Efeito da associação entre obesidade neuroendócrina e exócrina experimental sobre a pressão arterial de cauda e o metabolismo de glicose de ratos Wistar Effects of the association of experimental neuroendocrine and exocrine obesity on tail blood pressure and glucose metabolism in Wistar rats

Abstract

OBJETIVO: Estudar dois modelos de obesidade, exócrina e endócrina, e sua associação sobre a pressão arterial de cauda (PAC), o peso corporal (PC), o metabolismo glicídico (ISI) e gordura epididimal relativa (GER). MÉTODOS: Foram estudados ratos machos da cepa Wistar. O grupo MSG recebeu glutamato monossódico no período neonatal. Aos 3 meses de idade parte desses animais passou a receber dieta cafeteria (CAF). Os animais receberam controle salina no período neonatal. Durante 12 semanas foram pesados (PC) e tiveram a pressão arterial de cauda (PAC) aferida. O Teste de Tolerância Oral à Glicose foi realizado e o Índice de Sensibilidade à Insulina (ISI), calculado. O peso ventricular relativo (PVR) e a gordura epididimal relativa (GER) também foram calculados. RESULTADOS: Não se verificou alterações no PC e na PAC. A obesidade induzida pela administração de MSG e CAF, isoladamente, promoveu aumento da resistência à insulina (WST = 23,25 ± 9,31; CAF = 15,92 ± 9,10*; MSG = 13,41 ± 3,84* mg-1mU-1, p OBJECTIVE: To study two different models of obesity, exocrine and endocrine, and its association on tail arterial pressure (TAP), body weight (BW), glucose metabolism and visceral fat content. METHODS: Male Wistar rats were studied. The MSG group was composed by rats that received of MSG in neonatal period. At the 3rd month of life, part of these animals received cafeteria diet. Animals received saline control in the neonatal period. In the 12 weeks of study, body weight and blood pressure were measured twice a week. In the end of this period on, Oral Glucose Tolerance Test (OGTT) was performed and the Insulin Sensitivity Index (ISI) was calculated, also the left Relative Ventricular Weight (RLW) and Relative Epididimal Fat Weight (REFW) were obtained. RESULTS: No changes on BW and TAP were verified. The obesity induced by MSG and CAF, individually, let to increases on insulin resistance (WST = 23,25 ± 9,31; CAF = 15,92 ± 9,10*; MSG = 13,41 ± 3,84* mg-1mU-1, p < 0,05 vs WST) and relative epididimal fat content (WST = 6,20 ± 0,57; CAF = 8,27 ± 1,53*; MSG = 8,23 ± 1,98* g/100 g, *p < 0,05) when these rats were compared to control rats. An enhanced effect upon these parameters was observed with the association of both obesity models (MSG+CAF = 9,34 ± 5,77 mg-1mU-1, p < 0,05 vs MSG and CAF) and visceral fat content (MSG+CAF = 11,12 ± 3,85 g/100g, p < 0,05 vs MSG and CAF). CONCLUSION: The association of these two experimental models of obesity aggravates insulin resistance that probably is due at least in part to the increase of visceral fat content.

Keywords

• obesidade
• pressão arterial
• resistência à insulina
• síndrome X metabólica
• ratos Wistar
• obesity
• blood pressure
• insulin resistance
• metabolic syndrome X
• Wistar rats