Perinatal exposure to high dietary advanced glycation end products in transgenic NOD8.3 mice leads to pancreatic beta cell dysfunction

Danielle J Borg; Felicia Y. T Yap; Sahar Keshvari; David G Simmons; Linda A Gallo; Amelia K Fotheringham; Aowen Zhuang; Robyn M Slattery; Sumaira Z Hasnain; Melinda T Coughlan; Phillip Kantharidis; Josephine M Forbes

doi:10.1080/19382014.2017.1405189

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Perinatal exposure to high dietary advanced glycation end products in transgenic NOD8.3 mice leads to pancreatic beta cell dysfunction

Journal article

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Perinatal exposure to high dietary advanced glycation end products in transgenic NOD8.3 mice leads to pancreatic beta cell dysfunction

Danielle J Borg, Felicia Y. T Yap, Sahar Keshvari, David G Simmons, Linda A Gallo, Amelia K Fotheringham, Aowen Zhuang, Robyn M Slattery, Sumaira Z Hasnain, Melinda T Coughlan, …

Islets, Vol.10(1), pp.10-24

2018

DOI: https://doi.org/10.1080/19382014.2017.1405189

PMCID: PMC5796486

PMID: 29157116

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Abstract

advanced glycation end products

dietary intervention

insulin

insulitis

islet

NOD8.3

Type 1 diabetes

The contribution of environmental factors to pancreatic islet damage in type 1 diabetes remains poorly understood. In this study, we crossed mice susceptible to type 1 diabetes, where parental male (CD8+ T cells specific for IGRP206-214; NOD8.3) and female (NOD/ShiLt) mice were randomized to a diet either low or high in AGE content and maintained on this diet throughout pregnancy and lactation. After weaning, NOD8.3+ female offspring were identified and maintained on the same parental feeding regimen for until day 28 of life. A low AGE diet, from conception to early postnatal life, decreased circulating AGE concentrations in the female offspring when compared to a high AGE diet. Insulin, proinsulin and glucagon secretion were greater in islets isolated from offspring in the low AGE diet group, which was akin to age matched non-diabetic C57BL/6 mice. Pancreatic islet expression of Ins2 gene was also higher in offspring from the low AGE diet group. Islet expression of glucagon, AGEs and the AGE receptor RAGE, were each reduced in low AGE fed offspring. Islet immune cell infiltration was also decreased in offspring exposed to a low AGE diet. Within pancreatic lymph nodes and spleen, the proportions of CD4+ and CD8+ T cells did not differ between groups. There were no significant changes in body weight, fasting glucose or glycemic hormones. This study demonstrates that reducing exposure to dietary AGEs throughout gestation, lactation and early postnatal life may benefit pancreatic islet secretion and immune infiltration in the type 1 diabetic susceptible mouse strain, NOD8.3.

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Title: Perinatal exposure to high dietary advanced glycation end products in transgenic NOD8.3 mice leads to pancreatic beta cell dysfunction
Authors: Danielle J Borg (Author) - Inflammatory Diseases Biology and Therapeutics, Mater Research Institute- The University of Queensland, Translational Research Institute
Felicia Y. T Yap (Author) - Baker Heart and Diabetes Institute
Sahar Keshvari (Author) - The University of Queensland
David G Simmons (Author) - The University of Queensland
Linda A Gallo (Author) - The University of Queensland
Amelia K Fotheringham (Author) - The University of Queensland
Aowen Zhuang (Author) - The University of Queensland
Robyn M Slattery (Author) - Monash University
Sumaira Z Hasnain (Author) - The University of Queensland
Melinda T Coughlan (Author) - Monash University
Phillip Kantharidis (Author) - Baker Heart and Diabetes Institute
Josephine M Forbes (Author) - The University of Queensland
Publication details: Islets, Vol.10(1), pp.10-24
Publisher: Taylor & Francis Inc.
Date published: 2018
DOI: 10.1080/19382014.2017.1405189
ISSN: 1938-2022; 1938-2014
PMID: 29157116; PMC5796486
Copyright note: © 2018 The Author(s). Published by Taylor & Francis© Danielle J. Borg, Felicia Y. T. Yap, Sahar Keshvari, David G. Simmons, Linda A. Gallo, Amelia K. Fotheringham, Aowen Zhuang, Robyn M. Slattery, Sumaira Z. Hasnain, Melinda T. Coughlan, Phillip Kantharidis, and Josephine M. Forbes. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.
Organisation Unit: School of Health - Biomedicine; University of the Sunshine Coast, Queensland; School of Health and Behavioural Sciences - Legacy
Language: English
Record Identifier: 99620607202621
Output Type: Journal article

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Web Of Science research areas: Endocrinology & Metabolism

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