Obesity is becoming a major health problem in developing countries such as Australia, North America, Europe and other developing countries. The Australian Diabetes, Obesity and Lifestyle Study (AUSDIAB) predicts changes in glucose indices; health behavior and diabetes incidence in 5-year follow-up experiments among 5842 participants (Barr et al., 2007). This study suggests that large numbers of Australians suffered mortality each year due to cardiovascular disease associated with abnormal glucose metabolism. The Framingham Heart Study revealed that hypertension, diabetes, and left ventricular remodeling lead to the development of congestive heart failure (Levy et al., 1996). The Framingham Heart Study also found that a 5 percent weight gain increased the chance of hypertension by 30 percent over a four-year period. An increase in sympathetic activity, an alteration of the renin-angiotensin system, fluid volume retention, peripheral vasoconstriction, dyslipidemia, increased blood viscosity due to increased hematocrit and fibrinogen may increase the overload pressure on the heart in obesity (Schunkert, 2002). Several studies also suggest that the cause of hypertension itself may contribute to left ventricular hypertrophy in obese individuals as increasing BMI increases the possibility of hypertension (De Simone et al., 1994; Avelar et al., 2007). High dietary fat intake increases the expression of angiotensin IB (AT1B) and endothelin A (ETA) receptors (Neilsen et al., 2004; Zhang et al., 2005). Plasma concentrations of angiotensin II and endothelin 1 (physiological vasoconstrictor agents) were increased in both obese patients and animal models (Barton et al., 2000; Neilsen et al., 2004; Zhang et al., 2005). Recent studies have shown that reduced synthesis of nitric oxide (NO; an important vasodilator) from L-arginine in endothelial cells is an important factor contributing to the impaired action of insulin in the vasculature of obese and diabetic subjects. Obesity results from an imbalance between energy intake and expenditure. Growing evidence suggests that arginine plays an important role in regulating the metabolism of energy substrates in mammals (Frank et al. 2007; Jobgen et al. 2006). NO is synthesized from L-arginine by NO synthase. As a signaling molecule, physiological levels of NO stimulate glucose uptake, as well as glucose and fatty acid oxidation in skeletal muscle, heart, liver, and adipose tissues (Jobgen et al. 2006). Nitric oxide also inhibits the synthesis of glucose, glycogen, and lipids in the liver and adipose tissues and enhances lipolysis in subcutaneous adipocytes (Jobgen et al..