PMID- 9748106
OWN - NLM
STAT- MEDLINE
DCOM- 19981209
LR  - 20190712
IS  - 0031-9384 (Print)
IS  - 0031-9384 (Linking)
VI  - 64
IP  - 3
DP  - 1998 Jun 1
TI  - Intracerebroventricular glucagon-like peptide-1 (7-36) amide inhibits sham 
      feeding in rats without eliciting satiety.
PG  - 367-72
AB  - Glucagonlike peptide-1 (7-36) amide (GLP-1) and its receptors are present in 
      several brain regions and may play a role in the physiological control of 
      feeding. To investigate the effect of GLP-1 on eating in the absence of 
      postingestive food stimuli, rats were implanted with gastric cannulas for sham 
      feeding and lateral ventricular cannulas for infusion of GLP-1. Rats (n = 10) 
      sham fed 0.8 mol/L sucrose for 45 min, beginning 5 min after 
      intracerebroventricular (icv) infusion of 2.5 microL of artificial cerebrospinal 
      fluid with 0-30 microg of GLP-1 . Behaviors were observed each minute using a 
      time-sampling technique. Additionally, lick-by-lick records of the 
      microstructural pattern of sucrose intake were made during the first 15 min of 
      each test for five rats receiving 3 and 10 microg of GLP-1. GLP-1 decreased 
      sham-fed intake by as much as 50%, but GLP-1 did not terminate sham feeding. The 
      frequency of observations of feeding was decreased, but the frequency of resting, 
      the terminal item in the behavioral sequence of postprandial satiety in real 
      feeding rats, did not reliably increase. No abnormal behaviors were observed. 
      Although GLP-I did not affect the latency to begin sham feeding, it significantly 
      reduced the initial rate of licking. GLP-I did not affect the motor aspects of 
      licking, because the interlick intervals within individual bursts of licking or 
      overall lick efficiency were normal. These data suggest that 
      intracerebroventricular infusions of GLP-1 inhibit sham feeding by decreasing the 
      orosensory positive feedback that drives licking, rather than by activating 
      physiological satiating mechanisms or nonspecific mechanisms such as aversion or 
      motor incapacity.
FAU - Asarian, L
AU  - Asarian L
AD  - E.W. Bourne Laboratory, New York Hospital-Cornell Medical Center, White Plains 
      10605, USA.
FAU - Corp, E S
AU  - Corp ES
FAU - Hrupka, B
AU  - Hrupka B
FAU - Geary, N
AU  - Geary N
LA  - eng
GR  - MH 18390/MH/NIMH NIH HHS/United States
GR  - MH 51135/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Physiol Behav
JT  - Physiology & behavior
JID - 0151504
RN  - 0 (Dietary Sucrose)
RN  - 0 (Peptide Fragments)
RN  - 107444-51-9 (glucagon-like peptide 1 (7-36))
RN  - 62340-29-8 (Glucagon-Like Peptides)
RN  - 89750-14-1 (Glucagon-Like Peptide 1)
RN  - 9007-92-5 (Glucagon)
SB  - IM
MH  - Animals
MH  - Dietary Sucrose/pharmacology
MH  - Feeding Behavior/*drug effects
MH  - Glucagon
MH  - Glucagon-Like Peptide 1
MH  - Glucagon-Like Peptides
MH  - Injections, Intraventricular
MH  - Male
MH  - Peptide Fragments/administration & dosage/*pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Satiety Response/*drug effects
EDAT- 1998/09/25 00:00
MHDA- 1998/09/25 00:01
CRDT- 1998/09/25 00:00
PHST- 1998/09/25 00:00 [pubmed]
PHST- 1998/09/25 00:01 [medline]
PHST- 1998/09/25 00:00 [entrez]
AID - S0031-9384(98)00089-4 [pii]
AID - 10.1016/s0031-9384(98)00089-4 [doi]
PST - ppublish
SO  - Physiol Behav. 1998 Jun 1;64(3):367-72. doi: 10.1016/s0031-9384(98)00089-4.