Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P01275 (
glucagon
)
26,492
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
In the rat, the
glucagon-like peptide 1
(
GLP-1
)(7-36) amide inhibits neurones in the central nervous system responsible for food and water intake.
GLP-1
-induced inhibition of food intake may involve the hypothalamic arcuate nucleus, whereas rostral sensory circumventricular organs may be responsible for the inhibitory action of
GLP-1
on drinking. To further investigate the role of these blood-brain-barrier-free areas in
GLP-1
-induced inhibition of ingestive behavior, neonatal Wistar rats were subjected to monosodium glutamate (MSG) treatment, which causes extensive damage to the arcuate nucleus as well as to parts of the sensory circumventricular organs. The inhibitory effect of
GLP-1
on feeding induced by food deprivation was completely abolished in MSG-lesioned rats. This effect was not due to either a loss of sensitivity to anorectic agents or a
loss of taste
aversion because MSG-treated animals displayed normal anorectic responses to central administration of corticotropin-releasing factor and normal aversive responses to peripheral administration of both lithium chloride and D-amphetamine. In non-lesioned rats, neuropeptide Y (NPY)-induced feeding was significantly reduced by concomitant
GLP-1
administration. In contrast,
GLP-1
had no effect on NPY-induced feeding in MSG-lesioned rats, suggesting that the
GLP-1
receptors that mediate inhibition of feeding are localized upstream to the NPY-sensitive neurones inducing feeding behavior. The inhibitory effect of
GLP-1
on water intake was tested using an ANG II-elicited drinking paradigm. Central administration of
GLP-1
inhibited ANG II drinking in both MSG-treated rats and their nontreated littermates. In contrast, peripheral administration of
GLP-1
did not inhibit ANG II-induced drinking behavior in MSG-treated rats. Thus it is evident that centrally acting
GLP-1
modulates feeding and drinking behavior via neurones sensitive to MSG lesioning in the arcuate nucleus and circumventricular organs, respectively.
...
PMID:Glucagon-like peptide 1(7-36) amide's central inhibition of feeding and peripheral inhibition of drinking are abolished by neonatal monosodium glutamate treatment. 956 83
