Polydatin attenuates AGEs-induced upregulation of fibronectin and ICAM-1 in rat glomerular mesangial cells and db/db diabetic mice kidneys by inhibiting the activation of the SphK1-S1P signaling pathway

Chen, Cheng; Huang, Kaipeng; Hao, Jie; Huang, Junying; Yang, Zhao; Xiong, Fengxiao; Liu, Peiqing; Huang, Heqing

doi:10.1016/j.mce.2016.03.003

Cited by 30 publications

(22 citation statements)

References 67 publications

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“…In animal models of the western diet, high in fats and fructose, increased ceramide de novo synthesis has been reported, in relation with reduced insulin sensitivity [65,66]. In parallel, two very recent studies highlighted a possible role for diet-derived AGEs on this unbalance among sphingolipid intermediates through the action of the AGE-receptor RAGE [67,68]. In particular, according to the work from Geoffrey and colleagues, the dose- and time-dependent effect of exposition to AGEs on mesangial cells proliferation was mediated by the modulation of the sphingolipids intermediates ceramide/sphingosine/sphingosine-1-phospahate and activities of related enzymes [67].…”

Section: Dietary Sugar-induced Glycation: Interference On Cell Funmentioning

confidence: 99%

“…In particular, according to the work from Geoffrey and colleagues, the dose- and time-dependent effect of exposition to AGEs on mesangial cells proliferation was mediated by the modulation of the sphingolipids intermediates ceramide/sphingosine/sphingosine-1-phospahate and activities of related enzymes [67]. Similarly, the findings from Chen et al demonstrated that polydatin, through its anti-glicative effect, evokes the reduction of sphingosine kinase activity and its byproduct sphingosine-1-phosphate, and this may be the underlying mechanism for the prevention of diabetic nephropathy and glomerular mesangial cells’ pro-fibrogenic signalling [68]. The pro-inflammatory profile induced by high levels of ceramide and sphingosine-1-phosphate has been demonstrated to contribute to cardiac impairment and peripheral insulin resistance, and the modulation of enzymes involved in their accumulation has been shown to ameliorate metabolic derangements [69,70].…”

Section: Dietary Sugar-induced Glycation: Interference On Cell Funmentioning

confidence: 99%

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Dietary Sugars and Endogenous Formation of Advanced Glycation Endproducts: Emerging Mechanisms of Disease

2017

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The rapid increase in metabolic diseases, which occurred in the last three decades in both industrialized and developing countries, has been related to the rise in sugar-added foods and sweetened beverages consumption. An emerging topic in the pathogenesis of metabolic diseases related to modern nutrition is the role of Advanced Glycation Endproducts (AGEs). AGEs can be ingested with high temperature processed foods, but also endogenously formed as a consequence of a high dietary sugar intake. Animal models of high sugar consumption, in particular fructose, have reported AGE accumulation in different tissues in association with peripheral insulin resistance and lipid metabolism alterations. The in vitro observation that fructose is one of the most rapid and effective glycating agents when compared to other sugars has prompted the investigation of the in vivo fructose-induced glycation. In particular, the widespread employment of fructose as sweetener has been ascribed by many experimental and observational studies for the enhancement of lipogenesis and intracellular lipid deposition. Indeed, diet-derived AGEs have been demonstrated to interfere with many cell functions such as lipid synthesis, inflammation, antioxidant defences, and mitochondrial metabolism. Moreover, emerging evidence also in humans suggest that this impact of dietary AGEs on different signalling pathways can contribute to the onset of organ damage in liver, skeletal and cardiac muscle, and the brain, affecting not only metabolic control, but global health. Indeed, the most recent reports on the effects of high sugar consumption and diet-derived AGEs on human health reviewed here suggest the need to limit the dietary sources of AGEs, including added sugars, to prevent the development of metabolic diseases and related comorbidities.

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Section: Dietary Sugar-induced Glycation: Interference On Cell Funmentioning

confidence: 99%

Section: Dietary Sugar-induced Glycation: Interference On Cell Funmentioning

confidence: 99%

Dietary Sugars and Endogenous Formation of Advanced Glycation Endproducts: Emerging Mechanisms of Disease

2017

View full text Add to dashboard Cite

show abstract

“…In particular, the work from Geoffrey and colleagues, the dose-and time-dependent effect of exposition to AGEs on mesangial cells proliferation was mediated by the modulation of the sphingolipids intermediates ceramide/sphingosine/sphingosine-1-phospahate and activities of related enzymes [61]. Similarly, the findings from Chen et al demonstrated that polydatin, through its anti-glicative effect evokes the reduction of sphingosine kinase activity and its byproduct sphingosine-1-phosphate, and this may be the underlying mechanism for the prevention of diabetic nephropathy and glomerular mesangial cells pro-fibrogenic signalling [62]. The pro-inflammatory profile induced by high levels of ceramide and sphingosine-1-phosphate has been demonstrated to contribute to cardiac impairment and peripheral insulin resistance, and the modulation of enzymes involved in their accumulation has been shown to ameliorate metabolic derangements [63,64].…”

Section: Interference On Sphingolipids Metabolismmentioning

confidence: 90%

“…In animal models of western diet, high in fats and fructose, the increased ceramide de novo synthesis has been reported, in relation with reduced insulin sensitivity [59,60]. In parallel, two very recent studies highlighted a possible role for diet-derived AGEs on this unbalance among sphingolipids intermediates through the action of the AGE-receptor RAGE [61,62]. In particular, the work from Geoffrey and colleagues, the dose-and time-dependent effect of exposition to AGEs on mesangial cells proliferation was mediated by the modulation of the sphingolipids intermediates ceramide/sphingosine/sphingosine-1-phospahate and activities of related enzymes [61].…”

Section: Interference On Sphingolipids Metabolismmentioning

confidence: 94%

Dietary Sugars and Endogenous Formation of Advanced Glycation Endproducts: Emerging Mechanisms of Disease

Aragno¹,

Mastrocola²

2017

Preprint

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Abstract.The rapid increase in metabolic diseases occurred in the last three decades in both industrialized and developing countries has been related to the rise in sugar-added foods and sweetened beveragesconsumption. An emerging topic in the pathogenesis of metabolic diseases related to modern nutrition is the role of Advanced Glycation Endproducts (AGEs). AGEs can be ingested with high temperature processed foods, but also endogenously formed as consequence of a high dietary sugars intake. Animal models of high sugars consumption, in particular fructose, have reported AGEs accumulation in different tissues in association with peripheral insulin resistance and lipid metabolism alterations. The in vitro observation that fructose is one of the most rapid and effective glycating agent when compared to other sugars has prompted the investigation of the in vivo fructose-induced glycation. In particular, the widespread employment of fructose as sweetener has been ascribed by many experimental and observational studies for the enhancement of lipogenesis and intracellular lipid deposition. Indeed, diet-derived AGEs have been demonstrated to interfere with many cell functions such as lipid synthesis, inflammation, antioxidant defences, and mitochondrial metabolism. Moreover, emerging evidences also in humans suggest that this impact of dietary AGEs on different signalling pathways can contribute to the onset of organ damage in liver, skeletal and cardiac muscle, and brain, affecting not only metabolic control, but global health.Indeed, the here reviewed most recent reports on the effects of high sugars consumption and dietderived AGEs on human health suggest the need to limit the dietary sources of AGEs, including added sugars, to prevent the development of metabolic diseases and related comorbidities.

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“…S1P can cross-activate the transforming growth factor-β (TGF-β) pathway, inducing pro-fibrotic factors and fibronectin (FN) via activation of S1P receptors in renal mesangial cells [16]. It has been demonstrated that inhibiting Sphk1/S1P activation could delay the progression of diabetic nephropathy [17]. In acute liver failure, C5a/C5aR pathway is essential for upregulating Sphk1 expression, and blocking C5aR could play a protective role through reducing the expression of Sphk1, indicating the possible relationship between complement and Sphk1 [18].…”

Section: Introductionmentioning

confidence: 99%

Resveratrol Attenuates Adriamycin-Induced Focal Segmental Glomerulosclerosis through C3aR/C5aR- Sphingosine Kinase 1 Pathway

et al. 2017

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Background/Aim: Focal segmental glomerulosclerosis (FSGS) typically presents with nephrotic range proteinuria, which could eventually develop into end-stage renal disease. Resveratrol (RSV) is a natural polyphenol compound, which has been reported to suppress inflammatory response and renal interstitial fibrosis. This study is aimed at evaluating the renoprotective effect of RSV treatment on adriamycin-induced FSGS. Methods: In Balb/c mice, adriamycin nephropathy was induced by adriamycin (10 mg/kg body weight, diluted in normal saline) via a tail vein on day 0. Then the mice were treated with RSV (40 mg/kg body weight) once daily by oral gavage, again starting on the day of adriamycin injection and continued for 6 weeks. At 6 weeks, the mice were sacrificed; kidneys and blood samples were collected for further analysis. Results: When treated with adriamycin, the expressions of C3aR, C5aR, sphingosine kinase 1 (Sphk1), and soluble urokinase-type plasminogen activator receptor (suPAR) were upregulated, while RSV treatment could inhibit the expressions of C3aR, C5aR, Sphk1, and suPAR, eventually leading to anti-inflammatory and anti-fibrosis conditions. Conclusion: RSV attenuates adriamycin-induced FSGS through C3aR/C5aR-Sphk1 pathway.

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Polydatin attenuates AGEs-induced upregulation of fibronectin and ICAM-1 in rat glomerular mesangial cells and db/db diabetic mice kidneys by inhibiting the activation of the SphK1-S1P signaling pathway

Cited by 30 publications

References 67 publications

Dietary Sugars and Endogenous Formation of Advanced Glycation Endproducts: Emerging Mechanisms of Disease

Dietary Sugars and Endogenous Formation of Advanced Glycation Endproducts: Emerging Mechanisms of Disease

Dietary Sugars and Endogenous Formation of Advanced Glycation Endproducts: Emerging Mechanisms of Disease

Resveratrol Attenuates Adriamycin-Induced Focal Segmental Glomerulosclerosis through C3aR/C5aR- Sphingosine Kinase 1 Pathway

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