Nonenzymatic Glycosylation of Hemoglobin and Total Plasmatic Proteins in End-Stage Renal Disease

Abstract

In order to ascertain whether there are abnormalities of nonenzymatic glycosylation in uremia, the levels of nonenzymatically glycosylated hemoglobin (GHb), and total plasmatic glycosylated proteins (PGP) were studied using the thiobarbituric acid (TBA) method, a procedure not interfered with by carbamylation. Total hemoglobin A₁ (HbA₁) and the A_1c fraction were also determined by ion exchange chromatographic methods. Sixty-six end-stage renal disease patients (29 nondiabetic and 8 diabetic uremic patients on conservative treatment, 29 non-diabetic hemodialysis patients) and 56 controls (32 nonuremic diabetic patients and 24 healthy controls) were studied. High levels of GHb and total PGP were found in the nondiabetic uremic group on conservative treatment with all the methods used, but the persistence of high chromatographically determined HbA₁ levels in hemodialysis patients contrasts with the results obtained with the other techniques, which showed lower values on hemodialysis. Nondiabetic uremic patients with abnormal oral glucose tolerance curves had significantly higher levels of TBA-determined GHb and PGP. Uremic diabetic patients had the highest glycosylation levels of all the studied groups. We conclude that there is an abnormal nonenzymatic glycosylation of proteins in uremia, independent of carbamylation reactions and partially corrected by hemodialysis.

Oxidative stress and protein glycation in primary hypothyroidism. Male/female difference

“…Therefore, we propose that hyperlipidaemia in hypothyroidism provides a pool of substrates that in the presence of decreased antioxidant activity facilitates the rate of lipid peroxidation for generation of excess free radicals. Earlier reports from our laboratory and others [34,35] indicate the link between lipid peroxidation and protein glycation. Jain and Palmer have suggested that the protein glycation is facilitated by MDA per se, the major oxidative product of lipid peroxidation [32].…”

“…Two other important factors that contribute to protein glycation are the levels of lipid peroxides and reduced GSH [32,33], the markers of OS. Therefore, in the present study, we have assessed the correlation of fructosamine with OS, as reports have indicated a rise in fructosamine level with OS in conditions without hyperglycaemia [34,35]. OS ensues whenever there is increased production of FRs or decreased effective activity of antioxidants or a combination of both [36].…”

Increased plasma malondialdehyde and fructosamine in anemicH pyloriinfected patients: Effect of treatment

“…T he rate of for mation of glycated protein is considered to depend on the ambient concentration of glucose and half life of the protein [9] . However, there is convincing evidence that concentrations of nonenzymatically glycated protein are increased in many non-diabetic pathological states [10][11][12][13] . Elevated concentrations of glycated hemoglobin have been found in myocardial infarction, chronic renal failure, and nephrotic syndrome patients with normal blood glucose concentrations [10][11][12] .…”

“…However, there is convincing evidence that concentrations of nonenzymatically glycated protein are increased in many non-diabetic pathological states [10][11][12][13] . Elevated concentrations of glycated hemoglobin have been found in myocardial infarction, chronic renal failure, and nephrotic syndrome patients with normal blood glucose concentrations [10][11][12] . Similarly high concentrations of fructosamine are reported in non-diabetic chronic renal failure and rheumatic arthritis patients [12,13] .…”

“…Elevated concentrations of glycated hemoglobin have been found in myocardial infarction, chronic renal failure, and nephrotic syndrome patients with normal blood glucose concentrations [10][11][12] . Similarly high concentrations of fructosamine are reported in non-diabetic chronic renal failure and rheumatic arthritis patients [12,13] . Increased levels of glycated hemoglobin (HbA1C) have also been documented in iron deficiency anemic patients without any history of diabetes [14][15][16] .…”