
(at 0 min), and at subsequent time intervals. In Experiment
1, we measured plasma insulin levels with an ELISA test. We
inferred a CPIR if plasma insulin increased significantly between
the 0 and 5 min measurements. Both strains of mice exhibited
a significant CPIR after oral stimulation, but not after post-oral
stimulation with glucose. The fact that both strains exhibited a
CPIR of similar magnitude indicates that T1r3 is not necessary
for eliciting the CPIR. In Experiment 2, we measured blood
glucose levels at 0, 15, 30, 60 and 120 min. We found that both
strains exhibited significantly better glucose tolerance when the
glucose was administered orally than post-orally; the benefit
of oral administration was especially pronounced in the Tas1r3
KO mice. These results indicate that oral stimulation by sugars
elicits a CPIR via a T1r3-independent taste mechanism, and that
this CPIR substantially improves the ability of mice to tolerate
glucose challenges. Acknowledgements: Summer Undergraduate
Research Fellowship Program, Columbia University
As American as Apple Pie Gum: A Study of Satiety
Jack Hirsch 1 , Michele Soto 2 , Alan Hirsch 2
1
Adlai E. Stevenson High School Lincolnshire, IL, USA,
2
Smell & Taste Treatment and Research Foundation Chicago, IL, USA
Purpose: The aim of this study is to determine the satiety
value of Wrigley’s Extra Dessert Delight Apple Pie Sugar-Free
Gum as compared to a 100 calorie slice of apple pie. Procedure:
Thirteen girls and 11 boys self-assessed their degree of satiety
on a visual analog scale before and after chewing Wrigley’s
Extra Dessert Delight Apple Pie Sugar-Free Gum for one, 15,
and 30 minutes. This was repeated on a separate day with a 100
calorie slice of Market Pantry Apple Pie (Target) or vice-versa
(the order of presentation being counter balanced). A satiety
value was computed for each and statistical significance was
determined for difference in satiety index between the two and
effect of order of presentation (pie versus gum first). Conclusion:
No statistically significant difference was seen in satiety value
in response to eating a slice of apple pie or chewing apple
pie-flavored gum (p=0.096). No effect of order presentation was
seen. The gum imbued the same satiety value as apple pie, with
less than 1/20 of the calories. The results suggest that chewing
Wrigley’s Extra Dessert Delight Apple Pie Sugar-Free Gum may
have a role in the promotion of satiety in children as part of a
weight loss program.
#P171 POSTER SESSION IV:
CHEMICAL SIGNALING AND BEHAVIOR;
ANIMAL BEHAVIOR/PSYCHOPHYSICS;
CHEMOSENSATION AND METABOLISM;
VOMERONSASAL AND CHEMICAL
COMMUNICATION
Pre-absorptive insulin release to glutamate taste
Matthew C Kochem 1 , Suzanne M Alarcon 1 , Paul AS Breslin 1,2
1
Rutgers University New Brunswick, NJ, USA, 2 Monell Chemical
Senses Center Philadelphia, PA, USA
Glutamate, like glucose, requires insulin to be transported out
of blood into tissue. Glutamate is detected in the mouth by
taste cells, in the intestine by L-cells and in the pancreas by Beta
cells. In addition, glutamate stimulates glucagon release from
pancreatic alpha cells. It is unknown, however, whether preabsorptive
insulin release (PIR) occurs in response to the taste of
glutamate. The purpose of this study was to determine whether
glutamate causes PIR and whether the magnitude of PIR was
related to glutamate taste sensitivity, which is variable among
individuals. To assess PIR, human subjects tasted and consumed
a glutamate test meal at a dose of 100mg/kg body weight. The
glutamate dose was comprised of a mixture of monosodium
POSTER PRESENTATIONS
Abstracts are printed as submitted by the author(s).
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