Low glucose-induced ghrelin secretion is mediated by an ATP-sensitive potassium channel

Oya, Manami; Kitaguchi, Tetsuya; Harada, Kazuki; Sato, Takahiro; Kojima, Masayasu; Tsuboi, Takashi

doi:10.1530/joe-15-0090

Cited by 6 publications

(4 citation statements)

References 59 publications

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“…Oya et al showed that low (1 mM), normoglycemic (5 mM) and high (10 mM) concentrations of d -glucose increased ghrelin secretion compared to 25 mM d -glucose in MGN3-1 cells [38]. …”

Section: Discussionmentioning

confidence: 99%

“…However, inhibitors for SGLT1 and the GLUT family could not confirm an involvement of these proposed glucose-sensors in the effect of d -glucose on octanoyl ghrelin secretion. Previous studies also suggested that ATP-sensitive potassium (K ATP ) channels are involved in the effect of 25 mM d -glucose on ghrelin secretion in MGN3-1 cells [38]. However, tolbutamide (a potassium channel blocker) and diazoxide (a potassium channel activator) neither enhanced nor inhibited 1, 5 or 10 mM glucose-induced ghrelin secretion in primary cultures of gastric mucosal cells [37].…”

Section: Discussionmentioning

confidence: 99%

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The Sweetener-Sensing Mechanisms of the Ghrelin Cell

2016

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Carbohydrate administration decreases plasma levels of the ‘hunger hormone’ ghrelin. The ghrelin cell is co-localized with the sweet taste receptor subunit, TAS1R3, and the gustatory G-protein, gustducin, both involved in the sensing of sweeteners by entero-endocrine cells. This study investigated the role of gustducin-mediated sweet taste receptor signaling on ghrelin secretion in a gastric ghrelinoma cell line, tissue segments and mice. The monosaccharide d-glucose and low-intensity sweetener oligofructose (OFS) decreased (p < 0.001) ghrelin secretion while the high-intensity sweetener sucralose increased (p < 0.001) ghrelin secretion in vitro. These effects were not mediated via the sweet taste receptor or glucose transporters (the sodium-dependent glucose cotransporter SGLT-1 and GLUT2). The effect of these compounds was mimicked ex vivo in gastric and jejunal segments from both wild type (WT) and α-gustducin knockout (α-gust−/−) mice. In vivo, the sensing of d-glucose was polarized since intragastric but not intravenous administration of d-glucose decreased (p < 0.05) ghrelin levels in an α-gustducin independent manner which involved inhibition of duodenal ghrelin release. In contrast, neither OFS nor sucralose affected ghrelin secretion in vivo. In conclusion, α-gustducin-mediated sweet taste receptor signaling does not play a functional role in the sensing of carbohydrates, or low- or high-intensity sweeteners by the ghrelin cell.

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“…Oya et al showed that low (1 mM), normoglycemic (5 mM) and high (10 mM) concentrations of d -glucose increased ghrelin secretion compared to 25 mM d -glucose in MGN3-1 cells [38]. …”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The Sweetener-Sensing Mechanisms of the Ghrelin Cell

2016

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“…Another metabolic regulatory hormone, ghrelin, is secreted pre-prandially from cells in the gut and is thought to help prepare the body for nutrient uptake (Muller, T. D., et al, 2015). Recently, a ghrelin-expressing cell line was shown to secrete in a manner dependent upon K ATP channels (Oya, et al, 2015). In contrast, using the diazoxide paradigm in primary ghrelin cells, no function was found for K ATP channels in ghrelin secretion (Sakata, et al, 2012).…”

Section: Metabolic Amplification Of Hormone Secretion From Non-β Cellsmentioning

confidence: 99%

Mechanisms of the amplifying pathway of insulin secretion in the β cell

Kalwat

Cobb

2017

Pharmacology & Therapeutics

121

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Pancreatic islet β cells secrete insulin in response to nutrient secretagogues, like glucose, dependent on calcium influx and nutrient metabolism. One of the most intriguing qualities of β cells is their ability to use metabolism to amplify the amount of secreted insulin independent of further alterations in intracellular calcium. Many years studying this amplifying process have shaped our current understanding of β cell stimulus-secretion coupling; yet, the exact mechanisms of amplification have been elusive. Recent studies utilizing metabolomics, computational modeling, and animal models have progressed our understanding of the metabolic amplifying pathway of insulin secretion from the β cell. New approaches will be discussed which offer in-roads to a more complete model of β cell function. The development of β cell therapeutics may be aided by such a model, facilitating the targeting of aspects of the metabolic amplifying pathway which are unique to the β cell.

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“…Dopamine, isoproterenol, oxytocin, muscarine, and prostaglandin (E2) enhance ghrelin secretion, whereas lactate, palmitate, and somatostatin inhibit ghrelin secretion [10,11]. Chemicals, such as cinnamon, and changes in blood glucose levels also regulate ghrelin secretion, suggesting the existence of multiple regulatory mechanisms [12][13][14]. Ghrelin might be associated with gastrointestinal peristalsis, also known as the migrating motor complex, in humans and mice, although no conclusive results have been obtained [15,16].…”

Section: Introductionmentioning

confidence: 99%

Potential Role of TRPV4 in Stretch-Induced Ghrelin Secretion and Obesity

Hayakawa

Tanaka

Ogawa

et al. 2022

International Journal of Endocrinology

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Obesity is an important health problem, which can be prevented through appetite control. Ghrelin is an appetite-stimulating hormone considered to promote obesity. Thus, we examined whether gastric stretching affects ghrelin secretion. We investigated the role of transient receptor potential vanilloid 4 (TRPV4) in gastric glands in the regulation of ghrelin secretion. TRPV4 immunostaining was performed in tissue samples from 57 patients who underwent gastrectomy. TRPV4 expression was compared between patients with (body mass index (BMI) ≥ 30) and without (BMI <30) obesity. For in vitro experiments, we used MGN3-1 cells, a ghrelin-producing cell line derived from mice. To investigate the bioactivity of TRPV4, MGN3-1 cells were treated with TRPV4 agonists and antagonists, and changes in intracellular Ca2+ concentration were confirmed. The concentration of ghrelin in the cell supernatant was measured using the ELISA with and without 120% stretch stimulation. TRPV4 expression was significantly higher in patients with obesity than in those without at all sites, except the fornix. Immunostaining confirmed the expression of TRPV4 in MGN3-1 cells. TRPV4 agonist administration increased intracellular Ca2+ concentration and ghrelin secretion in MGN3-1 cells, whereas the administration of the agonist combined with the antagonist decreased intracellular Ca2+ concentration and ghrelin secretion. Ghrelin secretion significantly increased in response to a 120% stretch in MGN3-1 cells. However, secretion was not increased by stretch when cells were treated with a TRPV4 antagonist. TRPV4 regulates ghrelin secretion in response to stretch in the stomach, which may affect body weight.

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Low glucose-induced ghrelin secretion is mediated by an ATP-sensitive potassium channel

Cited by 6 publications

References 59 publications

The Sweetener-Sensing Mechanisms of the Ghrelin Cell

The Sweetener-Sensing Mechanisms of the Ghrelin Cell

Mechanisms of the amplifying pathway of insulin secretion in the β cell

Potential Role of TRPV4 in Stretch-Induced Ghrelin Secretion and Obesity

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