Revista Brasileira de Ginecologia e Obstetrícia. 2004;26(5):369-375
OBJECTIVE: to assess the action of antiretroviral drugs on glycid metabolism and on the pancreas of pregnant Wistar rats. METHODS: adult pregnant Wistar rats weighing 200-230g were used. Azidothymidine, lamivudine and nelfinavir were administered to the animals at doses 10 times higher than those administered to pregnant women. The animals were divided into seven groups of 10 animals, including a control group. The animals were sacrificed on the 21st day of pregnancy and glycemia, insulinemia, glucagonemia, free fatty acids (FFA) and hepatic glycogen were measured. Direct counts of the number of immunohistochemically labeled insulin- and glucagon-producing cells were used to determine pancreatic damage. Data were analyzed statistically by the Student’s t-test comparing each treated group with the control group. RESULTS: increased serum glucagon (control group: 88.2 pg/ml; treated groups: 99.7-120.7 pg/ml) and reduced insulin (control group: 6.2 muIU/ml; treated groups: 2.1-2.7 muIU/ml) were observed in all groups treated with antiretroviral drugs after 21 days of pregnancy. There was no significant difference between the experimental groups and the control in glycemia, plasma FFA or hepatic glycogen. Also, there was no significant difference in number of insulin- and glucagon-producing cells between the treated groups and the control. CONCLUSION: treatment of noninfected rats with antiretroviral drugs during pregnancy altered maternal glycid metabolism causing insulin decrease and glucagon elevation, with normal glycemia and unchanged number of pancreatic cells.
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OBJECTIVE: to assess the action of antiretroviral drugs on glycid metabolism and on the pancreas of pregnant Wistar rats. METHODS: adult pregnant Wistar rats weighing 200-230g were used. Azidothymidine, lamivudine and nelfinavir were administered to the animals at doses 10 times higher than those administered to pregnant women. The animals were divided into seven groups of 10 animals, including a control group. The animals were sacrificed on the 21st day of pregnancy and glycemia, insulinemia, glucagonemia, free fatty acids (FFA) and hepatic glycogen were measured. Direct counts of the number of immunohistochemically labeled insulin- and glucagon-producing cells were used to determine pancreatic damage. Data were analyzed statistically by the Student's t-test comparing each treated group with the control group. RESULTS: increased serum glucagon (control group: 88.2 pg/ml; treated groups: 99.7-120.7 pg/ml) and reduced insulin (control group: 6.2 muIU/ml; treated groups: 2.1-2.7 muIU/ml) were observed in all groups treated with antiretroviral drugs after 21 days of pregnancy. There was no significant difference between the experimental groups and the control in glycemia, plasma FFA or hepatic glycogen. Also, there was no significant difference in number of insulin- and glucagon-producing cells between the treated groups and the control. CONCLUSION: treatment of noninfected rats with antiretroviral drugs during pregnancy altered maternal glycid metabolism causing insulin decrease and glucagon elevation, with normal glycemia and unchanged number of pancreatic cells.
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