Adipate, together with Suberate and Ethylmalonate are all functional markers for deficiency of carnitine.

Carnitine is needed to move fatty acids into the mitochondria where they are converted to energy using vitamin B2.

If carnitine is sufficient long-chain fatty acids go through beta-oxidation in the mitochondria.

When insufficient levels of carnitine or vitamin B2 slow down this process, other parts of the cellular machinery take over and make adipate and suberate.

A similar block in another pathway causes high ethylmalonate. Since most of our bodies’ energy is produced from the burning of fatty acids, our muscles and brain suffer when this cellular energy pathway is blocked. Anything that interferes with the normal fatty acid oxidation may reveal high levels of these metabolites.

Dietary fatty acids are metabolized into fuel sources using beta-oxidation. Fatty acid conversion into Acetyl-CoA requires transport across the mitochondrial membrane via the carnitine shuttle. When beta-oxidation is impaired, fats are metabolized using an alternate pathway called omega-oxidation. Omega-oxidation results in elevated levels of dicarboxylic acids such as adipic acid and suberic acid. Impaired beta-oxidation occurs in carnitine deficiency or enzymatic dysfunction due to lack of nutrient cofactors. Vitamin B2 and magnesium play a role in optimizing beta-oxidation.

Adipic Acid, together with Suberate and Ethylmalonate are all functional markers for deficiency of carnitine.

Adipic Acid, together with Suberate and Ethylmalonate are all functional markers for deficiency of carnitine.

Adipic Acid, together with Suberate and Ethylmalonate are all functional markers for deficiency of carnitine.

Adipic Acid, together with Suberate and Ethylmalonate are all functional markers for deficiency of carnitine.

Dietary fatty acids are metabolized into fuel sources using beta-oxidation. Fatty acid conversion into Acetyl-CoA requires transport across the mitochondrial membrane via the carnitine shuttle. When beta-oxidation is impaired, fats are metabolized using an alternate pathway called omega-oxidation. Omega-oxidation results in elevated levels of dicarboxylic acids such as adipic acid and suberic acid. Impaired beta-oxidation occurs in carnitine deficiency or enzymatic dysfunction due to lack of nutrient cofactors. Vitamin B2 and magnesium play a role in optimizing beta-oxidation.

Adipic acid is an organic compound commonly found in a variety of foods, especially those containing artificial flavors and additives. It is a significant component in the production of nylon and other synthetic fibers but is also present in small amounts in our bodies as a byproduct of fatty acid metabolism. In a nutritional context, the measurement of adipic acid levels can provide valuable insights into an individual's metabolic health. Elevated levels of adipic acid in the body may indicate issues related to the breakdown of fats, which could be influenced by dietary habits, metabolic disorders, or the overconsumption of processed foods. Monitoring adipic acid can help in identifying imbalances in fatty acid metabolism, guiding dietary adjustments, and potentially improving overall metabolic function. This marker is particularly useful for assessing how well the body is managing the breakdown and utilization of fats, which is crucial for maintaining energy balance and preventing the accumulation of harmful substances in the bloodstream. Understanding adipic acid levels can thus play a critical role in optimizing nutritional health and preventing metabolic complications.

Dietary fatty acids are metabolized into fuel sources using beta-oxidation. Fatty acid conversion into Acetyl-CoA requires transport across the mitochondrial membrane via the carnitine shuttle. When beta-oxidation is impaired, fats are metabolized using an alternate pathway called omega-oxidation. Omega-oxidation results in elevated levels of dicarboxylic acids such as adipic acid and suberic acid. Impaired beta-oxidation occurs in carnitine deficiency or enzymatic dysfunction due to lack of nutrient cofactors. Vitamin B2 and magnesium play a role in optimizing beta-oxidation.

Adipic Acid, together with Suberate and Ethylmalonate are all functional markers for deficiency of carnitine.

Adipic Acid, together with Suberate and Ethylmalonate are all functional markers for deficiency of carnitine.

The adiponectin blood test determines the levels of adiponectin in blood. It is used to diagnose metabolic disorders such as Type 2 diabetes. Adiponectin is a hormone that is released from fat cells and will help to control the inflammation of tissue. The hormone will also boost insulin sensitivity and increases the breakdown of fatty acid in the liver. This process will, in turn, decrease the manufacturing of glucose by the liver. A low result might suggest Type 2 diabetes mellitus or metabolic syndrome. 

Adiponectin is a crucial marker often included in metabolic test panels to provide insights into an individual's metabolic health. This protein hormone, produced and secreted by fat cells, plays a significant role in regulating glucose levels and fatty acid breakdown in the body. High levels of adiponectin are associated with a lower risk of several metabolic disorders, including type 2 diabetes, obesity, and cardiovascular disease. Essentially, adiponectin enhances the body's sensitivity to insulin, making it an important indicator of metabolic syndrome and insulin resistance.

Adjusted calcium is useful in the interpretation of calcium levels when albumin levels are low.

Adjusted calcium, also known as corrected calcium, is a critical marker on a Comprehensive Metabolic Panel (CMP), which is a blood test used to assess your overall health and detect various medical conditions. Calcium is an essential mineral in the body, crucial for bone health, muscle function, nerve signaling, and blood clotting. The CMP measures the total calcium in your blood, but this value can be influenced by the levels of albumin, a protein that binds calcium. Since only the unbound or "free" calcium is biologically active, it's important to adjust the total calcium level for the albumin level to get a more accurate understanding of your calcium status. This is particularly important for people with abnormal albumin levels, such as those with liver disease, kidney disease, or severe malnutrition. The adjusted calcium value helps doctors make better-informed decisions about diagnosing and treating conditions related to calcium imbalances, such as hypercalcemia (high calcium levels) or hypocalcemia (low calcium levels). By providing a clearer picture of the physiologically active calcium, the adjusted calcium marker is an invaluable tool for ensuring appropriate medical care.

ADMA/SDMA may be measured in individuals with multiple risk factors for the development of CVD.

One of the earliest manifestations of endothelial dysfunction is nitric oxide (NO) deficiency, which promotes atherosclerosis. Asymmetric dimethylarginine (ADMA) and symmetric dimethylarginine (SDMA), its structural isomer, are metabolites of L-arginine, an amino acid that is catalyzed to L-citrulline and NO by nitric oxide synthase (NOS).

Both ADMA and SDMA have distinct pathophysiologies and manifestations. ADMA is a competitive inhibitor of NOS thereby reducing NO production and promoting endothelial dysfunction. SDMA also interferes with NO production, but does so indirectly by reducing the cellular availability of arginine. ADMA is primarily cleared through enzymatic degradation in the bloodstream and its presence identifies subclinical cardiovascular disease (CVD). Conversely, SDMA is primarily excreted in the urine and identifies reduced renal function.

Adrenal reserve, represented by the marker THE+5α-THF+THF (tetrahydrocortisone, 5-alpha-tetrahydrocortisol, and tetrahydrocortisol) on a dried urine essential hormone profile, is a critical indicator of adrenal gland function, particularly in women during the luteal phase of their menstrual cycle. This phase, which occurs after ovulation and before menstruation, is characterized by significant hormonal fluctuations that can influence adrenal function. The adrenal reserve marker provides valuable insights into the body's ability to produce and metabolize cortisol, a vital stress hormone.