Differential effects of sham feeding and meal ingestion on ghrelin and pancreatic polypeptide levels: evidence for vagal efferent stimulation mediating ghrelin release1

Simonian, Hrair P.; Kresge, Karen; Boden, Günther; Parkman, HP

doi:10.1111/j.1365-2982.2004.00634.x

Cited by 76 publications

(47 citation statements)

References 29 publications

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“…Ghrelin is expressed mainly in the stomach, in neuroendocrine cells in the fundus, from which it is secreted into the circulation [26]. A prior study of ours has shown that in normal subjects there is an increase in ghrelin levels with sham feeding, suggesting that the increase in ghrelin is via a vagal efferent pathway [10]. This was also confirmed in this study.…”

Section: Discussionsupporting

confidence: 76%

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Abnormal Ghrelin and Pancreatic Polypeptide Responses in Gastroparesis

et al. 2006

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Vagal nerve dysfunction has been implicated in the pathogenesis of diabetic gastroparesis, but its role in idiopathic gastroparesis remains uncertain. The increase in pancreatic polypeptide with sham feeding is often used as a measure of vagal integrity. Ghrelin has been suggested to function as an appetite-stimulating hormone from the gut to the brain acting through vagal afferent pathways. Systemic ghrelin also rises in part due to vagal efferent pathways. Alterations in ghrelin and its effects on appetite could play a role in gastroparesis. In this study we aimed [1] to investigate the presence of vagal nerve dysfunction in patients with idiopathic and diabetic gastroparesis and [2] to determine if alterations in ghrelin concentrations occur in gastroparesis. Normal subjects and patients with diabetic, idiopathic, or postsurgical gastroparesis underwent a sham feeding protocol. Serial blood samples were obtained for plasma ghrelin and pancreatic polypeptide. Sham feeding was characterized by an increase in pancreatic polypeptide and ghrelin in normal controls and patients with idiopathic gastroparesis. The changes in pancreatic polypeptide and ghrelin levels in diabetic and postsurgical gastroparesis were significantly less than those in normal subjects. Vagal nerve dysfunction, as evidenced by an impaired pancreatic polypeptide response with sham feeding, is present in diabetic gastroparesis but not idiopathic gastroparesis. Systemic ghrelin concentrations increased with sham feeding in normal subjects and patients with idiopathic gastroparesis but not in diabetic or postsurgical gastroparesis. Vagal function and regulation of ghrelin levels are impaired in diabetic gastroparesis.

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Section: Discussionsupporting

confidence: 76%

“…Increases in ghrelin also occur in diet-induced weight loss; this is consistent with a role of ghrelin in the long term regulation of body weight [9]. Systemic ghrelin rises in part in response to the cephalic phase of vagal efferent stimulation [10]. Interestingly, ghrelin has also been shown to stimulate gastric contractility and emptying [11][12][13][14].…”

mentioning

confidence: 87%

Abnormal Ghrelin and Pancreatic Polypeptide Responses in Gastroparesis

et al. 2006

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“…However, although it is presumed that olive oil stimulates the vagus nerve, we did not incorporate vagus nerve activity into our study. On the other hand, there is evidence that exposure to fat for only 3 min is sufficient to elicit a pancreatic polypeptide response [40]. Secretion of pancreatic polypeptide, a polypeptide secreted by pancreatic peptide cells in the endocrine pancreas, is regulated by cholinergic stimulation [41].…”

Section: Discussionmentioning

confidence: 99%

Nicotinic Acetylcholine Receptor Expression and Susceptibility to Cholinergic Immunomodulation in Human Monocytes of Smoking Individuals

Zanden

Hilbers²,

Verseijden³

et al. 2012

Neuroimmunomodulation

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Objective: Smoking is generally accepted as a factor that affects the disease course in inflammatory bowel disease patients. Whether these effects can be contributed to the immunomodulatory effects of nicotine via nicotinic acetylcholine receptor (nAChR) activation is unclear. As previous data suggest that the α7 nicotinic acetylcholine receptor (CHRNA7) and its duplicated variant CHRFAM7A may specifically participate in the inflammatory response of monocytes, we evaluated whether repeated nicotine exposure or smoking affects monocyte CHRNA7 and CHRFAM7A expression and cholinergic immunomodulation. Methods: The human monocyte cell line THP-I was incubated with nicotine for different time points before endotoxin exposure. In a pilot volunteer study using smoking (n = 4) and nonsmoking (n = 7) individuals, vagal output was stimulated by olive oil administration after which monocytes were analyzed for nicotinic receptor expression. Serum tumor necrosis factor (TNF) levels were determined using ELISA and expression levels of the nAChR subunits CHRNA7, CHRNB2 or CHRFAM7A were analyzed using QPCR. Results: Repeated nicotine exposure upregulated CHRNA7 expression on THP-I monocytes and led to an enhanced potential of α7 nAChR agonist GSK1345038A to reduce TNF levels. Furthermore, CHRNA7 was only detectable in isolated blood monocytes of smokers. On the other hand, the expression of CHRFAM7A and CHRNB2 was not affected by nicotine exposure. Lipopolysaccharides-induced TNF secretion was inhibited by nicotinic receptor activation in THP-I monocytes, but this response was not consistently seen in blood monocytes from smoking individuals. Conclusions: We conclude that CHRNA7 expression on blood monocytes is upregulated in smoking individuals, which may contribute to cholinergic immunomodulation.

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“…Due to the interrupted afferent vagal signalling, exogenous compensatory ghrelin is unable to induce hunger in patients after vagotomy and esophageal or gastric surgery. Moreover, vagal activity is supposed to be responsible for the release of ghrelin from mucosal cells of the gastric fundus [11,12]. Despite inadequate data for assessment whether vagal nerve continuity is beneficial for the morbidly obese patient most bariatric surgeons aim for preserving the anterior vagal trunk that continuous together with the lower part of the posterior trunk down into the fatty tissue of the lesser curvature when constructing the gastric pouch.…”

mentioning

confidence: 99%

Vagal Nerve Dissection During Pouch Formation in Laparoscopic Roux-Y-Gastric Bypass for Technical Simplification: Does it Matter?

et al. 2008

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Differential effects of sham feeding and meal ingestion on ghrelin and pancreatic polypeptide levels: evidence for vagal efferent stimulation mediating ghrelin release¹

Abstract: Plasma ghrelin and pancreatic polypeptide concentrations increase with sham feeding. This suggests a vagal efferent pathway mediating ghrelin release. In contrast to pancreatic polypeptide which rises with actual meal ingestion, ghrelin levels did not change.

Cited by 76 publications

References 29 publications

Abnormal Ghrelin and Pancreatic Polypeptide Responses in Gastroparesis

Abnormal Ghrelin and Pancreatic Polypeptide Responses in Gastroparesis

Nicotinic Acetylcholine Receptor Expression and Susceptibility to Cholinergic Immunomodulation in Human Monocytes of Smoking Individuals

Vagal Nerve Dissection During Pouch Formation in Laparoscopic Roux-Y-Gastric Bypass for Technical Simplification: Does it Matter?

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