Abscisic Acid Stimulates Glucagon-Like Peptide-1 Secretion from L-Cells and Its Oral Administration Increases Plasma Glucagon-Like Peptide-1 Levels in Rats | Zendy

Santina Bruzzone | Zendy; Mirko Mag | Zendy; Elena Mannino | Zendy; Giovanna Sociali | Zendy; Laura Sturla | Zendy; Chiara Fresia | Zendy; Valeria Booz | Zendy; Laura Emionite | Zendy; Antonio De Flora | Zendy; Elena Zocchi | Zendy

Open Access

Abscisic Acid Stimulates Glucagon-Like Peptide-1 Secretion from L-Cells and Its Oral Administration Increases Plasma Glucagon-Like Peptide-1 Levels in Rats

Author(s) -

Santina Bruzzone,

Mirko Mag,

Elena Mannino,

Giovanna Sociali,

Laura Sturla,

Chiara Fresia,

Valeria Booz,

Laura Emionite,

Antonio De Flora,

Elena Zocchi

Publication year - 2015

Publication title -

plos one

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.99

H-Index - 332

ISSN - 1932-6203

DOI - 10.1371/journal.pone.0140588

Subject(s) - glucose homeostasis , glucagon like peptide 1 , endocrinology , abscisic acid , medicine , enteroendocrine cell , in vivo , glucagon , endogeny , secretion , homeostasis , hormone , chemistry , in vitro , insulin , biology , diabetes mellitus , type 2 diabetes , biochemistry , insulin resistance , endocrine system , microbiology and biotechnology , gene

In recent years, Abscisic Acid (ABA) has been demonstrated to be involved in the regulation of glucose homeostasis in mammals as an endogenous hormone, by stimulating both insulin release and peripheral glucose uptake. In addition, ABA is released by glucose- or GLP-1-stimulated β-pancreatic cells. Here we investigated whether ABA can stimulate GLP-1 release. The human enteroendocrine L cell line hNCI-H716 was used to explore whether ABA stimulates in vitro GLP-1 secretion and/or transcription. ABA induced GLP-1 release in hNCI-H716 cells, through a cAMP/PKA-dependent mechanism. ABA also enhanced GLP-1 transcription. In addition, oral administration of ABA significantly increased plasma GLP-1 and insulin levels in rats. In conclusion, ABA can stimulate GLP-1 release: this result and the previous observation that GLP-1 stimulates ABA release from β -cells, suggest a positive feed-back mechanism between ABA and GLP-1, regulating glucose homeostasis. Type 2 diabetes treatments targeting the GLP-1 axis by either inhibiting its rapid clearance by dipeptidyl-peptidase IV or using GLP-1 mimetics are currently used. Moreover, the development of treatments aimed at stimulating GLP-1 release from L cells has been considered as an alternative approach. Accordingly, our finding that ABA increases GLP-1 release in vitro and in vivo may suggest ABA and/or ABA analogs as potential anti-diabetic treatments.

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