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Nesfatin‐1 acts in brain to regulate water intake
Author(s) -
Yosten Gina LC,
Samson Willis K.
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1079.6
Subject(s) - water intake , thirst , food intake , medicine , endocrinology , angiotensin ii , sed , chemistry , receptor
Nesfatin‐1, a recently discovered brain and gut peptide, was originally described based on its ability to potently inhibit food intake when injected centrally in rats (Nature 443:709,2006). Because nesfatin‐1 was also shown to inhibit water intake in ad libitum fed and watered animals (Am J Physiol 297:R330,2009), and because nesfatin‐1 is produced in areas of the brain that are known to be important for both food and water intake (Neurosci 156:563,2008), we hypothesized that nesfatin‐1 would play an important role in water intake. We therefore examined the effect of nesfatin‐1 injected into the lateral cerebroventricle (i.c.v.) on water intake in overnight‐dehydrated animals (food present), and found that nesfatin‐1 decreased water drinking in rats in a dose‐related manner. We also investigated the ability of nesfatin‐1 to alter angiotensin II (AII)‐induced thirst. Rats were pretreated with nesfatin‐1 i.c.v. 10 minutes prior to the injection of a dipsogenic dose of AII. Pretreatment with nesfatin‐1 significantly reduced water drinking in AII‐treated rats, again in a dose‐related fashion. In both experimental models, the inhibitory effects of nesfatin‐1 had abated by 24 hr post injection. These data indicate that nesfatin‐1 may be an important regulator of water intake, in addition to role in modulating food intake. Supported by AHA Grant 4470043.