Abstract
Leptin is an adipocytokine that consists of 167 amino acids. It functions as a regulator of hunger and energy expenditure. Leptin loses its ability to carry out its physiological function at high serum levels, and many studies have associated this loss of function with the development of coronary artery disease (CAD). This literature review aims to outline the steps by which leptin leads to CAD and atherosclerosis. Two independent researchers extracted animal and human studies from PubMed and Google Scholar databases. We applied PubMed search builder options: pathology, pathophysiology, metabolism, and physiology to focus the search results. This study concluded that the mechanism by which leptin might lead to CAD via pressor and depressor effects on vascular tone, enhancing atherosclerotic plaques, and through numerous single nucleotide polymorphisms, the most common being that of the leptin receptor gene rs113701.
Highlights
BackgroundCoronary artery disease is a notable cause of death globally
These findings suggested that Leptin leads to hypertension, but the increased nitric oxide (NO) production and endothelial nitric oxide synthase (eNOS) activity with depressor effects on vascular tone with leptin infusion contradict this theory
Leptin binds to wild-type and ob/ob mice receptors, and its induction of inflammation and endothelial damage results in enhanced atherosclerotic plaque formation
Summary
Coronary artery disease is a notable cause of death globally. There were 485.6 million coronary artery disease (CAD) cases in 2020; this represents an increase of 28.5% from 2017 [1]. The Bielecka-Dabrowa et al study showed that hypertension was associated with increased leptin and arterial stiffness It concluded that leptin achieved its pressor effects through the sympathetic nervous systems [19]. The results allude to a dose, length, and route-dependent leptin-induced vasoconstriction These findings suggested that Leptin leads to hypertension, but the increased NO production and eNOS activity with depressor effects on vascular tone with leptin infusion contradict this theory. Singh et al demonstrated two crucial takeaway points in their study They saw increased CRP concentrations at very high serum leptin levels and concluded; CRP did not predict cardiovascular disease independently, unlike leptin, which maintained a statistically significant predictive power. An et al sought to determine whether LEPR polymorphisms at Q223R (rs1137101) and K109R (rs1137100) were associated with increased risk of non-alcohol fatty liver disease (NAFLD) and coronary atherosclerosis in the Chinese Han population. Whether this is a practical approach to determining an individual's risk for CAD will depend on the availability of resources and overall cost
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