Oleoyl-lysophosphatidylinositol enhances glucagon-like peptide-1 secretion from enteroendocrine L-cells through GPR119

Arifin, Syamsul; Paternoster, Silvano; Carlessi, Rodrigo; Casari, Ilaria; Ekberg, Jeppe H.; Maffucci, Tania; Newsholme, Philip; Falasca, Marco

doi:10.1016/j.bbalip.2018.06.007

Cited by 18 publications

(9 citation statements)

References 45 publications

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“…However, considering the insignificant influence on GLP-1 release and additional membrane perforation caused by 1-GA-LPC ( Figure 8 D,E), only 1-CA-LPC was chosen to investigate whether GPR40, GPR55, GPR119, and GPR120 receptors were required for 1-CA-LPC -stimulated GLP-1 release. To this end, GLUTag cells were incubated with selective antagonists before stimulation with 1-CA-LPC, since the expression of GPCRs studied hereby was confirmed previously [ 25 , 26 , 27 ].…”

Section: Resultssupporting

confidence: 55%

Isoprenoid Derivatives of Lysophosphatidylcholines Enhance Insulin and GLP-1 Secretion through Lipid-Binding GPCRs

Drzazga

Kamińska

Gliszczyńska

et al. 2021

IJMS

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Insulin plays a significant role in carbohydrate homeostasis as the blood glucose lowering hormone. Glucose-induced insulin secretion (GSIS) is augmented by glucagon-like peptide (GLP-1), a gastrointestinal peptide released in response to ingesting nutriments. The secretion of insulin and GLP-1 is mediated by the binding of nutrients to G protein-coupled receptors (GPCRs) expressed by pancreatic β-cells and enteroendocrine cells, respectively. Therefore, insulin secretagogues and incretin mimetics currently serve as antidiabetic treatments. This study demonstrates the potency of synthetic isoprenoid derivatives of lysophosphatidylcholines (LPCs) to stimulate GSIS and GLP-1 release. Murine insulinoma cell line (MIN6) and enteroendocrinal L cells (GLUTag) were incubated with LPCs bearing geranic acid (1-GA-LPC), citronellic acid (1-CA-LPC), 3,7-dimethyl-3-vinyloct-6-enoic acid (GERA-LPC), and (E)-3,7,11-trimethyl- 3-vinyldodeca-6,10-dienoic acid (1-FARA-LPC). Respective free terpene acids were also tested for comparison. Besides their insulin- and GLP-1-secreting capabilities, we also investigated the cytotoxicity of tested compounds, the ability to intracellular calcium ion mobilization, and targeted GPCRs involved in maintaining lipid and carbohydrate homeostasis. We observed the high cytotoxicity of 1-GERA-LPC and 1-FARA-LPC in contrast 1-CA-LPC and 1-GA-LPC. Moreover, 1-CA-LPC and 1-GA-LPC demonstrated the stimulatory effect on GSIS and 1-CA-LPC augmented GLP-1 secretion. Insulin and GLP-1 release appeared to be GPR40-, GPR55-, GPR119- and GPR120-dependent.

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Section: Resultssupporting

confidence: 55%

Isoprenoid Derivatives of Lysophosphatidylcholines Enhance Insulin and GLP-1 Secretion through Lipid-Binding GPCRs

Drzazga

Kamińska

Gliszczyńska

et al. 2021

IJMS

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“…The primary source of AC is adenosine triphosphate (ATP) mediated by the Class-III AC/ADCY (adenylate cyclase) family. PKA enhances intracellular calcium influx through the phosphorylation of voltage-dependent calcium channel (VDCC), thus increasing insulin secretion [ 86 ] (see Fig. 2 ).…”

Section: Introductionmentioning

confidence: 99%

Targeting the GPR119/incretin axis: a promising new therapy for metabolic-associated fatty liver disease

Zhao

et al. 2021

Cell Mol Biol Lett

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In the past decade, G protein-coupled receptors have emerged as drug targets, and their physiological and pathological effects have been extensively studied. Among these receptors, GPR119 is expressed in multiple organs, including the liver. It can be activated by a variety of endogenous and exogenous ligands. After GPR119 is activated, the cell secretes a variety of incretins, including glucagon-like peptide-1 and glucagon-like peptide-2, which may attenuate the metabolic dysfunction associated with fatty liver disease, including improving glucose and lipid metabolism, inhibiting inflammation, reducing appetite, and regulating the intestinal microbial system. GPR119 has been a potential therapeutic target for diabetes mellitus type 2 for many years, but its role in metabolic dysfunction associated fatty liver disease deserves further attention. In this review, we discuss relevant research and current progress in the physiology and pharmacology of the GPR119/incretin axis and speculate on the potential therapeutic role of this axis in metabolic dysfunction associated with fatty liver disease, which provides guidance for transforming experimental research into clinical applications.

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“…An obvious candidate mechanism for such actions could be the activation of the b-arrestin pathway, which is not only capable of desensitizing and downregulating Gproteinecoupled receptors but can also activate the ERK1/2 MAPK cascade (Pouysségur, 2000). In line with this, in a recent study, effects of oleoyl-lysophosphatidylinositol on glucagon-like peptide-1 secretion from L-cells were found to be mediated via GPR119 and the subsequent activation of ERK1/2 MAPK as well as the cAMP/protein kinase A/CREB pathways (Arifin et al, 2018), whereas in another study, activation of GPR119 was followed by cAMP accumulation, Ca 2þ signal, and ERK1/2 MAPK activation (Zhang et al, 2014). In our hands, OEA (50 mM) had no effect on the Ca 2þ homeostasis of the sebocytes (acute treatment; Supplementary Figure S5) and only tended to elevate cAMP level of the sebocytes (60 minutes; Figure 4c).…”

Section: Discussionmentioning

confidence: 74%

GPR119 Is a Potent Regulator of Human Sebocyte Biology

Markovics

Angyal

Tóth

et al. 2020

Journal of Investigative Dermatology

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We have shown previously that endocannabinoids promote sebaceous lipogenesis, and sebocytes are involved in the metabolism of the endocannabinoid-like substance oleoylethanolamide (OEA). OEA is an endogenous activator of GPR119, a recently deorphanized receptor, which currently is being investigated as a promising antidiabetic drug target. In this study, we investigated the effects of OEA as well as the expression and role of GPR119 in human sebocytes. We found that OEA promoted differentiation of human SZ95 sebocytes (elevated lipogenesis, enhanced granulation, and the induction of early apoptotic events), and it switched the cells to a proinflammatory phenotype (increased expression and release of several proinflammatory cytokines). Moreover, we could also demonstrate that GPR119 was expressed in human sebocytes, and its small interfering RNAemediated gene silencing suppressed OEA-induced sebaceous lipogenesis, which was mediated via c-Jun N-terminal kinase, extracellular signaleregulated kinase 1/2, protein kinase B, and CRE-binding protein activation. Finally, our pilot data demonstrated that GPR119 was downregulated in the sebaceous glands of patients with acne, arguing that GPR119 signaling may indeed be disturbed in acne. Collectively, our findings introduce the OEA/GPR119 signaling as a positive regulator of sebocyte differentiation and highlight the possibility that dysregulation of this pathway may contribute to the development of seborrhea and acne.

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Oleoyl-lysophosphatidylinositol enhances glucagon-like peptide-1 secretion from enteroendocrine L-cells through GPR119

Cited by 18 publications

References 45 publications

Isoprenoid Derivatives of Lysophosphatidylcholines Enhance Insulin and GLP-1 Secretion through Lipid-Binding GPCRs

Isoprenoid Derivatives of Lysophosphatidylcholines Enhance Insulin and GLP-1 Secretion through Lipid-Binding GPCRs

Targeting the GPR119/incretin axis: a promising new therapy for metabolic-associated fatty liver disease

GPR119 Is a Potent Regulator of Human Sebocyte Biology

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