Cardiometabolic
65 biomarkers of 5 different classes from 200μl sample volume on GC- and LC-MS/MS platforms. Contact our experts for any questions or inquiries.
Why did we design this panel?
We developed this targeted metabolomics panel for investigating cardiometabolic health to achieve high specificity and sensitivity in identifying biomarkers and metabolites, understanding disease mechanisms, and supporting research and personalized medicine. This approach aids in:
Early Detection: Enabling early identification of individuals at risk of cardiometabolic diseases, such as diabetes, hypertension, and heart disease, before symptoms appear.
Precise Diagnosis: The panel provides a more accurate diagnosis by targeting specific biomarkers associated with cardiometabolic health, allowing for tailored interventions.
Monitoring Disease Progression: Longitudinal assessments can track changes in profiles over time, helping clinicians understand disease progression and the impact of lifestyle or therapeutic interventions.
Treatment Optimization: The panel can help in selecting the most effective treatment options and adjusting them according to the individual’s specific metabolic profile.
Integration with Other Omics: Combined with genomic, proteomic, or lipidomic data, the cardiometabolic panel can offer a more comprehensive understanding of the disease, advancing research and enabling the development of novel therapeutics.
Improved Outcomes in Population Health: On a larger scale, the cardiometabolic panel can help in population screening and identify trends or high-risk groups, informing public health strategies and interventions.
Applications: Atherosclerosis and peripheral artery disease (PAD), cardiovascular diseases, chronic kidney disease (CKD), metabolic syndrome, neurodegenerative diseases, metabolic dysfunction-associated fatty liver disease (MAFLD), obesity, polycystic ovary syndrome (PCOS), type 2 diabetes and prediabetes.
Amino acids and catabolites
31 markers by GC-MS/MS
Abnormal concentrations of free amino acids in plasma have been associated with risk of cancer, metabolic syndrome, diabetes. Low levels are observed in frail, elderly persons. Elevated branched chain amino acids (BCAA; Leu, Ile and Val) are associated with insulin resistance, diabetes type 2, cardiovascular disease and early kidney disease. The valine catabolite, 3-hydroxyisobutyrate (3HIB) is belived to play a key role in the development of insulin resistance. β-Aminoisobutyrate (BAIBA) increases with exercise and is inversely association with cardiometabolic risk factors.
Alanine, Arginine, Asparagine, Aspartic acid, Glutamic acid, Glutamine, Glycine, Histidine, Isoleucine, Kynurenine, Leucine, Lysine, Methionine, Ornithine, Phenylalanine, Proline, Sarcosine, Serine, Threonine, Total cysteine, Tryptophan, Tyrosine, Valine, 2-Aminoadipic acid, 2-Hydroxybutyrate, 3-Hydroxysiobutyrate, α-Hydroxyglutaric acid, β-Alanine, β-Aminoisobutyrate, β-Hydroxy B-methylbutyric acid, Phenylacetylglutamine
Acylcarnitines
23 markers by LC-MS/MS
Acylcarnitine esters are formed from the CoASH esters of acetate, propionate, butyrate, medium-chain, long-chain and very-long-chain fatty acids. Acylcarnitines cross the mitochondrial membrane, and such transport is required for beta-oxidation of long-chain fatty acids for energy production. Carnitine is mainly obtained through the diet, can be consumed as supplement, but about 30% is supplied by de novo synthesis from trimethyllysine (TML), which takes place in liver and kidney. The final step in the synthesis is catalyzed by the α-ketoglutarate-dependent enzyme, gamma-butyrobetaine dioxygenase (BBOX) that converts gamma-butyrylbetaine (BB) into carnitine. Circulating levels of carnitine and acylcarnitines have been related to risk of insulin resistance, diabetes 2, MAFLD and cardiovascular disease.
BB, C0, C2, C3, C3-DC, C4, C4-OH, C4-DC, iC5, C5-DC, C5:1, C6, C8, C10, C12, C14, C14-OH, C16, C16-OH, C18, C18-OH, C18:1, C18:2
TCA metabolites
7 markers by GC-MS/MS
Studies on metabolomics involving Krebs cycle intermediates in relation to human health and disease usually include few patients and have been performed only recently. These metabolites have been related to BMI, cardiovascular disease (pyruvate, citrate, succinate), diabetes (pyruvate, isocitrate, succinate), MAFLD (isocitrate and citrate), longevity (isocitrate), asthma (succinate), disease activity in rheumatoid arthritis patients (itaconate), and worsening of clinical outcome in cancer patients (succinate, fumarate and α-hydroxyglutarate).
α-Ketoglutarate, Citrate, Fumarate, Isocitrate, Lactate, Malate, Pyruvate
Ketone bodies
2 markers by GC-MS/MS
3-Hydroxybutyrate (bHB) is the most abundant ketone body. It is synthesized from acyl-CoA primarily in the liver. Increasing serum/plasma bHB concentrations reflect upregulated fatty acid β-oxidation as well as ketogenic amino acids catabolism in the liver and skeletal muscle to compensate insufficient glucose supply. bHB synthesis is stimulated and serum/plasma levels increase under conditions of fasting, endurance exercise, malnutrition or metabolic disorders including diabetes mellitus. Acetoacetate (AcAc) is a ketone body primarily produced in the liver under conditions of excessive fatty acid breakdown, including diabetes mellitus leading to diabetic ketoacidosis. High levels of ketone bodies, like bHB and AcAc, are not only indicators of diabetic hyperglycemia, but also markers of disturbed glucose metabolism in the prediabetic state.
Acetoacetate, 3-Hydroxybutyrate
AGEs
2 markers by LC-MS/MS
N(ε)-(carboxymethyl)lysine (CML) and N(6)-(1-carboxyethyl)-L-lysine (CEL) are advanced glycation end products (AGEs) generated by the Maillard reaction (MR) during thermal treatment of foods or are formed in vivo by nonenzymatic chemical reactions, taking place in tissues or fluid where significant concentration of glucose, fructose, or more reactive dicarbonyls react with proteins. CEL is primarily formed by reaction between methylglyoxal and lysine (the AGE path), which is dependent on hyperglycaemia. Thus, the pathways contributing to CEL formation appear to be more limited compared with CML. Like CML, CEL in tissues and serum/plasma increase with age, and have been assigned a role in the pathogenesis of age-related, chronic diseases, including diabetes, cardiovascular disease, Alzheimer’s disease and renal dysfunction.
Carboxyethyllysine, Carboxymethyllysine