Obesity and hypertension, major risk factors for the metabolic syndrome, render individuals susceptible to an increased risk of cardiovascular complications, such as adverse cardiac remodeling and heart failure. There has been much investigation into the role that an increase in the renin-angiotensin-aldosterone system (RAAS) plays in the pathogenesis of metabolic syndrome and in particular, how aldosterone mediates left ventricular hypertrophy and increased cardiac fibrosis via its interaction with the mineralocorticoid receptor (MR). Here, we review the pertinent findings that link obesity with elevated aldosterone and the development of cardiac hypertrophy and fibrosis associated with the metabolic syndrome. These studies illustrate a complex cross-talk between adipose tissue, the heart, and the adrenal cortex. Furthermore, we discuss findings from our laboratory that suggest that cardiac hypertrophy and fibrosis in the metabolic syndrome may involve cross-talk between aldosterone and adipokines (such as adiponectin). 1. Introduction The metabolic syndrome is characterized by a collection of cardiovascular risk factors that include obesity, dyslipidemia, hypertension, and glucose intolerance/insulin resistance and together predispose individuals to an increased risk of heart disease, stroke and diabetes [1, 2]. The increased prevalence of obesity and the metabolic syndrome portends a greater risk of cardiovascular disease such as heart failure and premature death [3–6]. Nearly 70 million adults in the USA are obese (defined as a body mass index (BMI) ≥30？kg/m2) [7, 8]. Although the pathogenesis of the metabolic syndrome has yet to be fully elucidated, increasing evidence has linked the renin-angiotensin-aldosterone system (RAAS) with the associated risk factors, including obesity and hypertension [9–11]. Elevated plasma aldosterone levels are found in patients with the metabolic syndrome [12], in resistant hypertension [13, 14], and are associated with the development of left ventricular (LV) hypertrophy (LVH) and increased cardiac fibrosis [13, 15, 16]. In addition, elevated RAAS activity is evident in patients with congestive heart failure [17]. Importantly, patients with obesity, hypertension, or diabetes mellitus are prone to diastolic heart failure which may be characterized by LVH. Profibrotic and proinflammatory effects observed in heart failure patients have been attributed to elevated angiotensin II (Ang-II) levels [18, 19]; however, it is now believed that an elevation in plasma aldosterone may also be in part responsible for these events
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