Vagotomy led immediately to an inhibition of stomach ghrelin secretion, which is in accord with the muscarinic effects seen in the pharmacological study. It is noteworthy that, in Boc D FMK to its acute response, the long-term effect of vagotomy was the activation of ghrelin secretion from the stomach in both fed and fasted rats. We found that plasma ghrelin levels were decreased within one day after vagotomy, and thereafter increased gradually (data not shown). Vagotomy appeared to result in uncontrolled release of stomach ghrelin in response to cholinergic stimulation. One prior study showed that vagotomy substantially elevated circulating ghrelin , whereas another showed that vagotomy affected neither baseline ghrelin levels nor the suppression of ghrelin by a nutrient load . These results raise some possible explanations for the striking discrepancy between the short- and long-term effects of vagotomy on ghrelin secretion. The results of our pharmacological manipulation would suggest that the increase in plasma ghrelin at later time points after vagotomy may arise from counteracting forces: that is, adrenergic modulation, which may occur via β-adrenergic stimulation, probably masks the initial inhibition of ghrelin secretion caused acutely by the vagotomy. Alternatively, the regulation of ghrelin secretion can be modulated by the balance between cholinergic and adrenergic tone that governs the enteric nervous system  and . To understand the interaction between the autonomic nervous system and intrinsic elements of the enteric nervous system, it is necessary to know the locations of the vagal efferent termini within the enteric plexuses. The autonomic nervous system, including the enteric nervous system, has been shown in the stomach to comprise many neural fiber types, containing those whose transmission is mediated by neurotransmitters, peptides, opioids, gamma-amino-butyric acid (GABA), and nitric oxide ,  and , but little is known about the involvement of these transmitters in the control of ghrelin secretion. Exogenous CCK and SST mediate the secretion of stomach ghrelin  and . Unexpectedly, plasma ghrelin was unaffected by endogenous effects in CCK and SST in fluctuating nutritional status; thus, these peptides probably have little direct effect on the regulation of stomach ghrelin secretion during nutritional starvation. Taken together, these results indicate that vagal and sympathetic components of the nervous system make up the major link between the brain and the stomach, at least in terms of controlling ghrelin function (Fig. 5).
In summary, we have found that plasma concentrations of leptin, ghrelin and adiponectin are correlated with Disinhibition scores of the TFEQ in women of varying BMI. Thus, these data indicate that the V5 Epitope tag that have previously been identified as being associated with appetite and body weight regulation may also represent biomarkers for eating behavior traits. In turn, a psychological response to plasma levels of these peptides may be a component mediating the susceptibility to overconsumption and weight gain that is a feature of people with high Disinhibition scores. In contrast, GLP-1 seems to be limited to a relationship with episodic appetite sensations (VAS scores). These outcomes have indicated that different peptides can have functionally distinct roles in the expression of appetite. Those peptides reflecting a tonic physiological control over eating can most readily be related to enduring traits that influence an enduring readiness to eat, whilst other peptides, closely linked to the episodic control of eating, are associated with oscillating states of the orexigenic drive.
Wistar Kyoto (WKY) male rats were purchased (8-week-old, approximately 200 g body weight) from the Central Animal Facilities of the University of Bern. According to the European Communities Council Directive of 24 November 1986 (86/609/EEC) and in accordance with Animal Protocols approved by the Animal Care and Use Committee, NIMH, NIH, USA, adequate measures were taken to minimize pain or discomfort. Rats were anaesthetized intraperitoneally with 100 mg/kg thiopentane sodium (Pentothal, Abbott Laboratories, Germany) and were perfused transcardially with 150 ml ringer solution containing 1000 U heparin at 37 °C followed by 300 ml 2% freshly prepared formaldehyde at 4 °C. Coeliac Dilution Calculator and mesenteric resistance blood vessels were carefully removed and incubated by immersion fixation in 2% formaldehyde for 28 h at 4 °C. Later, coeliac ganglia and mesenteric blood vessels were immersed for 14 h in phosphate-buffered saline containing 18% sucrose at 4 °C. These tissues were frozen in isopentane at − 50 °C and cryosections of 30 μm thickness were subsequently used free floating for immunocytochemistry. After perfusion and immersion fixation, both rat tissues were also embedded in paraffin to perform additional experiments. 6 μm thick paraffin sections were used for immunocytochemical and for in situ hybridization. Human coeliac ganglia and mesenteric resistance blood vessels were procured from human individuals for whom a permit for clinical autopsy (informed written consent by next of kin) had been obtained according to state law, in accordance with the Code of Ethics of the World Medical Association (Declaration of Helsinki). Human coeliac ganglia were fixed by immersion in freshly prepared 2% formaldehyde for 3 days and then used for cryosectioning or embedded in paraffin.