Abstract
Nutrients in the intestine inhibit food intake via an action on the vagal afferent pathway. The aim of the present study was to use immunochemical detection of Fos protein-like immunoreactivity (FLI) in the brainstem to trace the neuronal pathways activated by intestinal nutrients. Perfusion of the intestine of awake rats via an indwelling duodenal catheter with iso-osmotic mannitol, hydrochloric acid or casein hydrolysate had no effect on the number of FLI neurons in the nucleus of the solitary tract (NTS). Lipid emulsion (20%) and 2.7 M glucose significantly increased the number of immunopositive cells in the NTS. There was a significant increase in the number of immunopositive cells from caudal to rostral NTS. Nutrients effective at decreasing food intake (carbohydrate and fat) produced significant increases in Fos-like immunopositive cells in the NTS.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 266-270 |
| Number of pages | 5 |
| Journal | Brain Research |
| Volume | 663 |
| Issue number | 2 |
| DOIs | |
| State | Published - Nov 14 1994 |
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Keywords
- Carbohydrate
- Fos-like immunoreactivity
- Immunocytochemistry
- Lipid
- Nucleus of the solitary tract
- Small intestine
ASJC Scopus subject areas
- Developmental Biology
- Molecular Biology
- Clinical Neurology
- Neuroscience(all)
Cite this
Fos protein expression in the nucleus of the solitary tract in response to intestinal nutrients in awake rats. / Zittel, Tilman T.; De Giorgio, Roberto; Sternini, Catia; Raybould, Helen E.
In: Brain Research, Vol. 663, No. 2, 14.11.1994, p. 266-270.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Fos protein expression in the nucleus of the solitary tract in response to intestinal nutrients in awake rats
AU - Zittel, Tilman T.
AU - De Giorgio, Roberto
AU - Sternini, Catia
AU - Raybould, Helen E
PY - 1994/11/14
Y1 - 1994/11/14
N2 - Nutrients in the intestine inhibit food intake via an action on the vagal afferent pathway. The aim of the present study was to use immunochemical detection of Fos protein-like immunoreactivity (FLI) in the brainstem to trace the neuronal pathways activated by intestinal nutrients. Perfusion of the intestine of awake rats via an indwelling duodenal catheter with iso-osmotic mannitol, hydrochloric acid or casein hydrolysate had no effect on the number of FLI neurons in the nucleus of the solitary tract (NTS). Lipid emulsion (20%) and 2.7 M glucose significantly increased the number of immunopositive cells in the NTS. There was a significant increase in the number of immunopositive cells from caudal to rostral NTS. Nutrients effective at decreasing food intake (carbohydrate and fat) produced significant increases in Fos-like immunopositive cells in the NTS.
AB - Nutrients in the intestine inhibit food intake via an action on the vagal afferent pathway. The aim of the present study was to use immunochemical detection of Fos protein-like immunoreactivity (FLI) in the brainstem to trace the neuronal pathways activated by intestinal nutrients. Perfusion of the intestine of awake rats via an indwelling duodenal catheter with iso-osmotic mannitol, hydrochloric acid or casein hydrolysate had no effect on the number of FLI neurons in the nucleus of the solitary tract (NTS). Lipid emulsion (20%) and 2.7 M glucose significantly increased the number of immunopositive cells in the NTS. There was a significant increase in the number of immunopositive cells from caudal to rostral NTS. Nutrients effective at decreasing food intake (carbohydrate and fat) produced significant increases in Fos-like immunopositive cells in the NTS.
KW - Carbohydrate
KW - Fos-like immunoreactivity
KW - Immunocytochemistry
KW - Lipid
KW - Nucleus of the solitary tract
KW - Small intestine
UR - http://www.scopus.com/inward/record.url?scp=0028116708&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0028116708&partnerID=8YFLogxK
U2 - 10.1016/0006-8993(94)91272-6
DO - 10.1016/0006-8993(94)91272-6
M3 - Article
C2 - 7874510
AN - SCOPUS:0028116708
VL - 663
SP - 266
EP - 270
JO - Brain Research
JF - Brain Research
SN - 0006-8993
IS - 2
ER -