ArticleLipids in health and disease2017
Advanced glycation end products (AGEs) increase renal lipid accumulation: a pathogenic factor of diabetic nephropathy (DN).
Article in Lipids in health and disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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59 citing papers in PubMed, 107 citations in OpenAlex.
- Associations of dietary macronutrients and energy intake with diabetic kidney disease and all-cause mortality in diabetes: evidence from NHANES.BMJ open diabetes research & care · 2026Article
- An oral nanocombinatorial agent exhibits pleiotropic improvement in diabetic nephropathy via modulation of the SCAP/SREBPs pathway.Journal of nanobiotechnology · 2026Article
- Fibroblast growth factor 1 alleviates diabetic nephropathy by reducing renal lipid accumulation in diabetic kidney.World journal of diabetes · 2026Article
- Advances in Targeting the AGEs-RAGE Pathway for the Treatment of Diabetic Kidney Disease.Drug design, development and therapy · 2026Review
- Salvianolic Acids and Their Pharmacological Promise in Kidney Diseases: A Narrative Review.International journal of nephrology and renovascular disease · 2026Review
- Serum Levels of NBiomedicines · 2025Article
- Association between advanced glycation end products and estimated glomerular filtration rate: a cross-sectional analysis.Diabetology & metabolic syndrome · 2025Article
- Spinach Extract Reduces Kidney Damage in Diabetic Rats by Impairing the AGEs/RAGE Axis.International journal of molecular sciences · 2025Article
- FSTL1 aggravates high glucose-induced oxidative stress and transdifferentiation in HK-2 cells.Scientific reports · 2025Article
- Diabetic kidney disease: from pathogenesis to multimodal therapy-current evidence and future directions.Frontiers in medicine · 2025Review
- The relationship between advanced glycation end products, metabolic metrics, HbAFrontiers in endocrinology · 2025Article
- Potential pathways for natural active ingredients to intervene in diabetic kidney disease: targeting macrophage infiltration.Frontiers in physiology · 2025Review
- Lipid nephrotoxicity mediated by HIF-1α activation accelerates tubular injury in diabetic nephropathy.Renal failure · 2024Article
- Chlorogenic acid alleviates renal fibrosis by reducing lipid accumulation in diabetic kidney disease through suppressing the Notch1 and Stat3 signaling pathway.Renal failure · 2024Article
- Fermented Rice Bran Mitigated the Syndromes of Type 2 Diabetes in KK-Metabolites · 2024Article
- Targeting lipid droplets and lipid droplet-associated proteins: a new perspective on natural compounds against metabolic diseases.Chinese medicine · 2024Review
- FPS-ZM1 attenuates the deposition of lipid in the liver of diabetic mice by sterol regulatory element binding protein-1c.BMC endocrine disorders · 2024Article
- Advanced Glycation End-Products Acting as Immunomodulators for Chronic Inflammation, Inflammaging and Carcinogenesis in Patients with Diabetes and Immune-Related Diseases.Biomedicines · 2024Review
- Correlation between circulating advanced glycation end products and thioredoxin-interacting protein levels and renal fat content in type 2 diabetes mellitus patients.Diabetology & metabolic syndrome · 2024Article
- Vitamin D is involved in the effects of the intestinal flora and its related metabolite TMAO on perirenal fat and kidneys in mice with DKD.Nutrition & diabetes · 2024Article
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3 authors at 2 institutions in 1 country.
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Abstract
backgroundAdvanced glycation end products (AGEs) are pathogenic factors of diabetic nephropathy (DN), causing renal damage in various ways. The aim of this study is to investigate the ectopic lipid accumulation caused by AGEs in human renal tubular epithelial cell line (HK-2) cells and the kidney of type 2 diabetic rats.
methodsIn vivo study, diabetes was induced in male Sprague-Dawley rats through intraperitoneal injection of high-fat/high-sucrose diet and low-dose streptozocin (STZ). Two weeks after STZ injection, the diabetic rats were randomly divided into two groups, namely, untreated diabetic and Aminoguanidine Hydrochloride (AG, an AGEs formation inhibitor)-treated (100 mg/Kg/day, i.g., for 8 weeks) group. In vitro study, according to the different treatments, HK-2 were divided into 6 groups. Intracellular cholesterol content was assessed by Oil Red O staining and cholesterol enzymatic assay. Expression of mRNA and protein of molecules controlling cholesterol homeostasis in the treated cells was examined by real-time quantitative PCR and western blotting, respectively. SREBP cleavage-activating protein (SCAP) translocation was detected by confocal microscopy.
resultsHere we found Nε-(carboxymethyl) lysine (CML, a member of the AGEs family) increased Oil Red O staining and intracellular cholesterol ester (CE) in HK-2 cells; Anti-RAGE (AGEs receptor) reduced lipid droplets and the CE level. A strong staining of Oil Red O was also found in the renal tubules of the diabetic rats, which could be alleviated by AG. CML upregulated both mRNA and protein expression of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoAR), LDL receptor (LDLr), sterol regulatory element binding protein-2 (SREBP-2) and SCAP, which were inhibited by anti-RAGE. The upregulation of these molecules in the kidney of the diabetic rats was also ameliorated by AG. Furthermore, AG reduced serum and renal CML deposition, and improved urine protein and u-NGAL in type 2 diabetic rats.
conclusionsOverall, these results suggest that CML caused DN might be via disturbing the intracellular feedback regulation of cholesterol. Inhibition of CML-induced lipid accumulation might be a potential renoprotective role in the progression of DN.
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