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 with 5,842 participants (Barr et al., 2007). This study suggests that a large number of Australians suffer mortality each year from cardiovascular disease associated with abnormal glucose metabolism. The Framingham Heart Study found 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% weight gain increases the risk of hypertension by 30% over a four-year period. Increased sympathetic activity, impairment of the renin-angiotensin system, fluid volume retention, peripheral vasoconstriction, dyslipidemia, increased blood viscosity due to increased hematocrit and fibrinogen can increase overload of pressure on the heart in cases of obesity (Schunkert, 2002). Several studies also suggest that the cause of hypertension itself may contribute to left ventricular hypertrophy in obese individuals, as increased BMI increases the risk 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 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; a major vasodilator) from L-arginine in endothelial cells is a major factor contributing to impaired insulin action in the vascular system. obese and diabetic subjects. Obesity results from an imbalance between energy intake and expenditure. Increasing 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..