Direct effects of nutrients, acetylcholine, CCK, and insulin on ghrelin release from the isolated stomachs of rats

Shrestha, Yogendra B.; Wickwire, Kathie; Giraudo, Silvia Q.

doi:10.1016/j.peptides.2009.02.001

Cited by 36 publications

(27 citation statements)

References 43 publications

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“…Instead, because of the close association of ghrelin cells with the capillary network pervading the lamina propria (Date et al 2000), T1R3 expression might enable them to respond to signals emanating from the blood stream, particularly with regard to the serum concentrations of amino acids or glucose. Indeed, the intravenous application of various nutrients has been reported to affect ghrelin release (McCowen et al 2002;Qader et al 2005;Murray et al 2006;Shrestha et al 2009). Similarly, upon the transient rise in the concentrations of glucose and free amino acids in the blood serum after a meal (Kruger et al 2006), the release of ghrelin must be suppressed.…”

Section: Discussionmentioning

confidence: 99%

T1R3 is expressed in brush cells and ghrelin-producing cells of murine stomach

2010

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Various digestive and enteroendocrine signaling processes are constantly being adapted to the chemical composition and quantity of the chyme contained in the diverse compartments of the gastrointestinal tract. The chemosensory monitoring that underlies the adaptive capacity of the gut is thought to be performed by so called brush cells that share morphological and molecular features with gustatory sensory cells. A substantial population of brush cells is localized in the gastric mucosa. However, no chemosensory receptors have been found to be expressed in these cells so far, challenging the concept that they serve a chemosensory function. The canonical chemoreceptors for the detection of macronutrients are taste receptors belonging to the T1R family; these have been identified in several tissues in addition to the gustatory system including the small intestine. We demonstrate the expression of the T1R subtype T1R3, which is essential for the detection of both sugars and amino acids in the gustatory system, in two distinct cell populations of the gastric mucosa. One population corresponds to open-type brush cells, emphasizing the notion that they are a chemosensory cell type; T1R3 immunoreactivity in these cells is restricted to the apical cell pole, which might provide the basis for the detection of luminal macronutrient compounds. The second gastric T1R3-positive population consists of closed-type endocrine cells that produce ghrelin. This finding suggests that ghrelin-releasing cells, which lack access to the stomach lumen, might receive chemosensory input from macronutrients in the circulation via T1R3.

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Section: Discussionmentioning

confidence: 99%

T1R3 is expressed in brush cells and ghrelin-producing cells of murine stomach

2010

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“…It is important to note that the central gastroparetic action of CRF is independent of a stimulation of the hypothalamic-pituitary-adrenal axis based on the observation that the gastric-inhibitory response to CRF is still visible in hypophysectomized or adrenalectomized rats [68]. Since CRF is known to reduce vagal efferent activity [69] and acetylcholine stimulates ghrelin release from the stomach [70], the postoperative CRF-induced delay of gastric emptying may be mediated by a reduction of vagal efferent activity. These actions are likely to be CRF 1 mediated as in mice lacking the CRF 1 no postoperative gastric ileus following midline celiotomy, cecal exteriorization and palpation was observed [71] (Table 1).…”

Section: Modulation Of Postoperative Ileus By Brain Peptides and Neurmentioning

confidence: 99%

Brain peptides and the modulation of postoperative gastric ileus

Stengel¹,

Taché²

2014

Current Opinion in Pharmacology

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Postoperative ileus (POI) develops after abdominal surgery irrespective of the site of surgery. When prolonged, POI can lead to longer hospitalization times and higher healthcare costs. Moreover, it is associated with complaints for the patient. In order to develop new strategies to treat this condition, a deeper understanding of the pathophysiology of the POI is necessary. This review will focus on brain peptides (ghrelin, nesfatin-1, somatostatin, corticotropin-releasing factor, thyrotropin-releasing hormone and calcitonin gene-related peptide) involved in the mediation of POI and the possible modulation of these pathways to shorten the time of POI. Lastly, the role of vagal signaling and the possibility of reducing ambient temperature or chewing gum as potential treatment strategies of alleviating symptoms of POI is discussed.

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“…Moreover, differing patient hormonal states (other than ghrelin) may also affect ghrelin production. For instance, ghrelin secretion was reduced by insulin (Kamegai et al, 2004;Shrestha et al, 2009), and increased by cholecystokinin (CCK) (Shrestha et al, 2009) and glucagon (Kamegai et al, 2004). Finally, differing dietary choices by study subjects could be another confounding factor for ghrelin production, since a high-carbohydrate diet produced a more persistent postprandial inhibitory effect on ghrelin secretion than the high-fat diet (Monteleone et al, 2003;Sánchez et al, 2004), which was presumably due to the different satiating capacities of these diets.…”

Section: Other Possible Explanations For the Effect Of Sgas On Circulmentioning

confidence: 99%

The role of ghrelin signalling in second-generation antipsychotic-induced weight gain

Zhang¹,

Deng²,

Huang³

2013

Psychoneuroendocrinology

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Based on clinical and animal studies, this review suggests a tri-phasic effect of second-generation antipsychotics (SGAs) on circulating ghrelin levels: an initial increase exerted by the acute effect of SGAs; followed by a secondary decrease possibly due to the negative feedback from the SGA-induced body weight gain or hyperphagia; and a final re-increase to reach the new equilibrium. Moreover, the results can also vary depending on individual SGAs, other hormonal states, dietary choices, and other confounding factors including medical history, co-treatments, age, gender, and ghrelin measurement techniques. Interestingly, rats treated with olanzapine, an SGA with high weight gain liabilities, are associated with increased hypothalamic ghrelin receptor (GHS-R1a) levels. In addition, expressions of downstream ghrelin signalling parameters at the hypothalamus, including neuropeptide Y (NPY)/agouti-related peptide (AgRP) and proopiomelanocortin (POMC) are also altered under SGA treatments. Thus, understanding the role of ghrelin signalling in antipsychotic drug-induced weight gain should offer potential novel pharmacological targets for tackling the obesity side-effect of SGAs and its associated metabolic syndrome. ABSTRACTBased on clinical and animal studies, this review suggests a tri-phasic effect of second-generation antipsychotics (SGAs) on circulating ghrelin levels: an initial increase exerted by the acute effect of SGAs; followed by a secondary decrease possibly due to the negative feedback from the SGAinduced body weight gain or hyperphagia; and a final re-increase to reach the new equilibrium.Moreover, the results can also vary depending on individual SGAs, other hormonal states, dietary choices, and other confounding factors including medical history, co-treatments, age, gender, and ghrelin measurement techniques. Interestingly, rats treated with olanzapine, an SGA with high weight gain liabilities, are associated with increased hypothalamic ghrelin receptor (GHS-R1a) levels. In addition, expressions of downstream ghrelin signalling parameters at the hypothalamus, including neuropeptide Y (NPY)/ agouti-related peptide (AgRP) and proopiomelanocortin (POMC) are also altered under SGA treatments. Thus, understanding the role of ghrelin signalling in antipsychotic drug-induced weight gain should offer potential novel pharmacological targets for tackling the obesity side-effect of SGAs and its associated metabolic syndrome.

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Direct effects of nutrients, acetylcholine, CCK, and insulin on ghrelin release from the isolated stomachs of rats

Cited by 36 publications

References 43 publications

T1R3 is expressed in brush cells and ghrelin-producing cells of murine stomach

T1R3 is expressed in brush cells and ghrelin-producing cells of murine stomach

Brain peptides and the modulation of postoperative gastric ileus

The role of ghrelin signalling in second-generation antipsychotic-induced weight gain

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