Glycosylated haemoglobins and the oxygen affinity of whole blood

Samaja, Michele; Melotti, D.; Carenini, Angelo; Pozza, G.

doi:10.1007/bf00260950

Cited by 49 publications

(24 citation statements)

References 12 publications

(12 reference statements)

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“…Tissue 02 tension would also be reduced if erythrocyte 02 affinity were increased. Glycosylated Hb, which was present in greater concentrations in the diabetic animals than in the controls, has a greater 02 affinity than nonglycosylated Hb, but in diabetes there appears to be an increase in erythrocyte 2,3-diphosphoglycerate; the net result is little or no net shift in erythrocyte oxygen affinity (28).…”

Section: Discussionmentioning

confidence: 81%

Prevention of some electrophysiologic and biochemical abnormalities with oxygen supplementation in experimental diabetic neuropathy.

Low¹,

Tuck²,

Dyck³

et al. 1984

Proc. Natl. Acad. Sci. U.S.A.

108

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Endoneurial hypoxia has been suggested as a mechanism of human and experimental diabetic neuropathy (EDN). We found that rats rendered diabetic for 4 months had reduced nerve blood flow (NBF) and nerve oxygen tension (Pno2). The NBF was reduced by at least 33% in EDN and 60% of the oxygen tensions in the endoneurial 02 histogram were less than 25 mm Hg (3.3 kPa) in EDN compared with only 19% in the controls. To test the hypothesis that EDN may in part be due to hypoxia, we studied the effectiveness of oxygen supplementation in preventing some electrophysiologic and biochemical abnormalities. Rats with EDN had reduced caudal nerve conduction velocity and had a resistance to ischemic conduction block. When a matched groups of rats with EDN were 02 supplemented for 4 weeks, the time to 50% block of nerve conduction and nerve conduction velocity was no longer statistically different from controls. Endoneurial free sugars (glucose, fructose, sorbitol) were markedly increased in EDN. Oxygen supplementation resulted in no change in plasma glucose; by contrast, these increased endoneurial free sugars were significantly reduced (towards normal) by 60%, 33%, and 34%, respectively. myo-Inositol, however, was further decreased by oxygen supplementation. These findings of a partial prevention of electrophysiologic and biochemical abnormalities support a role of hypoxia in the pathogenesis of EDN.While the pathogenesis of diabetic neuropathy remains obscure (1), certain clues have been provided by some recent studies. These include reduced energy utilization (2), increased sorbitol and decreased nerve free myo-inositol concentrations (2, 3), increased intra-axonal sodium levels (4), and a reduced rate of incorporation of lipid and amino acids into myelin (5). Axonal transport rates are also reduced in experimental diabetic neuropathy (6, 4.5 (50 mg-ml-1; dose 1 ml-kg-1). The control groups received an intraperitoneal injection of citrate buffer (1 ml-kg-') alone. The rats were housed in cages with plastic floors covered with sawdust and wood shavings and were fed Purina Rat Chow (no. 5001) with an unrestricted supply of water. Rats were accepted as diabetic if fasting glucose exceeded 300 mg/dl 2 days after streptozotocin and remained >300 mg/dl at the time of sacrifice. NBF and Oxygen Tension Measurements. NBF was measured by using the hydrogen (H2) clearance method (8, 9); H2 and 02 were sensed in nerve with platinum microelectrodes (3-to 5-gm tip diameter) polarized +0.25 V and -0.65 V, respectively, using the principle of polarography (9-11). NBF was calculated from the time constant of the H2 washout curve (9-11). Sciatic Pno2 was sampled as for H2 by using identical microelectrodes but polarized -0.65 V. After in vitro calibration, the electrode was inserted into the nerve fascicle until the tip was at the center of the fascicle. Recordings were repeated at steps of 0.1 x radius as the micropipet was withdrawn. The electrode was recalibrated and the process was repeated at a different site three to five times...

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Section: Discussionmentioning

confidence: 81%

Prevention of some electrophysiologic and biochemical abnormalities with oxygen supplementation in experimental diabetic neuropathy.

Low¹,

Tuck²,

Dyck³

et al. 1984

Proc. Natl. Acad. Sci. U.S.A.

108

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“…In vitro, HbAlc has been shown to have altered oxygen saturation curves and/or decreased sensitivity to the allosteric effects of organic phosphate [17]. However, in vivo, the higher oxygen affinity of haemoglobin in diabetic patients appears to be independent of the state of glycosylation of haemoglobin [18], and whole blood oxygen saturation curves for normal and diabetic populations are essentially identical [19,20]. It is unlikely, therefore, that glycosylation of haemoglobin has any pathological effects.…”

Section: Erythrocyte Proteinsmentioning

confidence: 99%

Non-enzymatic glycosylation and the chronic complications of diabetes: an overview

Kennedy¹,

1984

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“…This hypothesis has been difficult to prove since intra-erythrocytic concentrations of 2,3-DPG are altered by many conditions frequently encountered among diabetic subjects [6][7][8]. While most authors have applied some exclusion criteria in order to select preferentially normoxic subjects when studying the relationship between 2,3-DPG synthesis and HbAtc formation [5,9], these criteria have not been exhaustive. In the present work particular care was taken to exclude from study any diabetic patients who had cause, symptoms or history of tissue hypoxia.…”

mentioning

confidence: 99%

Erythrocyte 2,3-bisphosphoglycerate concentrations and haemoglobin glycosylation in normoxic Type 1 (insulin-dependent) diabetes mellitus

1984

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Summary.Increased erythrocyte 2,3-bisphosphoglycerate concentrations are associated with increased haemoglobin glycosylation in patients with Type 1 diabetes mellitus who have no cause or symptoms of hypoxic stress. This change in 2,3-bisphosphoglycerate metabolism is additional to its response to changes in circulating haemoglobin concentration. Statistical analysis of data showed that erythrocyte 2,3-bisphosphoglycerate concentration did not correlate with the absolute concentration of circulating haemoglobin Ale, but with the proportion of haemoglobin glycosylated. This finding is consistent with the hypothesis that it is changes in the position of the erythrocyte oxygen dissociation curve which modulate the increase in 2,3-bisphosphoglycerate synthesis upon haemoglobin Alc formation.

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Glycosylated haemoglobins and the oxygen affinity of whole blood

Cited by 49 publications

References 12 publications

Prevention of some electrophysiologic and biochemical abnormalities with oxygen supplementation in experimental diabetic neuropathy.

Prevention of some electrophysiologic and biochemical abnormalities with oxygen supplementation in experimental diabetic neuropathy.

Non-enzymatic glycosylation and the chronic complications of diabetes: an overview

Erythrocyte 2,3-bisphosphoglycerate concentrations and haemoglobin glycosylation in normoxic Type 1 (insulin-dependent) diabetes mellitus

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