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    Nutritional Genetics Part 2: Labs
    Nutritional Genetics Part 2: Labs
    Nutritional Genetics Part 2: Labs
    Ebook116 pages50 minutes

    Nutritional Genetics Part 2: Labs

    By Ronald Steriti

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    About this ebook

    Nutritional Genetics is a very brief review of nutrition and genetics with a summary the published research, primarily from PubMed.
    Part 1 is an introduction, beginning with DNA damage and repair, nutrigenomics, nutrigenetics and epigenetics, genetic testing. It also contains sections on vitamins and nutrients and metabolism. Part 2 describes nutritional genetics lab tests.
    Parts 3 to 6 have sections on diseases. Part 3 includes Eyes, Ears, Respiratory, Cardiology, and Vascular diseases. Part 4 includes Gastrointestinal, Liver and Gallbladder, Pancreas, Thyroid, Urology, Gynecology, Obstetrics, and Men. Part 5 includes Neurology, Dermatology and Immunology. Part 6 includes Musculoskeletal, Hematology, Oncology, Psychiatry and Miscellaneous.

    Nutritional Genetics 2 - Labs

    1. Aldo-Keto Reductase
    2. Apolipoproteins
    3. Betaine-Homocysteine S-Methyltransferase, BHMT
    4. Breast Cancer (BRCA)
    5. Catalase
    6. Catechol-O-Methyltransferase (COMT)
    7. Coagulation Factor
    8. Cystathionine Beta Synthase (CBS)
    9. Cystathionine Gamma-Lyase, CSE
    10. Cytochrome P-450
    11. Dihydrofolate Reductase, DHFR
    12. Dopa Decarboxylase, DDC
    13. Gastric Intrinsic Factor, GIF
    14. Glucuronidation
    15. Glutamate Decarboxylase
    16. Glutathione
    17. Interleukin
    18. Kynurenine 3-Monooxygenase, KMO
    19. Methionine Adenosyltransferase, MAT
    20. Methionine Synthase
    21. Methylmalonic Acid
    22. Methylmalonyl-CoA Mutase, MCM
    23. Methylenetetrahydrofolate Reductase, MTHFR
    24. N-Acetyl Transferase, NAT
    25. PAPS Synthase
    26. Plasminogen Activators
    27. Platelet Glycoprotein
    28. Pyridoxal Kinase, PDX
    29. Renin-Angiotensin-Aldosterone
    30. S-Adenosyl Homocysteine Hydrolase, SAHH
    31. Serotonin Transporter
    32. Sulfonation, Sulfotransferase
    33. Superoxide Dismutase, SOD
    34. Transcobalamin
    35. Tumor Necrosis Factor, TNF
    36. Vitamin D Receptor, VDR

    LanguageEnglish
    PublisherRonald Steriti
    Release dateJun 23, 2016
    ISBN9781311611949
    Nutritional Genetics Part 2: Labs
    Author

    Ronald Steriti

    Dr. Ronald Steriti is a graduate of Southwest College of Naturopathic Medicine and currently is researcher for Jonathan V. Wright at the Tahoma Clinic.

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      Book preview

      Nutritional Genetics Part 2 - Ronald Steriti

      Chapter 1. Aldo-Keto Reductase

      The aldo-keto reductases (AKRs) are a superfamily of NAD(P)H-linked oxidoreductases, which reduce aldehydes and ketones to their respective primary and secondary alcohols. AKR enzymes are increasingly being recognized to play an important role in the transformation and detoxification of aldehydes and ketones generated during drug detoxification and xenobiotic metabolism. (Chen and Zhang, 2012)

      Hormone Metabolism

      AKR1C3 (type 5 17beta-HSD) reduces Delta(4)-androstene-3,17-dione to yield testosterone while AKR1C2 (type 3 3alpha-HSD) eliminates 5alpha-dihydrotestosterone (5alpha-DHT), and AKR1C1 forms 3beta-androstanediol (a ligand for ERbeta). In the breast, AKR1C3 forms testosterone, which is converted to 17beta-estradiol by aromatase or reduces estrone to 17beta-estradiol directly. AKR1C3 also acts as a prostaglandin (PG) F synthase and forms PGF(2alpha) and 11beta-PGF(2alpha), which stimulate the FP receptor and prevent the activation of PPARgamma by PGJ(2) ligands. This proproliferative signaling may stimulate the growth of hormone-dependent and -independent prostate and breast cancer. (Penning and Byrns, 2009)

      References

      Chen, WD and Y Zhang (2012), ‘Regulation of aldo-keto reductases in human diseases.’, Front Pharmacol, 3 35. PubMedID: 22408622

      Penning, TM and MC Byrns (2009), ‘Steroid hormone transforming aldo-keto reductases and cancer.’, Ann N Y Acad Sci, 1155 33-42. PubMedID: 19250190

      Chapter 2. Apolipoproteins

      Apolipoproteins are proteins that bind lipids (oil-soluble substances such as fat and cholesterol) to form lipoproteins, which transport lipids through the lymphatic and circulatory systems.

      There are several apolipoproteins.

      ApoA1 is the major protein component of high-density lipoproteins;

      ApoA4 is thought to act primarily in intestinal lipid absorption.

      ApoB’s form LDL, the so-called bad cholesterol particles.

      ApoE is a blood plasma protein that mediates the transport and uptake of cholesterol and lipid by way of its high affinity interaction with different cellular receptors, including the LDL receptor.

      Apolipoprotein A1 (APOA1)

      ApoA-I is a component of high-density lipoprotein (HDL). HDL transports cholesterol and phospholipids through the bloodstream from the body's tissues to the liver.

      Apolipoprotein A1 is a stronger prognostic marker than are HDL and LDL cholesterol for cardiovascular disease and mortality in elderly men. (Florvall et al., 2006)

      ApoA1 and ApoA1/ApoB ratio are better than HDL-cholesterol in assessing the severity of coronary damage. (Garfagnini et al., 1995)

      Lower ApoA1 levels correlate with dopaminergic system vulnerability in symptomatic PD patients and in asymptomatic individuals with physiological reductions in dopamine transporter density consistent with prodromal PD. Plasma ApoA1 may be a new biomarker for PD risk. (Qiang et al., 2013) (Swanson et al., 2014)

      Apolipoprotein E

      Apolipoprotein E (ApoE) is a class of apolipoprotein found in the chylomicron and Intermediate-density lipoprotein (IDLs) that is essential for the normal catabolism of triglyceride-rich lipoprotein constituents. In peripheral tissues, ApoE is primarily produced by the liver and macrophages, and mediates cholesterol metabolism in an isoform-dependent manner. In the central nervous system, ApoE is mainly produced by astrocytes, and transports cholesterol to neurons via ApoE receptors, which are members of the low density lipoprotein receptor gene family.

      APOE is 299 amino acids long and transports lipoproteins, fat-soluble vitamins, and cholesterol into the lymph system and then into the blood.

      ApoE is polymorphic, with three major alleles: ApoE2 (cys112, cys158), ApoE3 (cys112, arg158), and ApoE4 (arg112, arg158).

      The ApoE4 variant is the largest known genetic risk factor for late-onset sporadic Alzheimer's disease (AD). (Huang and Mahley, 2014)

      APOE polymorphism plays an important role in the development of BC, particularly when associated with higher serum triglyceride levels. (Cibeira et al., 2014)

      References

      Cibeira, GH, et al. (2014), ‘Apolipoprotein E genetic polymorphism, serum lipoprotein levels and breast cancer risk: A case-control study.’, Mol Clin Oncol, 2 (6), 1009-15. PubMedID: 25279190

      Florvall, G, S Basu, and A Larsson (2006), ‘Apolipoprotein A1 is a stronger prognostic marker than are HDL and LDL cholesterol for cardiovascular disease and mortality in elderly men.’, J Gerontol A Biol Sci Med Sci, 61 (12), 1262-66. PubMedID: 17234819

      Garfagnini, A, et al. (1995), ‘Relationship between HDL-cholesterol and apolipoprotein A1 and the severity of coronary artery disease.’, Eur Heart J, 16 (4), 465-70. PubMedID: 7671890

      Huang, Y and RW Mahley (2014), ‘Apolipoprotein E: structure and function in lipid metabolism, neurobiology, and Alzheimer’s diseases.’, Neurobiol Dis, 72 Pt A 3-12. PubMedID: 25173806

      Qiang, JK, et al. (2013), ‘Plasma apolipoprotein A1 as a biomarker for Parkinson disease.’, Ann Neurol, 74 (1), 119-27. PubMedID: 23447138

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