Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Small intestinal epithelial cells interact with a rather high concentration of fatty acids derived from the diet. These fatty acids directly or indirectly regulate the functions of the small intestine. We report here that linoleic acid and oleic acid markedly increased the influx of 45Ca2+ into the small intestinal epithelial cell line (IEC 6). By contrast, octanoic acid, methyl linoleate, and linolyl alcohol had no effect on the influx. Acidic amino acids, methyl linoleate, and linolyl alcohol, inhibited the linoleic acid-induced influx of 45Ca2+, indicating that activation of the influx by linoleic acid depended on the chain length and was affected by the presence of a carboxyl group. Of the gastrointestinal hormones, somatostatin specifically inhibited the linoleic acid-induced influx of 45Ca2+.
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PMID:The recognition system of dietary fatty acids by the rat small intestinal cells. 776 87

Valproate (VPA) can suppress absence and other seizures, but its precise mechanisms of action are not completely understood. We investigated whether VPA influences the expression of neuropeptide Y (NPY), an endogenous anticonvulsant. Chronic VPA administration to young rats (300-600 mg.kg(-1).d(-1) in divided doses over 4 d) resulted in a 30-50% increase in NPY mRNA and protein expression in the nucleus reticularis thalami (nRt) and hippocampus, but not in the neocortex, as shown by real-time PCR, radioimmunoassay, and immunohistochemistry. No increased expression was observed after a single acute dose of VPA. Chronic treatment with the pharmacologically inactive VPA analog octanoic acid did not elicit changes in NPY expression. No significant expression changes could be shown for the mRNAs of the Y1 receptor or of the neuropeptides somatostatin, vasoactive intestinal polypeptide, and choleocystokinin. Fewer synchronous spontaneous epileptiform oscillations were recorded in thalamic slices from VPA-treated animals, and oscillation duration as well as the period of spontaneous and evoked oscillations were decreased. Application of the Y1 receptor inhibitor N2-(diphenylacetyl)-N-[(4-hydroxyphenyl)methyl]-D-arginine-amide (BIBP3226) enhanced thalamic oscillations, indicating that NPY is released during those oscillations and acts to downregulate oscillatory strength. Chronic VPA treatment significantly potentiated the effect of BIBP3226 on oscillation duration but not on oscillation period. These results demonstrate a novel mechanism for the antiepileptic actions of chronic VPA therapy.
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PMID:Chronic valproic acid treatment triggers increased neuropeptide y expression and signaling in rat nucleus reticularis thalami. 1769 70