Evidence for glucagon-like peptide-1 receptor signaling to activate ATP-sensitive potassium channels in pancreatic beta cells

Kwon, Hye-Jung; Park, Hyunsun; Park, Sung-Hee; Park, Jae-Hyung; Shin, Su‐Kyung; Song, Suk-Won; Hwang, Meeyul; Cho, Ho-Chan; Song, Dae‐Kyu

doi:10.1016/j.bbrc.2015.11.127

Cited by 7 publications

(9 citation statements)

References 29 publications

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“…A new generation of antidiabetics, such as those acting as incretinomimetics, has an advantage over sulfonylureas. As with GLP-1, these drugs act by inactivating the K ATP channel at high glucose concentrations, but when glucose levels decrease, they may promote the opening of these channels by other mechanisms [ 34 ]. This duality of GLP-1 allows better control of insulin secretion and prevents beta cell overload.…”

Section: Discussionmentioning

confidence: 99%

Stevia Nonsweetener Fraction Displays an Insulinotropic Effect Involving Neurotransmission in Pancreatic Islets

Piovan

Pavanello

Peixoto

et al. 2018

International Journal of Endocrinology

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Stevia rebaudiana (Bert.) Bertoni besides being a source of noncaloric sweeteners is also an important source of bioactive molecules. Many plant extracts, mostly obtained with ethyl acetate solvent, are rich in polyphenol compounds that present insulinotropic effects. To investigate whether the nonsweetener fraction, which is rich in phenolic compounds isolated from Stevia rebaudiana with the solvent ethyl acetate (EAF), has an insulinotropic effect, including interference at the terminals of the autonomic nervous system of the pancreatic islets of rats. Pancreatic islets were isolated from Wistar rats and incubated with EAF and inhibitory or stimulatory substances of insulin secretion, including cholinergic and adrenergic agonists and antagonists. EAF potentiates glucose-stimulated insulin secretion (GSIS) only in the presence of high glucose and calcium-dependent concentrations. EAF increased muscarinic insulinotropic effects in pancreatic islets, interfering with the muscarinic receptor subfamily M3. Adrenergic inhibitory effects on GSIS were attenuated in the presence of EAF, which interfered with the adrenergic α 2 receptor. Results suggest that EAF isolated from stevia leaves is a potential therapy for treating type 2 diabetes mellitus by stimulating insulin secretion only in high glucose concentrations, enhancing parasympathetic signal transduction and inhibiting sympathetic signal transduction in beta cells.

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Section: Discussionmentioning

confidence: 99%

Stevia Nonsweetener Fraction Displays an Insulinotropic Effect Involving Neurotransmission in Pancreatic Islets

Piovan

Pavanello

Peixoto

et al. 2018

International Journal of Endocrinology

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“…[ 113 114 ] Besides, it has been used as alternative to conventional hypoglycemic agents and insulin injectable therapies since it has a lower risk of causing hypoglycemia[ 115 ] because the GLP-1 has alternative mechanisms may act as negative feedback pathway for insulin secretion, activating the K ATP channels through phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)-dependent pathway. [ 10 ]…”

Section: Discussionmentioning

confidence: 99%

“…The glucose is the most potent stimulator of insulin secretion and can achieve acute and long-term regulation of insulin secretion. [ 8 ] However, other nutrients also are capable of triggering insulin release or amplify glucose-stimulated insulin secretions (GSISs)[ 9 ] such as hormones,[ 10 ] proteins,[ 11 12 ] and pharmacological agents. [ 13 ]…”

Section: Introductionmentioning

confidence: 99%

Influence of flavonoids on mechanism of modulation of insulin secretion

Soares¹,

Leal²,

Silva³

et al. 2017

Phcog Mag

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Background:The development of alternatives for insulin secretion control in vivo or in vitro represents an important aspect to be investigated. In this direction, natural products have been progressively explored with this aim. In particular, flavonoids are potential candidates to act as insulin secretagogue.Objective:To study the influence of flavonoid on overall modulation mechanisms of insulin secretion.Methods:The research was conducted in the following databases and platforms: PubMed, Scopus, ISI Web of Knowledge, SciELO, LILACS, and ScienceDirect, and the MeSH terms used for the search were flavonoids, flavones, islets of Langerhans, and insulin-secreting cells.Results:Twelve articles were included and represent the basis of discussion on mechanisms of insulin secretion of flavonoids. Papers in ISI Web of Knowledge were in number of 1, Scopus 44, PubMed 264, ScienceDirect 511, and no papers from LILACS and SciELO databases.Conclusion:According to the literature, the majority of flavonoid subclasses can modulate insulin secretion through several pathways, in an indication that corresponding molecule is a potential candidate for active materials to be applied in the treatment of diabetes.SUMMARY The action of natural products on insulin secretion represents an important investigation topic due to their importance in the diabetes controlIn addition to their typical antioxidant properties, flavonoids contribute to the insulin secretionThe modulation of insulin secretion is induced by flavonoids according to different mechanisms. Abbreviations used: KATP channels: ATP-sensitive K+ channels, GLUT4: Glucose transporter 4, ERK1/2: Extracellular signal-regulated protein kinases 1 and 2, L-VDCCs: L-type voltage-dependent Ca+2 channels, GLUT1: Glucose transporter 1, AMPK: Adenosine monophosphate-activated protein kinase, PTP1B: Protein tyrosine phosphatase 1B, GLUT2: Glucose transporter 2, cAMP: Cyclic adenosine monophosphate, PKA: Protein kinase A, PTK: Protein tyrosine kinase, CaMK II: Ca2+/calmodulin-dependent protein kinase II, GSIS: Glucose-stimulated insulin secretion, Insig-1: Insulin-induced gene 1, IRS-2: Insulin receptor substrate 2, PDX-1: Pancreatic and duodenal homeobox 1, SREBP-1c: Sterol regulatory element binding protein-1c, DMC: Dihydroxy-6’-methoxy-3’,5’-dimethylchalcone, GLP-1: Glucagon-like peptide-1, GLP-1R: Glucagon-like peptide 1 receptor.

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“…The translocation of TRPM4 from a vesicular pool and its subsequent fusion with the plasma membrane via Ca 2+ -dependent exocyto- [37,38]. There have been many efforts to determine the mechanistic pathway by which GLP-1 elicits a positive effect on insulin secretion and to identify the type of ion channels responsible or to clarify the mechanistic site involved in this fundamentally pivotal physiology [15,[39][40][41][42][43][44][45][46]. Rapid progress and findings regarding these open questions were made following the report that TRPM2-deficient mice showed a lack of effect of GLP-1 on insulin secretion [17,36].…”

Section: Glucose-induced Regulation Of Trpm2-channel Current and Insumentioning

confidence: 99%

Glucose and GTP-binding protein-coupled receptor cooperatively regulate transient receptor potential-channels to stimulate insulin secretion [Review]

et al. 2016

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Abstract. In pancreatic β-cells, glucose-induced closure of the ATP-sensitive K + (KATP) channel is an initial process triggering glucose-stimulated insulin secretion (GSIS). This KATP-channel dependent pathway has been believed to be a central mechanism for GSIS. However, since the resting membrane potential of cells is determined by the balance of the net result of current amplitudes in outward and inward directions, it must be taken into consideration that not only KATP channel inhibition but also inward current via the basal opening of non-selective cation channels (NSCCs) plays a crucial role in membrane potential regulation. The basal activity of NSCCs is essential to effectively evoke depolarization in concert with KATP channel closure that is dependent on glucose metabolism. The present study summarizes recent findings regarding the roles of NSCCs in GSIS and GTP-binding protein coupled receptor-(GPCR) operated potentiation of GSIS. Key words: GPCR, Pancreatic β-cells, TRP channel, Insulin secretionTHE CONCEPT that glucose-stimulated insulin secretion (GSIS) in pancreatic β-cells is initiated by closure of the ATP-sensitive K + (KATP) channel as a result of an increase in the intracellular ATP/ADP ratio induced by glucose metabolism upon elevation of glucose concentration in the blood ( Fig. 1; the triggering pathway), was proposed a long time ago [1][2][3]. Inhibition of the KATP channel is followed by membrane depolarization and activation of voltage-dependent Ca 2+ channels (VDCCs) [4,5]. Opening of the VDCCs brings about firing of action potential, cytosolic Ca 2+ increase and initiation of GSIS [6,7]. The triggering pathway is followed by time-dependent increase in insulin secretion that is potentiated by glucose exposure (the second phase, potentiating pathway or KATP-independent pathway) [3,8] However, closure of the KATP channel alone is not sufficient to induce a shift in the membrane potential towards the threshold level and for the triggering pathway that can activate VDCCs, since membrane potential is theoretically determined by the overall balance of outward and inward currents. Modest background inward currents through opening of nonselective cation channels (NSCCs) are crucial for induction of membrane depolarization following KATP channel closure [9,10]. This idea further suggests that regulation of a class of NSCCs may play an important role in producing effective depolarization of the membrane. Several types of NSCCs have been reported to be expressed in pancreatic β-cells, which, in terms of ion selectivity, are permeable to Na + , K + , and Ca 2+ . In contrast to these ion channels, which have not been well studied, the classic-type ion channels; i.e., the voltage-dependent Na + channel, the voltage-dependent K + channel [11,12], the voltage-dependent Ca 2+ channel [13,14] and the KATP channel have attracted a large amount of interest for a long time, because the first three types of these ion channels play an important role in membrane excitability and the KATP

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Evidence for glucagon-like peptide-1 receptor signaling to activate ATP-sensitive potassium channels in pancreatic beta cells

Cited by 7 publications

References 29 publications

Stevia Nonsweetener Fraction Displays an Insulinotropic Effect Involving Neurotransmission in Pancreatic Islets

Stevia Nonsweetener Fraction Displays an Insulinotropic Effect Involving Neurotransmission in Pancreatic Islets

Influence of flavonoids on mechanism of modulation of insulin secretion

Glucose and GTP-binding protein-coupled receptor cooperatively regulate transient receptor potential-channels to stimulate insulin secretion [Review]

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