Induction of drinking by insulin in the rat

Spitz, Richard

doi:10.1016/0014-2999(75)90083-7

Cited by 12 publications

(2 citation statements)

References 7 publications

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“…Whether or not GLP-1R agonists affect sodium intake remains a topic for further investigation. Although insulin affects water intake, the direction of insulin's effect makes it unlikely that this explains GLP-1R-mediated hypodipsia because administration of insulin increases, rather than decreases, water intake in the absence of food (39). Increased blood pressure inhibits water intake (33), but the time course of the pressor response to GLP-1 and the suppression of intake do not support changes in blood pressure as a more direct cause of the observed effects on water intake.…”

Section: Discussionmentioning

confidence: 94%

Glucagon-like peptide-1 receptor agonists suppress water intake independent of effects on food intake

McKay

Kanoski²,

Hayes

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Glucagon-like peptide-1 (GLP-1) is produced by and released from the small intestine following ingestion of nutrients. GLP-1 receptor (GLP-1R) agonists applied peripherally or centrally decrease food intake and increase glucose-stimulated insulin secretion. These effects make the GLP-1 system an attractive target for the treatment of type 2 diabetes mellitus and obesity. In addition to these more frequently studied effects of GLP-1R stimulation, previous reports indicate that GLP-1R agonists suppress water intake. The present experiments were designed to provide greater temporal resolution and site specificity for the effect of GLP-1 and the long-acting GLP-1R agonists, exendin-4 and liraglutide, on unstimulated water intake when food was and was not available. All three GLP-1R ligands suppressed water intake after peripheral intraperitoneal administration, both in the presence of and the absence of food; however, the magnitude and time frame of water intake suppression varied by drug. GLP-1 had an immediate, but transient, hypodipsic effect when administered peripherally, whereas the water intake suppression by IP exendin-4 and liraglutide was much more persistent. Additionally, intracerebroventricular administration of GLP-1R agonists suppressed water intake when food was absent, but the suppression of intake showed modest differences depending on whether the drug was administered to the lateral or fourth ventricle. To the best of our knowledge, this is the first demonstration of GLP-1 receptor agonists affecting unstimulated, overnight intake in the absence of food, the first test for antidipsogenic effects of hindbrain application of GLP-1 receptor agonists, and the first test of a central effect (forebrain or hindbrain) of liraglutide on water intake. Overall, these results show that GLP-1R agonists have a hypodipsic effect that is independent of GLP-1R-mediated effects on food intake, and this occurs, in part, through central nervous system GLP-1R activation.

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Section: Discussionmentioning

confidence: 94%

Glucagon-like peptide-1 receptor agonists suppress water intake independent of effects on food intake

McKay

Kanoski²,

Hayes

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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“…This effect is unlikely to contribute to the observed effects, however, because any loss of water or NaCl would lead to increased, rather than decreased, fluid intake. Similarly, GLP‐1 enhances glucose‐stimulated insulin release but insulin increases water intake , which makes this another unlikely explanation for the present results. A more plausible possibility is that the observed effects are related to the pressor response of GLP‐1R agonists .…”

Section: Discussionmentioning

confidence: 70%

Glucagon‐Like Peptide‐1 Receptor Agonist Administration Suppresses Both Water and Saline Intake in Rats

McKay

Daniels

2013

J Neuroendocrinology

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Glucagon-like peptide-1 (GLP-1) plays an important role in energy homeostasis. Injections of GLP-1 receptor (GLP-1R) agonists suppress food intake, and endogenous GLP-1 is released when nutrients enter the gut. There is also growing evidence that the GLP-1 system is involved in the regulation of body fluid homeostasis. GLP-1R agonists suppress water intake independent of their effects on food intake. It is unknown, however, whether this suppressive effect of GLP-1R agonists extends to saline intake. Accordingly, we tested the effect of the GLP-1R agonists liraglutide (0.05 µg) and exendin-4 (0.05 µg) on water and saline intakes stimulated either by angiotensin II (AngII) or by water deprivation with partial rehydration (WD-PR). Each agonist suppressed AngII-induced water intake; however, only exendin-4 suppressed saline intake. WD-PR-induced water and saline intakes were both attenuated by each agonist. Analysis of drinking microstructure after WD-PR found a reliable effect of the agonists on burst number. Furthermore, exendin-4 conditioned a robust taste avoidance to saccharine; however, there was no similar effect of liraglutide. To evaluate the relevance of the conditioned taste avoidance, we tested whether inducing visceral malaise by injection of lithium chloride (LiCl) suppressed fluid intake. Injection of LiCl did not suppress water or saline intakes. Overall, these results indicate that the fluid intake suppression by GLP-1R activation is not selective to water intake, is a function of post-ingestive feedback, and is not secondary to visceral malaise.

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