Receptor for Advanced Glycation End Products (RAGE) in Type 1 Diabetes Pathogenesis

Leung, Sherman S.; Forbes, Josephine M.; Borg, Danielle J.

doi:10.1007/s11892-016-0782-y

Cited by 28 publications

(22 citation statements)

References 181 publications

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“…Thus far, less attention has been paid to the anti-glycative activities of RA, especially in the liver. The increase in the receptors of advanced glycative endproducts (RAGE) plays an important role in diabetic progression because RAGE reacts with AGEs and other ligands such as beta-amyloid, and the interactions of RAGE and its ligands further activates other signal pathways responsible for the production of oxidative, inflammatory, or angiogenic factors [ 10 – 12 ]. Thus, the decline of RAGE formation due to RA definitely contributes to diminishing glycative injury and other diabetic pathological stress.…”

Section: Introductionmentioning

confidence: 99%

The anti-inflammatory and anti-glycative effects of rosmarinic acid in the livers of type 1 diabetic mice

Wen

Yin

2017

Biomedicine (Taipei)

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Background: Rosmarinic acid (RA) is a polyphenol present in members of the Lamiaceae family. In this study, yhe anti-inflammatory and anti-glycative effects of RA in the livers of type 1 diabetic mice were examined.Methods: The diabetic mice were divided into three groups: diabetic mice with 0, low dose RA (25 mg/ml), and high dose RA (50 mg/ml). One group of non-diabetic mice was used as a control for comparison. RA was supplied via daily 200 μL oral injections for 9 weeks. The level of interleukin (IL)-6, the tumor necrosis factor (TNF)-alpha, the prostaglandin E2 (PGE2), and the activity of cyclooxygenase (COX)-2 in the livers were measured. The hepatic receptor of advanced glycative endproduct (RAGE), the sorbitol levels, and the glyoxalase 1 (GLO-1) activity were also determined.Results: Compared with diabetic group that received no RA, the groups with RA supplements at both levels of dosages had increased body weight and had both decreased water intake and feed intake (p < 0.05). RA intake was found to reduce plasma glucose level and elevate plasma insulin level when compared with the diabetic group that received no RA (p < 0.05). RA treatments lowered the hepatic level of IL-6, TNF-alpha, and PGE2, as well as the activity of COX-2 (p < 0.05). RA administration also decreased hepatic RAGE and sorbitol levels, and GLO-1 activity when compared with the diabetic group that received no RA (P < 0.05).Conclusion: These findings support the conclusion that rosmarinic acid (RA) could be a potent protective agent for the liver against diabetic injury.

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Section: Introductionmentioning

confidence: 99%

The anti-inflammatory and anti-glycative effects of rosmarinic acid in the livers of type 1 diabetic mice

Wen

Yin

2017

Biomedicine (Taipei)

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“…While further data would be required to confirm these processes in the NOD8.3 model, it is conceivable that AGEs can influence T cell polarization and T regulatory (Treg) cell function. 19 Previous reports suggest that naïve human CD4 + T cells increase RAGE expression 57 and secretion of Th17 and Th1 cytokines, when exposed to AGEs. 37 AGEs also appear to reduce Treg suppression in vitro 57 and, in an animal model with impaired AGE clearance, high levels of circulating AGEs associated with reduced Treg numbers.…”

Section: Discussionmentioning

confidence: 99%

“…Protein modifications termed advanced glycation end products (AGEs) are environmental factors which, together with modifications in their receptor, RAGE, associate with risk for islet autoimmunity and type 1 diabetes development. 19–21 AGEs are made endogenously 22 and may be absorbed from dietary sources. 23,24 Circulating levels of AGEs appear to correlate between mother and baby, 25 suggesting maternal transmission of AGEs to the fetus.…”

Section: Introductionmentioning

confidence: 99%

“…RAGE, which is expressed on cells from the innate and adaptive immune system, including antigen presenting cells 33,34 and T cells 35–38 allows for interaction with a number of ligands, including AGEs. 19 Manipulating AGE concentrations has been shown to affect macrophage proliferation in vitro , 39 CD4 + T cell proportions and their ability to proliferate in response to β-cell antigens in adult NOD/ShiLt mice. 28 These, and other studies reviewed elsewhere, 19 emphasize interplay of RAGE and its ligands in immunology and autoimmunity that is yet to be fully appreciated.…”

Section: Introductionmentioning

confidence: 99%

“… 19 Manipulating AGE concentrations has been shown to affect macrophage proliferation in vitro , 39 CD4 + T cell proportions and their ability to proliferate in response to β-cell antigens in adult NOD/ShiLt mice. 28 These, and other studies reviewed elsewhere, 19 emphasize interplay of RAGE and its ligands in immunology and autoimmunity that is yet to be fully appreciated.…”

Section: Introductionmentioning

confidence: 99%

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

Borg

Yap

Keshvari

et al. 2017

Islets

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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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Molecular Mechanisms Underlying Vascular Disease in Diabetes

Touyz

Eluwole

Camargo

et al. 2023

Blood Pressure Disorders in Diabetes Mellitus

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Receptor for Advanced Glycation End Products (RAGE) in Type 1 Diabetes Pathogenesis

Cited by 28 publications

References 181 publications

The anti-inflammatory and anti-glycative effects of rosmarinic acid in the livers of type 1 diabetic mice

The anti-inflammatory and anti-glycative effects of rosmarinic acid in the livers of type 1 diabetic mice

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

Molecular Mechanisms Underlying Vascular Disease in Diabetes

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