Exploratory metabolomics of metabolic syndrome: A status report

Abstract

Metabolic syndrome (MetS) is as a cluster of cardio-metabolic factors that greatly increase the risk of chronic diseases such as type II diabetes mellitus and atherosclerotic cardiovascular disease. In the United States, obesity, physical inactivity, aging, and genetics (to a minor extent) have arisen as risk factors for developing MetS. Although 35% of American adults suffer from MetS, its pathogenesis largely remains unknown. Worse, there is a lack of screening and optimum therapy for this disease. Researchers have consequently turned towards metabolomics to identify biomarkers to better understand MetS. The purpose of this review is to characterize various metabolites and their potential connections to MetS. Numerous studies have also characterized MetS as a disease of increased inflammation, and therefore this review also explores how metabolites play a role in various inflammatory pathways. Our review explores a broad range of metabolites including biogenic amines, branched chain amino acids, aromatic amines, phosphatidylcholines, as well as a variety of other molecules. We will explore their biochemical pathways and their potential role in serving as biomarkers.

Circulating Pro- and Anti-Inflammatory Metabolites and Its Potential Role in Rheumatoid Arthritis Pathogenesis

“…RA patients present several comorbidities including obesity, metabolic syndrome, and sarcopenia, probably triggered by a disbalance of proinflammatory cytokines including TNF and IL-6 among other causes [73][74][75][76][77], that will modify the circulating metabolites [78]. Several studies have investigated circulating metabolic changes related to the metabolic syndrome and obesity [79,80]. Of interest, a lot of circulating metabolites that are different in RA patients compared to controls could be related to associated metabolic syndrome, since choline metabolism (especially TMAO and carnitine), aminoacids (alanine, glutamine, glutamate, arginine, aspartate, asparagine, histidine, methionine, cysteine, lysine, branched-chain amino acids (BCAA), phenylaniline, tyrosine, and tryptophan) and phospholipids (phosphatydilcholines) also change in those with metabolic syndrome [80].…”

“…Several studies have investigated circulating metabolic changes related to the metabolic syndrome and obesity [79,80]. Of interest, a lot of circulating metabolites that are different in RA patients compared to controls could be related to associated metabolic syndrome, since choline metabolism (especially TMAO and carnitine), aminoacids (alanine, glutamine, glutamate, arginine, aspartate, asparagine, histidine, methionine, cysteine, lysine, branched-chain amino acids (BCAA), phenylaniline, tyrosine, and tryptophan) and phospholipids (phosphatydilcholines) also change in those with metabolic syndrome [80]. Several works on muscle mass have also suggested that some circulating metabolites can be biomarkers of muscle mass and sarcopenia [81].…”

Detection of Early Disease Risk Factors Associated with Metabolic Syndrome: A New Era with the NMR Metabolomics Assessment

“…The two major contributors of the GlycA signal are α1-acid glycoprotein and haptoglobin, synthesized and secreted by neutrophils granules, as well by the liver [66]. The potential risk associated with elevated GlycA would relate to activation of systemic inflammatory pathways, because GlycA identifies aggregates of glycan moieties on circulating glycoproteins, which the majority of them are acute phase reactants and immunologic proteins [62,180]. In a large study with apparently healthy individuals, CVD mortality was significantly associated with elevated levels of GlycA [66].…”

Altered Metabolic Profile and Adipocyte Insulin Resistance Mark Severe Liver Fibrosis in Patients with Chronic Liver Disease

“…Metabolomics and lipidomics are used to assess the metabolic factors involved in the onset of metabolic diseases, to understand the different metabolic pathways involved in organ damage [1,2]. Several studies have shown that in patients with chronic liver disease (CLD) and HCV infection, insulin resistance when present affects the liver, muscle and adipose tissue by altering both glucose and lipid homeostasis [3,4].…”