Oligonol, a low-molecular-weight polyphenol derived from lychee fruit, attenuates gluco-lipotoxicity-mediated renal disorder in type 2 diabetic &lt;i&gt;db/db&lt;/i&gt; mice

Park, Chan Hum; Noh, Jeong Sook; Fujii, H.; Roh, Seong‐Soo; Song, Yeonsu; Choi, Jae Sue; Chung, Hae Young; Yokozawa, Takako

doi:10.5582/ddt.2015.01003

Cited by 29 publications

(14 citation statements)

References 65 publications

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“…Resveratrol and anthocyanin-rich Seoritae extract prevents lipotoxic and glucotoxic effects through AMPK-PGC-1α axis in db/db mice [199,200]. The anti-lipotoxic effect of curcumin, berberine, oligonol-derived lychee fruit, and oryzanol-derived rice bran oil has also been demonstrated due to their capacity to reduce inflammatory, oxidative stress, and mitochondrial dysfunction markers in diabetic murine models [201][202][203][204][205]. Tangshen formula, a traditional Chinese formulation, was able to alleviate abnormal renal lipid accumulation and kidney damage in db/db mice by promoting ABCA1-mediated efflux cholesterol [206].…”

Section: Polyphenols Flavonoids and Nutraceuticalsmentioning

confidence: 99%

Lipotoxicity and Diabetic Nephropathy: Novel Mechanistic Insights and Therapeutic Opportunities

Opazo-Ríos

Mas

Marín-Royo

et al. 2020

IJMS

213

147

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Lipotoxicity is characterized by the ectopic accumulation of lipids in organs different from adipose tissue. Lipotoxicity is mainly associated with dysfunctional signaling and insulin resistance response in non-adipose tissue such as myocardium, pancreas, skeletal muscle, liver, and kidney. Serum lipid abnormalities and renal ectopic lipid accumulation have been associated with the development of kidney diseases, in particular diabetic nephropathy. Chronic hyperinsulinemia, often seen in type 2 diabetes, plays a crucial role in blood and liver lipid metabolism abnormalities, thus resulting in increased non-esterified fatty acids (NEFA). Excessive lipid accumulation alters cellular homeostasis and activates lipogenic and glycogenic cell-signaling pathways. Recent evidences indicate that both quantity and quality of lipids are involved in renal damage associated to lipotoxicity by activating inflammation, oxidative stress, mitochondrial dysfunction, and cell-death. The pathological effects of lipotoxicity have been observed in renal cells, thus promoting podocyte injury, tubular damage, mesangial proliferation, endothelial activation, and formation of macrophage-derived foam cells. Therefore, this review examines the recent preclinical and clinical research about the potentially harmful effects of lipids in the kidney, metabolic markers associated with these mechanisms, major signaling pathways affected, the causes of excessive lipid accumulation, and the types of lipids involved, as well as offers a comprehensive update of therapeutic strategies targeting lipotoxicity.

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Section: Polyphenols Flavonoids and Nutraceuticalsmentioning

confidence: 99%

Lipotoxicity and Diabetic Nephropathy: Novel Mechanistic Insights and Therapeutic Opportunities

Opazo-Ríos

Mas

Marín-Royo

et al. 2020

IJMS

213

147

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“…While this model is useful for studying glycation in T1D, it is not representative of the metabolic abnormalities seen in T2D—other animal models, such as the genetically‐ or diet‐induced obesity models, better reflect T2D in humans. In the LepR db/db mice, CML and other AGEs have been measured in plasma or serum, but only a few studies using genetically induced obesity models have analysed AGEs in organs or tissues such as kidneys, liver, or skin . Among the DIO models of T2D, HF and HF‐HS diets have successfully rendered the animals intolerant to glucose but have mixed results with respect to inducing hyperglycaemia.…”

Section: Introductionmentioning

confidence: 99%

“…In the LepR db/db mice, CML and other AGEs have been measured in plasma or serum, 21 but only a few studies using genetically induced obesity models have analysed AGEs in organs or tissues such as kidneys, liver, or skin. [22][23][24] Among the DIO models of T2D, HF and HF-HS diets have successfully rendered the animals intolerant to glucose but have mixed results with respect to inducing hyperglycaemia. Very few studies have used DIO models to observe the accumulation of AGEs in fluids, tissues, and organs.…”

Section: Introductionmentioning

confidence: 99%

The LepR^db/db mice model for studying glycation in the context of diabetes

Guilbaud

Howsam

Niquet-Léridon³

et al. 2019

Diabetes Metabolism Res

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Background Early (furosine) and advanced (carboxymethyllysine, CML) products of glycation (AGEs) have been reported as increased in plasma, tissues, and organs of diabetic people, indicating a direct link between glycation and type 2 diabetes (T2D). While murine models present some of the characteristics observed in diabetic humans, their pertinence as models of glycation, particularly for T2D, remains poorly described. The aim of this study was to characterize and compare glycation in several organs of two commonly studied murine models of T2D using stable isotope dilution liquid chromatography tandem mass spectrometry (LC‐MS/MS). Methods Defining parameters of type 2 diabetes including body weight, fasting glycaemia, and glucose intolerance were measured in three different C57BL6 mouse models of T2D—the genetic LepRdb/db (db/db) model and two diet‐induced obesity (DIO) models—and their respective controls. Furosine, free, and protein‐bound CML were quantified in kidneys, lungs, heart, and liver by LC‐MS/MS. Results The obesity, hyperglycaemia, and glucose intolerance in db/db mice was accompanied by an increase of furosine and protein‐bound CML levels in all organs relative to controls. The DIO models took several months to become obese, exhibited less severe hyperglycaemia and glucose intolerance, while glycation products were not significantly different between these groups (with the exception of furosine in liver and CML in lungs). Conclusions The db/db model better reflected the characteristics of human T2D compared with the DIO models and exhibited greater formation and accumulation of both furosine and protein‐bound CML in all of the organs tested here.

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“…Advanced Glycation and Lipoxidation End products (AGEs and ALEs) are now widely studied not only as biomarkers of oxidative stress but also because emerging data indicate their involvement as pathogenic factors and/or as damaging intermediates in several chronic diseases [1], [2], [3]. The identification, characterization and quantification of AGEs and ALEs in different physio-pathological conditions represent an emerging need, not only to find correlations with the onset and progression of diseases, but also to better understand the pathways dealing with their formation.…”

Section: Introductionmentioning

confidence: 99%

A capture method based on the VC1 domain reveals new binding properties of the human receptor for advanced glycation end products (RAGE)

et al. 2017

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The Advanced Glycation and Lipoxidation End products (AGEs and ALEs) are a heterogeneous class of compounds derived from the non-enzymatic glycation or protein adduction by lipoxidation break-down products. The receptor for AGEs (RAGE) is involved in the progression of chronic diseases based on persistent inflammatory state and oxidative stress. RAGE is a pattern recognition receptor (PRR) and the inhibition of the interaction with its ligands or of the ligand accumulation have a potential therapeutic effect. The N-terminal domain of RAGE, the V domain, is the major site of AGEs binding and is stabilized by the adjacent C1 domain. In this study, we set up an affinity assay relying on the extremely specific biological interaction AGEs ligands have for the VC1 domain. A glycosylated form of VC1, produced in the yeast Pichia pastoris, was attached to magnetic beads and used as insoluble affinity matrix (VC1-resin). The VC1 interaction assay was employed to isolate specific VC1 binding partners from in vitro generated AGE-albumins and modifications were identified/localized by mass spectrometry analysis. Interestingly, this method also led to the isolation of ALEs produced by malondialdehyde treatment of albumins. Computational studies provided a rational-based interpretation of the contacts established by specific modified residues and amino acids of the V domain. The validation of VC1-resin in capturing AGE-albumins from complex biological mixtures such as plasma and milk, may lead to the identification of new RAGE ligands potentially involved in pro-inflammatory and pro-fibrotic responses, independently of their structures or physical properties, and without the use of any covalent derivatization process. In addition, the method can be applied to the identification of antagonists of RAGE-ligand interaction.

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Oligonol, a low-molecular-weight polyphenol derived from lychee fruit, attenuates gluco-lipotoxicity-mediated renal disorder in type 2 diabetic <i>db/db</i> mice

Cited by 29 publications

References 65 publications

Lipotoxicity and Diabetic Nephropathy: Novel Mechanistic Insights and Therapeutic Opportunities

Lipotoxicity and Diabetic Nephropathy: Novel Mechanistic Insights and Therapeutic Opportunities

The LepR^db/db mice model for studying glycation in the context of diabetes

A capture method based on the VC1 domain reveals new binding properties of the human receptor for advanced glycation end products (RAGE)

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Oligonol, a low-molecular-weight polyphenol derived from lychee fruit, attenuates gluco-lipotoxicity-mediated renal disorder in type 2 diabetic <i>db/db</i> mice

Cited by 29 publications

References 65 publications

Lipotoxicity and Diabetic Nephropathy: Novel Mechanistic Insights and Therapeutic Opportunities

Lipotoxicity and Diabetic Nephropathy: Novel Mechanistic Insights and Therapeutic Opportunities

The LepRdb/db mice model for studying glycation in the context of diabetes

A capture method based on the VC1 domain reveals new binding properties of the human receptor for advanced glycation end products (RAGE)

Contact Info

Product

Resources

About

The LepR^db/db mice model for studying glycation in the context of diabetes