Glycation free adduct accumulation in renal disease: the new AGE
Abstract
Glycation adducts formed in the later stages of protein glycation reactions, advanced glycation endproducts (AGEs), are a class of uraemic toxin. Protein glycation was viewed originally as a post-translational modification that accumulated mostly on extracellular proteins. We now know that AGE residues are also formed on short-lived cellular and extracellular proteins. Cellular proteolysis forms AGE free adducts from these proteins, which are released into plasma for urinary excretion. AGE free adducts are also absorbed from food. AGE free adducts are the major molecular form by which AGEs are excreted in urine. They normally have high renal clearance, but this declines markedly in chronic renal failure patients, leading to profound increases in plasma AGE free adducts. Accumulation of plasma AGE free adducts is increased further in end stage renal disease patients on peritoneal dialysis and haemodialysis by increased AGE formation. The impact of AGEs absorbed from food is probably most marked for undialysed patients with mild uraemia. The toxicity of AGEs has been associated with resistance of the extracellular matrix to proteolysis and AGE receptor-mediated responses. AGE free adducts may also contribute to vascular disease in uraemia. They represent an important new age for glycation research in nephrology.
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Adipokine secretion profiles differ between subcutaneous and abdominal adipose tissues.
“In addition, the profile of adipokines produced is dissimilar between the subcutaneous and abdominal adipose tissues.”
From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [36]
Leptin is preferentially expressed and secreted by subcutaneous adipose tissue, while adiponectin, visfatin, omentin, resistin, PAI-1, IL-8, IL-7, IL-1a, MCP-1, TGF-b, growth-related oncogene, CCL5 and MIP-1b are expressed more in abdominal fat.
“Thus, leptin is preferentially expressed and secreted by subcutaneous adipose tissue (52) , while the expression of adiponectin, visfatin, omentin, resistin, PAI-1, IL-8, IL-7, IL-1a, MCP-1, TGF-b, growth-related oncogena, CCL5 and MIP-1b is higher in abdominal fat.”
From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [36]
IL-6 and TNF-a appear to be synthesised equally by different adipose tissue sites.
“In contrast to such distributions, there are reports that IL-6 and TNF-a seem to be equally synthesised by the different sites (28,36,53 -59) .”
From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [36]
Adipose tissue macrophages may contribute to maintenance of the low-grade inflammatory state linked to obesity.
“Adipose tissue macrophages may contribute to the maintenance of the low-grade inflammatory state linked to obesity (36) .”
From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [36]
Reduced secretion of pro-inflammatory mediators from adipocytes or adipose tissue macrophages likely contributes to the effect of weight loss.
“On the other hand, it seems likely that reduced secretion of pro-inflammatory mediators from adipocytes or activated macrophages of adipose tissue contributes to the effect of weight loss (31,36,65,67,142) .”
From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [36]
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- Authors
- Thornalley, P. J.
- Affiliations
- University of Essex (GB)
- Corresponding author
- Thornalley, Paul J.
- ORCID
- Thornalley, Paul J.
- Venue
- Pediatric Nephrology
- Published
- 2005-08-24
- Volume
- 20
- Issue
- 11
- Pages
- 1515-1522
- ISSN
- 0931-041X (ISSN-L)
- 1432-198X
- OpenAlex
- W2135210722
- Cited by
- 53
- References
- 67
- Citations by year
- 2026: 2 · 2023: 1 · 2022: 4 · 2021: 1 · 2020: 2 · 2019: 2 · 2018: 1 · 2017: 6 · 2015: 5 · 2014: 3 · 2013: 2 · 2012: 1
- FWCI
- 0.50
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Pediatric Nephrology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Wellcome Trust
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Health Sciences › Medicine › Nephrology › Dialysis and Renal Disease Management
- Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
- Keywords
- advanced glycation end products, protein glycation, uremic toxins, chronic kidney disease, end-stage renal disease, dialysis, renal clearance, AGE receptor, extracellular matrix
- MeSH terms
- Amino Acid Oxidoreductases, Food Analysis, Humans, Imidazoles, Kidney, Kidney Diseases, Glycation End Products, Advanced
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