GLUT4 content decreases along with insulin resistance and high levels of inflammatory markers in rats with metabolic syndrome

Spontaneously hypertensive neonate rats (18/group) were treated with monosodium glutamate (MetS) during 9 days, and compared with Wistar-Kyoto (C) and saline-treated SHR (H). Blood pressure (BP) and lipid levels, C-reactive protein (CRP), interleukin 6 (IL-6), TNF-α and adiponectin were evaluated. GLUT4 protein was analysed in the heart, white adipose tissue and gastrocnemius. Studies were performed at 3 (3-mo), 6 (6-mo) and 9 (9-mo) months of age.MetS rats were more insulin resistant (p<0.001, all ages) and had higher BP (3-mo: p<0.001, 6-mo: p？=？0.001, 9-mo: p？=？0.015) as compared to C. At 6 months, CRP, IL-6 and TNF-α were higher (p<0.001, all comparisons) in MetS rats vs H, but adiponectin was lower in MetS at 9 months (MetS: 32？±？2, H: 42？±？2, C: 45？±？2 pg/mL; p<0.001). GLUT4 protein was reduced in MetS as compared to C rats at 3, 6 and 9-mo, respectively (Heart: 54%, 50% and 57%; Gastrocnemius: 37%, 56% and 50%; Adipose tissue: 69%, 61% and 69%).MSG-treated SHR presented all metabolic syndrome characteristics, as well as reduced GLUT4 content, which must play a key role in the impaired glycemic homeostasis of the metabolic syndrome.Metabolic syndrome is a highly prevalent condition [1] and a determinant of increased cardiovascular risk [2] and type 2 diabetes [3]. Insulin resistance is the key factor that leads to several of the abnormalities associated with the syndrome [4]. The link between insulin resistance and metabolic syndrome was suggested to be inflammation [5], which is the most widely accepted hypothesis for its development [5-9]. Besides, hypertension is related to insulin resistance [4], a feature that can be genetically induced [10,11].GLUT4 is the insulin-sensitive glucose transporter which main role is to provide the insulin-stimulated glucose uptake by adipose tissue, skeletal muscle and the heart, tissues that specifically express this protein [12]. It has been extensively reported that transgenic mice lacking or overexpressing GLUT4 respecti