| First Author | Kowluru RA | Year | 1992 |
| Journal | Metabolism | Volume | 41 |
| Issue | 2 | Pages | 160-4 |
| PubMed ID | 1310517 | Mgi Jnum | J:1603 |
| Mgi Id | MGI:50130 | Doi | 10.1016/0026-0495(92)90145-z |
| Citation | Kowluru RA, et al. (1992) Erythrocyte sodium-potassium ATPase activity and thiol metabolism in genetically hyperglycemic mice. Metabolism 41(2):160-4 |
| abstractText | Erythrocyte sodium pump activity, osmotic fragility, and thiol status were measured in genetically hyperglycemic (db/db) mice and compared with their nondiabetic littermates (db/m). The data showed no major differences in these parameters. However, erythrocytes from streptozotocin (Stz)-induced diabetic rats had significantly lower activity of sodium pump and thiols with an almost fourfold increase in osmotic fragility as compared with erythrocytes from nondiabetic rats. Sorbinil (an aldose reductase inhibitor) treatment of Stz-diabetic rats normalized all these lesions, suggesting a key role for polyol pathway. However, sorbitol levels in erythrocytes from db/db and db/m mice were undetectable. The data suggest that in db/db mice, the relative lack of polyol pathway, a potential consumer of NADPH, may provide erythrocytes with optimal NADPH for glutathione reductase system, thus maintaining normal GSH levels even at the height of hyperglycemia. Thus, the genetically hyperglycemic mice may serve as a useful model to study diabetes related complications without involving polyol pathway. |
