[The mechanism responding to tissue anoxia, with special reference to the effects of corticosteroid on erythrocyte 2,3-DPG].
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Biomedical subjects
Publications and source records attributed to M Oimomi.
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Serum creatine phosphokinase activity increased significantly four or six hours after the administration of prednisolone in patients with muscular dystrophy of various types, whereas it did not increase in other muscular disorders. The extent of the response correlated inversely with the grade of disability. The prednisolone test may help to differentiate muscular dystrophy from polymyositis.
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These experiments were undertaken to determine whether neuropeptide Y (NPY) could suppress a prostaglandin hyperthermia in conscious dogs. Prostaglandin E2 (PGE2) (5 micrograms), injected into the lateral cerebral ventricle (ILV), evoked a hyperthermia of approximately 1 degrees C. Addition of ILV NPY (5 micrograms) significantly attenuated the PGE2-induced hyperthermia, whereas pancreatic polypeptide (PP), another member of the PP family peptide, did not. These results provide evidence for a role of NPY on thermoregulation in the dog.
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Studies were carried out on the mechanism of action of glucocorticoids on erythrocyte glycolysis. Inosine increased the levels of 2,3-DPG, lactate, and ATP in red blood cell samples with very low glucose concentrations in which the glycolytic system was unable to utilize glucose. With inosine and hydrocortisone added to red blood cells, 2,3-DPG and lactate increased more than in red blood cells supplemented with inosine alone. There was no significant increase in the level of ATP when glucose and inosine were added compared to the addition of inosine only. There were no changes in the activity of enzymes such as PFK and PGK. From these findings, it is suggested that glucocorticoids increase the level of red blood cell 2,3-DPG, by activating the conversion of 1,3-DPG to 2,3-DPG during glycolysis, probably by stimulating 2,3-DPG mutase.
The effect of fructose on the formation of advanced Maillard reaction products which show fluorescence and have crosslinking was investigated. Type I collagen was added to various concentrations of glucose and fructose which were then incubated at 37 degrees C for 4 weeks. The level of furosine and the fluorescence intensity both increased in direct proportion to glucose and fructose levels and to the duration of incubation. Incubation with fructose produced less furosine but more intense fluorescence than incubation with glucose. Furthermore, collagen was significantly less soluble after incubation with fructose than after incubation with glucose. These results suggest that fructose in the polyol pathway plays an important role in the formation of advanced Maillard products.
The serum fructosamine level is influenced by the serum protein level. Therefore, we investigated the relationship between serum fructosamine levels and serum total protein and albumin levels measured simultaneously in non-diabetic and diabetic patients. Significant positive correlations were found between them. A correction formula was constructed to express the serum fructosamine level when the serum total protein level was 7 g/dl or when the serum albumin level was 4 g/dl: corrected fructosamine (mmol/l) = measured fructosamine (mmol/l) + A (7 (g/dl) or 4 (g/dl)--serum total protein (g/dl) or serum albumin (g/dl] where A is 0.28 for serum total protein and 0.30 for serum albumin in non-diabetic subjects; 0.29 for serum total protein and 0.31 for serum albumin in non-diabetic and diabetic subjects combined.
Patients with diabetes mellitus as well as those with renal failure had high hemoglobin A1 (HbA1) levels. However, the portion of HbA1a+b fractions was larger in patients with renal failure than in diabetic patients. Thus, if renal disorder is advanced, caution should be exercised in evaluating HbA1 data. Furthermore, not only is the collective determination of Hb minor components such as HbA1 required, but also investigation of changes in HbA1a+b in patients with renal failure or diabetic nephropathy.