Metformin, but not glimepiride, improves carotid artery diameter and blood flow in patients with type 2 diabetes mellitus.

OBJECTIVE: To compare the effects of glimepiride and metformin on vascular reactivity, hemostatic factors and glucose and lipid profiles in patients with type 2 diabetes. METHODS: A prospective study was performed in 16 uncontrolled patients with diabetes previously treated with dietary intervention. The participants were randomized into metformin or glimepiride therapy groups. After four months, the patients were crossed over with no washout period to the alternative treatment for an additional four-month period on similar dosage schedules. The following variables were assessed before and after four months of each treatment: 1) fasting glycemia, insulin, catecholamines, lipid profiles and HbA1 levels; 2) t-PA and PAI-1 (antigen and activity), platelet aggregation and fibrinogen and plasminogen levels; and 3) the flow indices of the carotid and brachial arteries. In addition, at the end of each period, a 12-hour metabolic profile was obtained after fasting and every 2 hours thereafter. RESULTS: Both therapies resulted in similar decreases in fasting glucose, triglyceride and norepinephrine levels, and they increased the fibrinolytic factor plasminogen but decreased t-PA activity. Metformin caused lower insulin and pro-insulin levels and higher glucagon levels and increased systolic carotid diameter and blood flow. Neither metformin nor glimepiride affected endothelial-dependent or endothelial-independent vasodilation of the brachial artery. CONCLUSIONS: Glimepiride and metformin were effective in improving glucose and lipid profiles and norepinephrine levels. Metformin afforded more protection against macrovascular diabetes complications, increased systolic carotid artery diameter and total and systolic blood flow, and decreased insulin levels. As both therapies increased plasminogen levels but reduced t-PA activity, a coagulation process was likely still ongoing.

Metformin, but not glimepiride, improves carotid artery diameter and blood flow in patients with type 2 diabetes mellitus

OBJECTIVE: To compare the effects of glimepiride and metformin on vascular reactivity, hemostatic factors and glucose and lipid profiles in patients with type 2 diabetes. METHODS: A prospective study was performed in 16 uncontrolled patients with diabetes previously treated with dietary intervention. The participants were randomized into metformin or glimepiride therapy groups. After four months, the patients were crossed over with no washout period to the alternative treatment for an additional four-month period on similar dosage schedules. The following variables were assessed before and after four months of each treatment: 1) fasting glycemia, insulin, catecholamines, lipid profiles and HbA1 levels; 2) t-PA and PAI-1 (antigen and activity), platelet aggregation and fibrinogen and plasminogen levels; and 3) the flow indices of the carotid and brachial arteries. In addition, at the end of each period, a 12-hour metabolic profile was obtained after fasting and every 2 hours thereafter. RESULTS: Both therapies resulted in similar decreases in fasting glucose, triglyceride and norepinephrine levels, and they increased the fibrinolytic factor plasminogen but decreased t-PA activity. Metformin caused lower insulin and pro-insulin levels and higher glucagon levels and increased systolic carotid diameter and blood flow. Neither metformin nor glimepiride affected endothelial-dependent or endothelial-independent vasodilation of the brachial artery. CONCLUSIONS: Glimepiride and metformin were effective in improving glucose and lipid profiles and norepinephrine levels. Metformin afforded more protection against macrovascular diabetes complications, increased systolic carotid artery diameter and total and systolic blood flow, and decreased insulin levels. As both therapies increased plasminogen levels but reduced t-PA activity, a coagulation process was likely still ongoing.

Método rápido para dosagem da insulinemia por radioimunoensaio e sua aplicaçäo para a localizaçäo intra-operatória de insulinoma / Quick method of dosage of insulinemia by radioimmunoassay and its utilization for intraoperative localization of insulinoma

Desenvolvemos método rápido de dosagem de insulina para atender à necessidade de diagnóstico urgente da causa de certas hipoglicemias do recém nascido e para auxiliar na localizaçäo de insulinomas cuja situaçäo anatômica näo tenha sido definida por métodos radiológicos e ultra-sonográficos. A dosagem de insulina é realizada em 100micronl de plasma, em tampäo TRIS 100 mM, pH 7,0, com BSA a 0,25% incubados a 37-C por 40 minutos com insulina marcada com iodo 125 e anticorpo anti-insulina. A separaçäo do hormônio ligado pelo anticorpo é conseguida com polietilenoglicol (P.M. 6000) a 17% e a contagem realizada de imediato. Para apressar o ensaio, a curva padräo é preparada na véspera. Os resultados säo obtidos em 90 minutos e para sua validaçäo comparamo-los com os do método convencional, ficando evidente a sua similaridade (p>0,05). Este método rápido foi utilizado para localizaçäo intra-operatória do insulinoma de uma paciente em que, embora o diagnóstico clínico e laboratorial fosse indubitável, a localizaçäo do tumor era duvidosa após o emprego dos métodos radiológicos e ultra-sonográficos. A colheita das amostras durante o ato cirúrgico, realizada em diversos pontos da veia pancreática e na veia esplénica, e as dosagens das insulinemias pelo método rápido permitiram a orientaçäo da ressecçäo do páncreas e a retirada do tumor

Contribuiçäo ao estudo do mecanismo da pertubaçäo da homeostase glicêmica no hipertiroidismo

Objetivando investigar a natureza da influência do hipertiroidismo no metabolismo dos carboidratos e aparecimento ou agravamento do diabete que pode ocorrer, estudamos dez pacientes tirotóxicos portadores de doença de Graves antes e após o tratamento, inicialmente com propranolol e, depois, com propiltiouracil. O uso do propranolol näo interferiu com a tolerância à glicose secreçäo de insulina ou receptores para insulina em eritrócitos. O tratamento com propiltiouracil reduziu a insulinemia basal e aumentou a ligaçäo específica máxima da insulina a eritrócitos (p < 0,005). Concluímos que o hipertiroidismo induz a resistência à insulina por diminuir a ligaçäo da insulina a seus recptores específicos nos tecidos. Essa resistência à insulina exige maior secreçäo do hormônio e pode causar intolerância à glicose em indivíduos suscetíveis. Isto é, portadores de reserva pancreática diminuída em funçäo da idade ou de herança diabética