The Hidden Price of Plenty: Oxidative Stress and Calorie-Induced Cardiometabolic Dysfunction

Abstract

Overnutrition is a predominant issue in contemporary society, increasing rapidly despite considerable progress in our comprehension of nutrition, the health consequences of different food categories, and the dangers linked to excessive calorie consumption. The pathways connecting obesity to associated disorders are intricate, although research has consistently identified oxidative stress as a principal facilitator of the progression of many diseases. In this paper, the synthesis of various reactive species at the molecular level is studied, and the influence of diet on their production is assessed, with a thorough examination of the cellular mechanisms involved. Furthermore, the correlation between oxidative stress and the development of cardiometabolic diseases is explored, highlighting the most recent and relevant research in the field.

Keywords: adiposity; metabolic cardiovascular syndrome; nitro-oxidative; nutrition; nutritional physiological phenomena; obesity; stress.

Figure 1

Schematic representation of obesity-induced pathophysiological mechanisms leading to HFpEF, highlighting endothelial dysfunction, systemic inflammation, and metabolic derangements. Abbreviations: FFA: free fatty acids; HF: heart failure; LA: left atria; RAAS: renin–angiotensin–aldosterone system; SNS: sympathetic nervous system. * See text for further information.

Figure 2

Integrated model of the cardio-renal-metabolic syndrome in obesity, with therapeutic targets highlighted in red. Abbreviations: CPAP: continuous positive airway pressure; DM: diabetes mellitus; GLP-1 RA: glucagon-like peptide-1 receptor agonists; RAAS: renin–angiotensin–aldosterone system; SGLT2i: Sodium/glucose cotransporter-2 inhibitors.