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Targeting Saliva for the Purpose of Modulating Feeding Behavior
Author(s) -
Hurtado Daniela Maria,
Acosta Andres,
La Sala Michael,
Zolotukhin Sergei
Publication year - 2010
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.24.1_supplement.lb279
Subject(s) - saliva , endocrinology , medicine , appetite , taste , salivary gland , hormone , transgene , taste aversion , obesity , biology , gene , neuroscience , biochemistry
In this report, we show that murine and human saliva contains gut peptide YY (PYY3‐36), a hormone characterized by its physiological function of increasing satiation but not altering appetite. The purpose of the study was to investigate whether changes in salivary PYY3‐36 concentration induced either pharmacologically (acute augmentation) or genetically (gene therapy) would modulate food intake (FI) and body weight (BW) in C57Bl6 mice. Short‐term augmentation resulted in transient decrease in FI followed by compensatory feeding. On the contrary, sustained PYY transgene expression in the salivary gland resulted in a significant reduction of FI and 24% decrease of BW in diet‐induced obese mice over the eight weeks study. A conditioned taste aversion (CTA) test was used to determine the mechanism of FI reduction. Intra‐peritoneal administration of PYY3‐36, or LiCl produced CTA to the paired flavored chow, whereas no such response was documented in response to the augmentation of the salivary PYY3‐36. Furthermore, hypothalamic c‐fos activation had been investigated in response to the acute salivary PYY3‐36 augmentation. Interestingly, the treatment induced hypothalamic nuclei similar to the ones activated during re‐feeding. In conclusion, we describe the existence of an alternative satiation pathway mediated by salivary PYY3‐36 suggesting novel pharmacological and/or genetic approaches to treat obesity.