Glucagon-like peptide–1 suppresses advanced glycation end product–induced monocyte chemoattractant protein–1 expression in mesangial cells by reducing advanced glycation end product receptor level

Ishibashi, Yuji; Nishino, Yoshinori; Matsui, Takanori; Takeuchi, Masayoshi; Yamagishi, Sho‐ichi

doi:10.1016/j.metabol.2011.01.010

Cited by 90 publications

(82 citation statements)

References 27 publications

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“…These changes might account for the finding indicating that, after 6 days, the wounds received Exe4 were more healed than those treated with NT, exendin-4(9-39) but also with Exendin-4(9-39) þExe4. Furthermore, we found, in line with that already described by Ishibashi et al (2011), myofibroblasts positive for GLP-1R immunostaining both at the plasma membrane and intracellular (Widmann et al, 1995;Roed et al, 2013). In addition, activation of the mitogenic ERK1/2, was described as part of the intracellular cascade activated by GLP-1R (Favaro et al, 2012).…”

Section: Discussionsupporting

confidence: 91%

The pro-healing effect of exendin-4 on wounds produced by abrasion in normoglycemic mice

Bacci

Laurino

Manni

et al. 2015

European Journal of Pharmacology

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Section: Discussionsupporting

confidence: 91%

The pro-healing effect of exendin-4 on wounds produced by abrasion in normoglycemic mice

Bacci

Laurino

Manni

et al. 2015

European Journal of Pharmacology

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“…Renoprotective effect of GLP-1R agonists through the direct action on the kidney was first reported in an animal model (Kodera et al 2011). Ishibashi et al (2011 also reported that GLP-1R agonist directly acts on mesangial cells via GLP-1R and that it could work as an anti-inflammatory agent via activation of cyclic adenosine monophosphate pathway.…”

Section: Discussionmentioning

confidence: 99%

The Glucagon-Like Peptide-1 Receptor Agonist, Liraglutide, Attenuates the Progression of Overt Diabetic Nephropathy in Type 2 Diabetic Patients

Imamura

Hirai

2013

Tohoku J. Exp. Med.

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Diabetic nephropathy (DN) is the leading cause of end-stage renal disease. Glucagon-like peptide-1 (GLP-1) is one of the incretins, gut hormones released from the intestine in response to food intake. GLP-1 receptor (GLP-1R) agonists have been used to treat type 2 diabetes. Here, we studied the effect of the administration of a GLP-1R agonist, liraglutide, on proteinuria and the progression of overt DN in type 2 diabetic patients. Twenty-three type 2 diabetic patients with overt DN, who had already been treated with blockade of renin-angiotensin system under dietary sodium restriction, were given liraglutide for a period of 12 months. Treatment with liraglutide caused a significant decrease in HbA1c from 7.4 ± 0.2% to 6.9 ± 0.3% (p = 0.04), and in body mass index (BMI) from 27.6 ± 0.9 kg/m 2 to 26.5 ± 0.8 kg/m 2 after 12 months (p < 0.001), while systolic blood pressure did not change. The progression of DN was determined as the rate of decline in estimated glomerular filtration rate (eGFR). The 12-month administration of liraglutide caused a significant decrease in proteinuria from 2.53 ± 0.48 g/g creatinine to 1.47 ± 0.28 g/g creatinine (p = 0.002). The administration of liraglutide also substantially diminished the rate of decline in eGFR from 6.6 ± 1.5 mL/min/1.73 m 2 /year to 0.3 ± 1.9 mL/min/1.73 m 2 /year (p = 0.003). Liraglutide can be used not only for reducing HbA1c and BMI, but also for attenuating the progression of nephropathy in type 2 diabetic patients.

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“…We have previously found that GLP-1 or GIP limits endothelial and mesangial cells' susceptibility toward pro-oxidative and pro-inflammatory effects of AGEs by suppressing RAGE gene expression and oxidative stress generation through the elevation of cyclic AMP, whose effect could be augmented by the addition of DPP-4 inhibitor. [28][29][30][31] In addition, the AGE-RAGE axis evokes oxidative stress generation in various cell types via NADPH oxidase activity, which is blocked by cAMP-elevating agents. 3,32,33 Aortic AGEs and oxidative stress levels have been shown to decrease in diabetic RAGE and apolipoprotein E double knockout Figure 1 AGE-modified protein levels (a and b) and RAGE gene expression (c) in the kidneys of Control, DPP-4-deficient, STZ or DPP-4-deficient STZ rats at 9 weeks old.…”

Section: Dpp-4 and Age-rage T Matsui Et Almentioning

confidence: 99%

Dipeptidyl peptidase-4 deficiency protects against experimental diabetic nephropathy partly by blocking the advanced glycation end products-receptor axis

Matsui

Nakashima

Nishino

et al. 2015

Laboratory Investigation

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Advanced glycation end products (AGEs) and their receptor (RAGE) have a role in diabetic nephropathy. We have recently found that linagliptin, an inhibitor of dipeptidyl peptidase-4 (DPP-4), could inhibit renal damage in type 1 diabetic rats by suppressing the AGE-RAGE axis. However, it remains unclear whether DPP-4 deficiency could also have beneficial effects on experimental diabetic nephropathy. To address the issue, we rendered wild-type F344/NSlc and DPP-4-deficient F344/DuCrl/Crlj rats diabetic by injection of streptozotocin, and then investigated whether DPP-4 deficiency could block the activation of AGE-RAGE axis in the diabetic kidneys and resultantly ameliorate renal injury in streptozotocin-induced diabetic rats. Compared with control rats at 9 and 11 weeks old, body weight and heart rates were significantly lower, while fasting blood glucose was higher in wild-type and DPP-4-deficient diabetic rats at the same age. There was no significant difference of body weight, fasting blood glucose and lipid parameters between the two diabetic rat strains. AGEs, 8-hydroxy-2′-deoxyguanosine (8-OHdG) and nitrotyrosine levels in the kidney, renal gene expression of RAGE and intercellular adhesion molecule-1, glomerular area, urinary excretion of 8-OHdG and albumin, and the ratio of renal to body weight were increased in wild-type diabetic rats at 9 and/or 11 weeks old compared with age-matched control rats, all of which except for urinary 8-OHdG levels at 11 weeks old were significantly suppressed in DPP-4-deficient diabetic rats. Our present study suggests that DPP-4 deficiency could exert beneficial actions on type 1 diabetic nephropathy partly by blocking the AGE-RAGE axis. DPP-4 might be a novel therapeutic target for preventing diabetic nephropathy. Sugars, including glucose and fructose, can react nonenzymatically with the amino groups of proteins, lipids and nucleic acids to form reversible Schiff bases, and then Amadori products. 1-3 These early glycation products undergo further complex reactions such as rearrangement, dehydration and condensation to become irreversibly cross-linked, heterogeneous fluorescent derivatives called 'advanced glycation end products (AGEs)'. 1-3 The process of non-enzymatic glycation is also known as Maillard reaction, and formation and accumulation of AGEs in various tissues have progressed at a physiological aging and at an extremely accelerated rate under diabetes. [1][2][3] There is a growing body of evidence that AGEs and their receptor (RAGE) interaction evoke oxidative stress generation and inflammatory and fibrotic reactions, thereby causing progressive alteration in renal architecture and loss of renal function in diabetes. [4][5][6][7][8] Furthermore, RAGEoverexpressing diabetic mice have been shown to exhibit progressive glomerulosclerosis with renal dysfunction, compared with diabetic littermates lacking the RAGE transgene. 9 Diabetic homozygous RAGE null mice displayed diminished albuminuria and glomerulosclerosis and failed to develop significantly increased mesan...

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Glucagon-like peptide–1 suppresses advanced glycation end product–induced monocyte chemoattractant protein–1 expression in mesangial cells by reducing advanced glycation end product receptor level

Cited by 90 publications

References 27 publications

The pro-healing effect of exendin-4 on wounds produced by abrasion in normoglycemic mice

The pro-healing effect of exendin-4 on wounds produced by abrasion in normoglycemic mice

The Glucagon-Like Peptide-1 Receptor Agonist, Liraglutide, Attenuates the Progression of Overt Diabetic Nephropathy in Type 2 Diabetic Patients

Dipeptidyl peptidase-4 deficiency protects against experimental diabetic nephropathy partly by blocking the advanced glycation end products-receptor axis

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