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.
Low levels of adipate can occur if there is insufficient dietary fat or digestive fat malabsorption. While adipate can be synthesized, it is primarily produced by the gastrointestinal microbiome from dietary fats and absorbed from the gastrointestinal system. Adipate and suberate levels may also be low if there are inherited low activity enzyme variants present in the synthesis pathway. An insufficiency of zinc or vitamin B3 may inhibit omega oxidation pathways and decrease adipate levels. Adipate can be used to synthesize succinate and support the Citric Acid Cycle.
Consider supporting adipate synthesis with vitamins B2, B3, CoQ10 (ubiquinone), L-carnitine, magnesium, and zinc.
Adipate may be combined with malonate and converted into succinate to drive the CAC forward. If adipate is low, but succinate is adequate and alpha-ketoglutarate is elevated, conversion to succinate may cause lower adipate levels. Consider increasing healthy fats and supporting fat digestion with digestive enzymes.
Celiac disease or inflammatory bowel syndrome (IBD) may impair digestion and absorption of fats, proteins, minerals, and vitamins. Fat malabsorption can present with gastrointestinal bloating and cramping with pale or greasy stools.
Consider US BIOTEK’S CELIAC PANEL to rule out Celiac disease as a cause of malabsorption.
Consider food allergy and sensitivity testing with IgG, IgA, IgG4, and IgE panels to rule out Ig-mediated inflammation as a cause of malabsorption or other gut symptoms.
Consider an evaluation of gastrointestinal function to determine the need for digestive supports and improved fat assimilation.
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High levels of adipate can occur if there is a high dietary fat load, during fasting, or if there are inherited low-activity enzyme variants in the beta-oxidation pathway. Metabolic syndrome or type II diabetes may increase adipate and suberate levels. An L-carnitine deficiency can inhibit normal beta-oxidation and promote omega-oxidation, increasing adipate and suberate levels. Adipate is converted into succinate and other products in the liver. Dicarboxylic acids (cis- aconitate, isocitrate, succinate, malate, suberate, and adipate) may be excreted in high amounts due to increased mobilization of fatty acids, beta-oxidation defects, increased gut permeability or fasting. In some autistic individuals, there is an inverse relationship between adipate levels and social deficit/communication scores and a direct association with adipate levels and total ASD symptom scores. Adipate levels may increase if liver disorders are present. Exposure to phthalates or butane can also increase adipate levels.
Consider supporting the beta-oxidation pathway with vitamins B2, B3, iron (if deficient), L-carnitine, sulforaphane and a lower-fat diet. Individuals with beta-oxidation defects may have trouble producing enough ketone bodies to successfully accommodate fasting or a “keto” or high-fat diet.
Omega oxidation products can be converted into products that support the CAC. Levels of dicarboxylic acids (cis-aconitate, isocitrate, succinate, malate, suberate, and adipate) can increase when this occurs.
Adipate is primarily produced by the gastrointestinal microbiome from dietary fats. A high dietary fat load may increase levels of adipate, suberate, and beta-hydroxybutyrate.
Type II diabetes or metabolic syndrome can increase not only adipate but suberate, alpha-hydroxybutyrate, lactate, and pyruvate.
Butane exposures may occur due to deliberate inhalation (“huffing”) or from industrial, aerosol propellant or petroleum exposures. Butane “huffing” may result in neurological and cardiovascular symptoms.
Phthalate exposures can inhibit beta-oxidation and increase levels of adipate, suberate, ethylmalonate, and methylsuccinate.
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2-Decenedioic Acid, 2-ET-3-OH-Propionic, 2-Hydroxyadipic, 2-Hydroxybutyric, 2-Hydroxyglutaric, 2-Hydroxyisocaproic, 2-Hydroxyisovaleric, 2-Methyl, 3-Hydroxybutyric, 2-Methylacetoacetic, 2-Methylbutrylglycine, 2-Methylglutaconic Acid, 2-Octenedioic acid, 2-Octenoic Acid, 2-OH-3ME-Valeric, 2-Oxo-3-methylvaleric, 2-OXO-Butyric Acid, 2-OXOADIPIC, 2-Oxoglutaric, 2-Oxoisocaproic, 2-Oxoisovaleric, 2OH-Phenylacetic Acid, 3-Hydroxyadipic, 3-Hydroxybutyric, 3-Hydroxyglutaric, 3-Hydroxyisobutyric, 3-Hydroxyisovaleric, 3-Hydroxypropionic, 3-Hydroxysebacic, 3-Hydroxyvaleric, 3-Methylcrotonylglycine, 3-Methylglutaconic, 3-Methylglutaric, 3-OH-3-Methylglutaric, 3OH-2-Methylvaleric Acid, 3OH-Dodecanedioic Acid, 3OH-Dodecanoic Acid, 4 HYDROXYCYCLOHEX- ANEACETIC, 4-Hydroxphenyllactic, 4-Hydroxybutyric, 4-Hydroxyphenylacetic, 4-Hydroxyphenylpyruvic, 4OH-Pheylpropionic Acid, 5-HIAA, 5-Oxoproline, 5OH-Hexanoic Acid, Acetoacetic, Aconitic, Ur, Adipic, Butyrylglycine, Citric, Crotonylglycine, Decadienedioic, Dodecanedioic, Ethylmalonic, Fumaric, Glutaconic, Glutaric, Glyceric Acid, Hexanoylglycine, Homogentisic, HOMOVANILLIC ACID, Isobutyrylglycine, Isocitric, Isovaleryglycine, Lactic, Lactic Acid, Malic, Malonic, Methylcitric, Methylmalonic, Methylsuccinic, Mevalonolactone, N ACETYLASPARTIC, N-AcetylTyrosine, N-Valerylglycine, Octanoic, Orotic, Phenylacetic, Phenyllactic, Phenylpropionylglycine, Phenylpyruvic, Propionylglycine, Pyruvic, Sebacic, Suberic, Suberylglycine, Succinic, Succinylacetone, Thymine, Tiglylglycine, Trans-Cinnamoylglycine, Uracil, VMA