RESUMO
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.
Assuntos
Glicemia/análise , Dieta Hiperlipídica , Hipoglicemiantes/administração & dosagem , Insulina/administração & dosagem , Lipídeos/sangue , Redução de Peso/efeitos dos fármacos , Animais , Glicemia/efeitos dos fármacos , Hipoglicemiantes/farmacologia , Insulina/farmacologia , Masculino , Radioimunoensaio , Ratos , Ratos WistarRESUMO
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.
Assuntos
Animais , Masculino , Ratos , Glicemia/análise , Redução de Peso/efeitos dos fármacos , Dieta Hiperlipídica , Hipoglicemiantes/administração & dosagem , Insulina/administração & dosagem , Lipídeos/sangue , Glicemia/efeitos dos fármacos , Radioimunoensaio , Ratos Wistar , Hipoglicemiantes/farmacologia , Insulina/farmacologiaRESUMO
The aim of this study was to analyze the correlation between triglyceride (TG) serum levels in obese and non-obese patients in a simulated postprandial state. Both groups showed TG levels < 150 mg/dL when fasting. After 12 h fasting, the subjects ingested a lipid overload diet and blood samples were collected. The variation between fasting and the postprandial TG peak levels were analyzed. The peak of postprandial TG levels occurred 4 h after the lipid overload in both groups. When the subjects were not fasting, the majority of non-obese subjects remained within the range of normal TG values, but the values for the obese group remained elevated. There was a significant correlation between Body Mass Index (BMI) and TG at each time point until 2 h after the meal, but the data did not show a correlation after 3 h. According to the receiver-operating characteristics (ROC) curve, postprandial TG values were not a good predictor of obesity (based on BMI), but they were a predictor of non-obesity. This study reinforces the importance of measuring non-fasting TG levels in obese and non-obese subjects, because some non-obese patients probably had altered fat metabolism, indicating that this examination could be an indicator of metabolic risk.