The potential role of glutamate in the current diabetes epidemic

Alberto M. Davalli, Carla Perego, Franco B. Folli

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

In the present article, we propose the perspective that abnormal glutamate homeostasis might contribute to diabetes pathogenesis. Previous reports and our recent data indicate that chronically high extracellular glutamate levels exert direct and indirect effects that might participate in the progressive loss of β-cells occurring in both T1D and T2D. In addition, abnormal glutamate homeostasis may impact all the three accelerators of the "accelerator hypothesis" and could partially explain the rising frequency of T1D and T2D.

Original languageEnglish (US)
Pages (from-to)167-183
Number of pages17
JournalActa Diabetologica
Volume49
Issue number3
DOIs
StatePublished - Jun 2012

Fingerprint

Glutamic Acid
Homeostasis

Keywords

  • Diabetes
  • Glutamate toxicity
  • l-Glutamic acid
  • Monosodium glutamate
  • Obesity
  • Pancreatic β-cells

ASJC Scopus subject areas

  • Endocrinology
  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Cite this

The potential role of glutamate in the current diabetes epidemic. / Davalli, Alberto M.; Perego, Carla; Folli, Franco B.

In: Acta Diabetologica, Vol. 49, No. 3, 06.2012, p. 167-183.

Research output: Contribution to journalArticle

Davalli, Alberto M. ; Perego, Carla ; Folli, Franco B. / The potential role of glutamate in the current diabetes epidemic. In: Acta Diabetologica. 2012 ; Vol. 49, No. 3. pp. 167-183.
@article{adbb0c647b4e4835acf3aece41d013b7,
title = "The potential role of glutamate in the current diabetes epidemic",
abstract = "In the present article, we propose the perspective that abnormal glutamate homeostasis might contribute to diabetes pathogenesis. Previous reports and our recent data indicate that chronically high extracellular glutamate levels exert direct and indirect effects that might participate in the progressive loss of β-cells occurring in both T1D and T2D. In addition, abnormal glutamate homeostasis may impact all the three accelerators of the {"}accelerator hypothesis{"} and could partially explain the rising frequency of T1D and T2D.",
keywords = "Diabetes, Glutamate toxicity, l-Glutamic acid, Monosodium glutamate, Obesity, Pancreatic β-cells",
author = "Davalli, {Alberto M.} and Carla Perego and Folli, {Franco B.}",
year = "2012",
month = "6",
doi = "10.1007/s00592-011-0364-z",
language = "English (US)",
volume = "49",
pages = "167--183",
journal = "Acta Diabetologica",
issn = "0940-5429",
publisher = "Springer-Verlag Italia",
number = "3",

}

TY - JOUR

T1 - The potential role of glutamate in the current diabetes epidemic

AU - Davalli, Alberto M.

AU - Perego, Carla

AU - Folli, Franco B.

PY - 2012/6

Y1 - 2012/6

N2 - In the present article, we propose the perspective that abnormal glutamate homeostasis might contribute to diabetes pathogenesis. Previous reports and our recent data indicate that chronically high extracellular glutamate levels exert direct and indirect effects that might participate in the progressive loss of β-cells occurring in both T1D and T2D. In addition, abnormal glutamate homeostasis may impact all the three accelerators of the "accelerator hypothesis" and could partially explain the rising frequency of T1D and T2D.

AB - In the present article, we propose the perspective that abnormal glutamate homeostasis might contribute to diabetes pathogenesis. Previous reports and our recent data indicate that chronically high extracellular glutamate levels exert direct and indirect effects that might participate in the progressive loss of β-cells occurring in both T1D and T2D. In addition, abnormal glutamate homeostasis may impact all the three accelerators of the "accelerator hypothesis" and could partially explain the rising frequency of T1D and T2D.

KW - Diabetes

KW - Glutamate toxicity

KW - l-Glutamic acid

KW - Monosodium glutamate

KW - Obesity

KW - Pancreatic β-cells

UR - http://www.scopus.com/inward/record.url?scp=84862737626&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84862737626&partnerID=8YFLogxK

U2 - 10.1007/s00592-011-0364-z

DO - 10.1007/s00592-011-0364-z

M3 - Article

C2 - 22218826

AN - SCOPUS:84862737626

VL - 49

SP - 167

EP - 183

JO - Acta Diabetologica

JF - Acta Diabetologica

SN - 0940-5429

IS - 3

ER -