Prostaglandin E ₂ : a Neuromodulator in the Central Control of Gastrointestinal Motility and Feeding Behavior by Calcitonin

Abstract

Two micrograms of prostaglandin E2 injected into the lateral ventricle of the brain in rats had the same anorectic and gastrointestinal motor effect as central administration of 0.02 unit of calcitonin. The effects of calcitonin were blocked by a previous intracerebroventricular administration of 0.25 milligram of indomethacin. These results suggest that both anorectic and gastrointestinal motor effects of calcitonin are centrally mediated by the release of prostaglandins.

Procalcitonin N-Terminal Peptide Causes Catabolic Effects via the Hypothalamus and Prostaglandin-Dependent Pathways

“…Our results also show that ICV administered N-PCT has similar effects on body temperature and feeding behavior as those elicited by ICV injection of CT [2, 3] and proinflammatory cytokines via the eicosanoid cyclooxygenase pathway [39, 47]. This study did not address the issue of whether N-PCT induces c-Fos in CT-like receptors or cytokine containing neurons in the hypothalamus, but the response occurs rapidly.…”

“…The reduction in the intake of food and the hyperthermia, following the ICV injection of a single dose of N-PCT, coincide with the effects observed following the ICV administration of CT and other CT-like peptides [1,2,3, 41]. These findings, together with the localization of N-PCT in hypothalamic areas associated with thermogenesis and feeding behavior in which the CT-R was abundantly expressed [2, 3], suggest that N-PCT could elicit its catabolic effects via the CT-like receptors. However, this hypothesis is not supported by the data in the present study.…”

“…Intracerebroventricular (ICV) administration of CT has various physiological actions affecting energy homeostasis (i.e., diminution of appetite, hyperthermia and reduction of locomotor activity) [1]. These effects of CT are supposed to be mediated through direct action on the CNS, by specific binding to CT receptors (CT-R) and subsequently formation and release of prostaglandins (PGs) [2, 3]. Expression of the CT-R gene and specific CT-R for biologically active CT has been recognized in rat brain [4,5,6,7].…”

Pathogenic Importance of Intestinal Hypermotility in NSAID-Induced Small Intestinal Damage in Rats

“…Since the intraluminal pressure measured in the present study is more affected by contraction of circular smooth muscle than longitudinal smooth muscle, the method to measure intestinal motility would account for the different results. On the other hand, Fargeas and co-workers [31, 32]reported that intracerebroventricular indomethacin affects intestinal motility, probably by decreasing the level of PG in the hypothalamus, and suggested a possible role for PG as a central neuromodulator of gut motility. Thus, it is possible that NSAIDs produce intestinal hypermotility mediated by central as well as peripheral actions.…”

The role of genetic variation across IL-1β, IL-2, IL-6, and BDNF in antipsychotic-induced weight gain

“…In addition, prostaglandins, especially PGE 2 , and their precursors have been shown to reduce food intake and influence GI motility [381][382][383][384][385][386] . C-fos mRNA studies show that central injection of PGE 2 activates neurons within the PVN 387 .…”