Gut vagal afferent lesions increase meal size but do not block gastric preload-induced feeding suppression

Citation
Gj. Schwartz et al., Gut vagal afferent lesions increase meal size but do not block gastric preload-induced feeding suppression, AM J P-REG, 45(6), 1999, pp. R1623-R1629
Citations number
31
Categorie Soggetti
Physiology
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
ISSN journal
03636119 → ACNP
Volume
45
Issue
6
Year of publication
1999
Pages
R1623 - R1629
Database
ISI
SICI code
0363-6119(199906)45:6<R1623:GVALIM>2.0.ZU;2-1
Abstract
Subdiaphragmatic vagal afferent (SVA) signals arising from gut sites may pr ovide critical feedback for the control of food intake within a meal. To ev aluate the role of SVAs in both spontaneous and scheduled meals, food intak e was assessed in two paradigms in male Sprague-Dawley rats. In the first s tudy, control(Con) rats (n = 6) and rats with subdiaphragmatic vagal deaffe rentation (SDA) (n = 7) had 12-h nightly access to Ensure liquid diet (1 kc al/ml). SDA rats had larger and fewer meals and maintained initial rapid ra tes of licking, yet total numbers of licks were unaffected. In the second s tudy, Con (n = 8) and SDA (n = 7) rats had scheduled access to 12.5% liquid glucose after overnight food deprivation. Glucose intake was assessed afte r 5-ml gastric preloads of 0.9% saline or glucose, peptone, and Intralipid solutions at three concentrations (0.5, 1, and 2 kcal/ml). Glucose and pept one preloads suppressed intake similarly in Con and SDA rats, whereas Intra lipid was ineffective. These results suggest that meal-related SVA signals 1) are not critical in determining preload-induced feeding suppression afte r deprivation, yet 2) contribute to satiety during spontaneous meals.