dc.creatorDa-Silva C.A.
dc.creatorGoncalves A.A.
dc.date1997
dc.date2015-06-30T14:50:09Z
dc.date2015-11-26T15:06:51Z
dc.date2015-06-30T14:50:09Z
dc.date2015-11-26T15:06:51Z
dc.date.accessioned2018-03-28T22:17:15Z
dc.date.available2018-03-28T22:17:15Z
dc.identifier
dc.identifierBrazilian Journal Of Medical And Biological Research. , v. 30, n. 5, p. 657 - 661, 1997.
dc.identifier0100879X
dc.identifier
dc.identifierhttp://www.scopus.com/inward/record.url?eid=2-s2.0-0030912953&partnerID=40&md5=1a35e965d718a51f1505dd3ce789bba8
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/100280
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/100280
dc.identifier2-s2.0-0030912953
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1257320
dc.descriptionErythrocytes may play a role in glucose homeostasis during the postprandial period. Erythrocytes from diabetic patients are defective in glucose transport and metabolism, functions that may affect glycogen storage. Phenobarbital, a hepatic enzyme inducer, has been used in the treatment of patients with non-insulin-dependent diabetes mellitus (NIDDM), increasing the insulin-mediated glucose disposal. We studied the effects of phenobarbital treatment in vivo on glycemia and erythrocyte glycogen content in control and alloxan-diabetic rats during the postprandial period. In control rats (blood glucose, 73 to 111 mg/dl in femoral and suprahepatic veins) the erythrocyte glycogen content was 45.4 ± 1.1 and 39.1 ± 0.8 μg/g Hb (mean ± SEM, N = 4-6) in the femoral artery and vein, respectively, and 37.9 ± 1.1 in the portal vein and 47.5 ± 0.9 in the suprahepatic vein. Diabetic rats (blood glucose, 300-350 mg/dl) presented low (P < 0.05) erythrocyte glycogen content, i.e., 9.6 ± 0.1 and 7.1 ± 0.7 μg/g Hb in the femoral artery and vein, respectively, and 10.0 ± 0.7 and 10.7 ± 0.5 in the portal and suprahepatic veins, respectively. After 10 days of treatment, phenobarbital (0.5 mg/ml in the drinking water) did not change blood glucose or erythrocyte glycogen content in control rats. In diabetic rats, however, it lowered (P < 0.05) blood glucose in the femoral artery (from 305 ± 18 to 204 ± 45 mg/dl) and femoral vein (from 300 ± 11 to 174 ± 48 mg/dl) and suprahepatic vein (from 350 ± 10 to 174 ± 42 mg/dl), but the reduction was not sufficient for complete recovery. Phenobarbital also stimulated the glycogen synthesis, leading to a partial recovery of glycogen stores in erythrocytes. In treated rats, erythrocyte glycogen content increased to 20.7 ± 3.8 μg/g Hb in the femoral artery and 30.9 ± 0.9 μg/g Hb in the suprahepatic vein (P < 0.05). These data indicate that phenobarbital activated some of the insulin-stimulated glucose metabolism steps which were depressed in diabetic erythrocytes, supporting the view that erythrocytes participate in glucose homeostasis.
dc.description30
dc.description5
dc.description657
dc.description661
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dc.languageen
dc.publisher
dc.relationBrazilian Journal of Medical and Biological Research
dc.rightsaberto
dc.sourceScopus
dc.titlePartial Recovery Of Erythrocyte Glycogen In Diabetic Rats Treated With Phenobarbital
dc.typeArtículos de revistas


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