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Obesity is a complex, multifactorial condition contributing to a chronic prooxidant and proinflammatory state and to deterioration of glucose and lipid metabolism. It increases the risk of several noncommunicable diseases, including type 2 diabetes (T2D), cardiovascular disease (CVD), and some types of cancer [7,8]. Known contributing factors include imbalances in pathways of glucose and lipid metabolism that occur because of variations in quantity and quality of the diet, sedentary lifestyle, and genetic predisposition [9,10]. Obesity arises as a consequence of how the body regulates energy intake, energy expenditure, and energy storage, and it reflects a state of positive energy balance largely caused by westernized environmental pressures [11] resulting in an energy mismatch. This operates through dietary behaviors that do not trigger strong biological opposition [12]. A vicious cycle ensues, involving a state of excessive insulin secretion and a series of metabolic responses that produce systemic insulin resistance [13]. Desensitization to insulin action is accompanied by increased oxidative stress [14] and increased leptin secretion, inflammation, and a decreased ability to metabolize lipid and default energy storage as adipose tissue [15]. Furthermore, changes in the action of endocrine regulators including insulin, leptin, ghrelin, and glucagon-like peptide-1 (GLP-1) disturb appetite regulation in the obese state, rendering sustained weight loss difficult to achieve [16]. In this setting, the regulation of energy balance is biased toward protection against weight loss, further fat accumulation, and disease progression [12,17].
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