Insulin resistance and salt-sensitive hypertension in metabolic syndrome

Metabolic syndrome, which is caused by obesity, is now a global pandemic. Metabolic syndrome is an aggregation of dyslipidaemia, hypertension and diabetes. Moreover, metabolic syndrome is a highly predisposing condition for cardiovascular disease. Recent clinical studies have shown that metabolic syndrome also increases the risk for proteinuria and chronic kidney disease (CKD) [1]. For a definition of metabolic syndrome, indeed, visceral obesity is essential and more than two of the following components: blood pressure, glucose and lipid abnormalities. However, insulin resistance is a key factor to developing these components of metabolic syndrome. Based on recent progress of research on adipocytes, visceral obesity plays a critical role in the development of insulin resistance. Indeed, angiotensionogen, one of adipokines such as TNF-a and NEFA, which are produced by visceral fat, might contribute to the development of insulin resistance in the muscle and adipose tissues [2]. In contrast, lack of insulin resistance in the kidney increases tubular sodium reabsorption by hyperinsulinaemia, leading to sodium retention in the body, and resultant salt-sensitive hypertension [3]. Therefore, there is an intimate relationship between insulin resistance and salt-sensitive hypertension in obese hypertensive patients with metabolic syndrome [4–7]. Insulin resistance in metabolic syndrome