ABSTRACT Introduction/Aim: The gut has shown to have a pivotal role on the pathophysiology of metabolic disease. Food stimulation of distal intestinal segments promotes enterohormones secretion influencing insulin metabolism. In diabetic rats, oral insulin has potential to change intestinal epithelium behavior. This macromolecule promotes positive effects on laboratorial metabolic parameters and decreases diabetic intestinal hypertrophy. This study aims to test if oral insulin can influence metabolic parameters and intestinal weight in obese non-diabetic rats. Methods: Twelve weeks old Wistar rats were divided in 3 groups: control (CTRL) standard chow group; high fat diet low carbohydrates group (HFD) and HFD plus daily oral 20U insulin gavage (HFD+INS). Weight and food consumption were weekly obtained. After eight weeks, fasting blood samples were collected for laboratorial analysis. After euthanasia gut samples were isolated. Results: Rat oral insulin treatment decreased body weight gain (p<0,001), fasting glucose and triglycerides serum levels (p<0,05) an increased intestinal weight of distal ileum (P<0,05). Animal submitted to high fat diet presented higher levels of HOMA-IR although significant difference to CT was not achieved. HOMA-beta were significantly higher (p<0.05) in HFD+INS. Visceral fat was 10% lower in HFD+INS but the difference was not significant. Conclusions: In non-diabetic obese rats, oral insulin improves metabolic malfunction associated to rescue of beta-cell activity.

A utilização do iodo antes de cirurgias de tireóide visa a redução do fluxo sangüíneo para a glândula e melhora da hemostasia. Para tentar elucidar o mecanismo pelo qual a vasoconstricção se instala, foi determinada a atividade colinesterásica em tireóides de ratos Wistar machos (240-250g de peso corporal), submetidos a uma sobrecarga oral de iodo pela oferta de solução aquosa de iodato de potássio (KIO3 3mig/ml) como água de beber, por 3 e 7 dias; o grupo controle recebeu água durante o mesmo período. Ao final do tratamento os animais foram sacrificados e suas tireóides retiradas, limpas e pesadas; o rim direito e o lobo direito do fígado foram usados como controles da atividade colinesterásica. Foram preparados homogeneizados em tampão fosfato (pH=8,0), contendo 0,32M de sacarose, na concentração de 40mg de tecido/ml. Os ratos que receberam KIO3 por 7 dias tiveram diminuição no peso da tireóide quando comparados aos controles (p<0,05), o mesmo não acontecendo aos 3 dias de tratamento. Aos 3 dias de tratamento, a atividade colinesterásica tireóidea foi de 5,38±0,36 nmol/min.mg para o grupo controle (n=12) e de 5,43±0,98 nmol/min.mg para o grupo tratado (n=11) (NS); valores bastante similares foram também encontrados com o tratamento de 7 dias (controles: 5,42±0,27 nmol/min.mg (n=8) e tratados: 5,63±0,88 nmol/min.mg (n=8); NS). Nossos resultados sugerem que, a despeito da vasoconstricção, não há alteração da atividade colinesterásica na tireóide em resposta a sobrecarga oral de iodo.

Iodine is given during the 7 to 10 days immediately preceding thyroid operation to decrease the vascularity of the gland, making it less friable and decreasing difficulties for the surgeon. The present work evaluated cholinesterase activity in rat thyroid glands on high iodine intake to establish a possible relationship between high iodine-induced vasoconstriction and parasympathetic activity. Male Wistar rats weighing 240-250g were given KIO3 (3mug/ml) as drinking water for 3 and 7 days; the control groups received tap water. At the end of the treatment period rats were sacrificed and their thyroid glands taken out, washed and weighed; the liver and the kidney were used as parameters of cholinesterase activity. Rats that received KIO3 for 7 days had a decreased thyroid gland weight compared to controls (p<0.05). However, no significant decrease in thyroid weight occurred after 3 days of treatment. At 3 days thyroid gland cholinesterase activity (nmol of acetylthiocholine hydrolysed/min.mg of protein) was 5.38±0.36 (mean±SD) in the control group (n=12) and 5.43±0.98 in the treated group (n=11) (NS). After 7 days of treatment cholinesterase activity was 5.42±0.27 in the control group (n=8) and 5.63±0.88 in the treated group (n=8) (NS). Our results suggest that the iodine-induced thyroid gland vasoconstriction is not due to changes in thyroid cholinesterase activity.