NUTRITION AND
METABOLISM
VITAMINS
PRESENTED
Dr. Alhaji Gbla
VITAMINS
• Vitamin A Also called retinol.
• FUNCTION Antioxidant; constituent of visual pigment(retinal); essential for normal differentiation of
epithelial cells into specialized tissue (pancreatic cells, mucus-secreting cells);prevents squamous metaplasia.
• Used to treat measles and acute promyelocytic leukemia
• Retinol is vitamin A, so think retin-A (usedtopically for wrinkles and Acne).
• Found in liver and leafy vegetables.
• Use oral isotretinoin to treat severe cystic acne.
• Night blindness (nyctalopia); dry, scaly skin(xerosis cutis); corneal squamous metaplasia
• Bitot spots (keratin debris; foamy appearance on conjunctiva A ); corneal degeneration(keratomalacia);
immunosuppression.
• AA Fig .A Showing Bitot spot
• EXCESS VITAMIN A
• Acute toxicity—nausea, vomiting, vertigo, and blurred vision.
• Chronic toxicity—alopecia, dry skin (eg,scaliness), hepatic toxicity and enlargement,arthralgias, and
idiopathic intracranial hypertension.
• Teratogenic (cleft palate, cardiac abnormalities),therefore a ⊝ pregnancy test and two forms of contraception
are required before isotretinoin (vitamin A derivative) is prescribed.
• Vitamin B1 Also called thiamine.
• FUNCTION In thiamine pyrophosphate (TPP), a cofactor for several dehydrogenase enzyme reactions:
• . Branched-chain ketoacid dehydrogenase
• . α-ketoglutarate dehydrogenase (TCA cycle)
• . Pyruvate dehydrogenase (links glycolysis to TCA cycle)
• . Transketolase (HMP shunt)
• DEFICIENCY Impaired glucose breakdown ATP depletion worsened by glucose infusion; highly aerobic
• tissues (eg, brain, heart) are affected first.
• In alcoholic or malnourished patients give thiamine before dextrose to reduce risk of precipitating Wernicke
encephalopathy.
• Diagnosis made by increasing RBC transketolase activity following vitamin B1 administration
• Wernicke-Korsakoff syndrome—confusion ,ophthalmoplegia, ataxia (classic triad) +confabulation,
personality change, memory loss (permanent).
• Damage to medial dorsal nucleus of thalamus, mammillary bodies.
• Dry beriberi—polyneuropathy, symmetrical muscle wasting.
• Wet beriberi—high-output cardiac failure (dilated cardiomyopathy), edema.
• Vitamin B2 Also called riboflavin.
• FUNCTION Component of flavins FAD and FMN, used as cofactors in redox reactions, eg, the succinate
dehydrogenase reaction in the TCA cycle.
• DEFICIENCY Cheilosis (inflammation of lips, scaling and fissures at the corners of the mouth), Corneal
Vascularisation .
• Vitamin B3 Also called niacin.
• FUNCTION Constituent of NAD+, NADP+ (used in redoxreactions).
• Derived from tryptophan. Synthesis requires vitamins B2 and B6.
• Used to treat dyslipidemia; lowers levels of VLDL and raises levels of HDL
• DEFICIENCY
• Glossitis. Severe deficiency leads to pellagra,which can also be caused by Hartnup disease,malignant
carcinoid syndrome (increase Tryptophan metabolism )
• Symptoms of pellagra: Diarrhea, Dementia (also hallucinations),Dermatitis (C3/C4dermatome
circumferential “broad collar” rash[Casal necklace], hyperpigmentation of sun exposed limbs ).
• Hartnup disease—autosomal recessive.
• Deficiency of neutral amino acid (eg,tryptophan) transporters in proximal renal tubular cells and on
enterocytes neutral aminoaciduria decrease absorption from the gut and lead to decrease Tryptophan for
conversion to niacin
• pellagra-like symptoms. Treat with high protein diet and nicotinic acid.
• EXCESS
• Facial flushing (induced by prostaglandin, not histamine; can avoid by taking aspirin with niacin),
hyperglycemia, hyperuricemia.
• Excess of vitamin B3 podagra.
• Vitamin B5 Also called pantothenic acid.
• FUNCTION Essential component of coenzyme A (CoA, a cofactor for acyl transfers) and fatty acid Synthase
• DEFICIENCY Dermatitis, enteritis, alopecia, adrenal insufficiency.
• Vitamin B6 Also called pyridoxine.
• FUNCTION Converted to pyridoxal phosphate (PLP), a cofactor used in transamination (eg, ALT and AST),
• decarboxylation reactions, glycogen phosphorylase. Synthesis of cystathionine, heme, niacin,
• histamine, and neurotransmitters including serotonin, epinephrine, norepinephrine (NE),
• dopamine, and GABA.
• DEFICIENCY Convulsions, hyperirritability, peripheral neuropathy (deficiency inducible by isoniazid and oral
• contraceptives), sideroblastic anemia (due to impaired hemoglobin synthesis and iron excess).
• - Vitamin B7 Also called biotin.
• FUNCTION Cofactor for carboxylation enzymes (which add
• a 1-carbon group):
• . Pyruvate carboxylase: pyruvate (3C)
• oxaloacetate (4C)
• . Acetyl-CoA carboxylase: acetyl-CoA (2C)
• malonyl-CoA (3C)
• . Propionyl-CoA carboxylase: propionyl-CoA
• (3C) methylmalonyl-CoA (4C)
• Vitamin B7 Also called biotin.
• FUNCTION
• Cofactor for carboxylation enzymes (which add a 1-carbon group):
• Pyruvate carboxylase: pyruvate – Oxaloacetate
• Acetyl-CoA carboxylase: acetyl-CoA - Malonyl-CoA
• DEFICIENCY Relatively rare. Dermatitis, enteritis, alopecia.
• Caused by long-term antibiotic use or excessive ingestion of raw egg whites.
• Vitamin B9 Also called folate.
• FUNCTION
• Converted to tetrahydrofolic acid (THF), a coenzyme for 1-carbon transfer/methylation reactions.
• Important for the synthesis of nitrogenous bases in DNA and RNA.
• Found in leafy green vegetables. Absorbed in jejunum and Small reserve pool stored primarily in the liver.
• DEFICIENCY
• Macrocytic, megaloblastic anemia; hypersegmented polymorphonuclear cells(PMNs); glossitis; no neurologic
symptoms (as opposed to vitamin B12 deficiency).
• Labs : increase homocysteine, normal methylmalonic acid levels.
• Seen in alcoholism and pregnancy
• Deficiency can be caused by several drugs (eg,phenytoin, sulfonamides, methotrexate).
• Supplemental maternal folic acid at least 1 month prior to conception and during early pregnancy to reduce risk of
neural tube defects. Give vitamin B for the 9 months of pregnancy.
• Vitamin B12 Also called cobalamin.
• FUNCTION
• Cofactor for methionine synthase (transfers CH3 groups as methylcobalamin) and methylmalonyl-CoA
mutase. Important for DNA Synthesis
• Found in animal products.
• Synthesized only by microorganisms. Very large reserve pool (several years) stored primarily in the liver.
Deficiency caused by malabsorption (eg, sprue, enteritis, Diphyllobothrium latum, achlorhydria, bacterial
overgrowth, alcohol excess), lack of intrinsic factor (eg, pernicious anemia, gastric bypass surgery), absence
of terminal ileum (surgical resection, eg, for Crohn disease), certain drugs (eg, metformin),or insufficient
intake (eg, veganism).Anti-intrinsic factor antibodies diagnostic for pernicious anemia.
• Folate supplementation can mask the hematologic symptoms of B12 deficiency, but not the neurologic
symptoms.
• DEFICIENCY
• Macrocytic, megaloblastic anemia;hypersegmented PMNs; paresthesias and subacute combined degeneration
(degeneration of dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts)
• due to abnormal myelin. Associated with increased homocysteine and methylmalonic acid levels, along with
2° folate deficiency. Prolonged deficiency causes irreversible nerve damage.
• Vitamin C Also called ascorbic acid.
• FUNCTION
• Antioxidant; also facilitates iron absorption by reducing it to Fe2+ state.
• Necessary for hydroxylation of proline and lysine in collagen synthesis.
• Necessary for dopamine β-hydroxylase, which converts dopamine to NE.
• Found in fruits and vegetables.
• Ancillary treatment for methemoglobinemia by reducing Fe3+ to Fe2+.
• DEFICIENCY Scurvy—swollen gums, easy bruising,petechiae, hemarthrosis, anemia, poor wound healing,
perifollicular and subperiosteal hemorrhages, “corkscrew” hair.
• Weakened immune response.
• EXCESS
• Nausea, vomiting, diarrhea, fatigue, calcium oxalate nephrolithiasis. Can increase Iron toxicity in
• predisposed individuals by increasing dietary iron absorption (ie, can worsen hereditary hemochromatosis or
transfusion-related iron overload ).
• Vitamin D D3 (cholecalciferol) from exposure of skin (stratum basale) to sun, ingestion of fish, milk, plants.
• D2 (ergocalciferol) from ingestion of plants, fungi, yeasts.
• Both converted to 25-OH D3 (storage form) in liver and to the active form 1,25-(OH)2 D3 (calcitriol) in the
Kidney .
• FUNCTION
• Increase intestinal absorption of Ca2+ and PO4
• Increase in bone mineralization at low levels.
• Increase in bone resorption at higher levels.
• REGULATION
• Increase PTH , decreases Ca2+,decrease PO4 and increases 1,25-(OH)2D3 production.
• 1,25-(OH)2D3 feedback inhibits its own production.
• Increase PTH and increasing Ca2+ and decreasing PO4 absorption in Kidney disease
• DEFICIENCY
• A
• Rickets in children (deformity, such as genu varum “bowlegs”), osteomalacia in adults (bone
• pain and muscle weakness), hypocalcemic tetany.
• Caused by malabsorption, decrease sun exposure, poor diet, chronic kidney disease (CKD), advanced liver
disease.
• Give oral vitamin D to breastfed infants.
• Deficiency is exacerbated by pigmented skin, premature birth.
• EXCESS
• Hypercalcemia, hypercalciuria, loss of appetite, stupor.
• Seen in granulomatous diseases increasing activation of vitamin D by epithelioid macrophages).
• Vitamin E Includes tocopherol, tocotrienol.
• FUNCTION
• Antioxidant (protects RBCs and membranes from free radical damage).
• DEFICIENCY Hemolytic anemia, acanthocytosis, muscle weakness, demyelination of posterior columns
• (Decrease position and vibration sensation) and spinocerebellar tract (ataxia).
• Neurologic presentation may appear similar to vitamin B12 deficiency, but without megaloblastic anemia,
hypersegmented neutrophils, or increase serum methylmalonic acid levels .
• EXCESS
• Risk of enterocolitis in infants. High-dose supplementation may alter metabolism of vitamin K and enhanced
anticoagulant effects of warfarin.
• Vitamin K Includes phytomenadione, phylloquinone, phytonadione, menaquinone.
• FUNCTION
• Activated by epoxide reductase to the reduced form, which is a cofactor for the γ-carboxylation of glutamic
acid residues on various proteins required for blood clotting.
• Synthesized by intestinal flora.
• Necessary for the maturation of clotting factors II, VII, IX,X, and proteins C and S.
• Warfarin inhibits vitamin K–dependent synthesis of these factors .
• DEFICIENCY Neonatal hemorrhage with increase PT and increase APTT
• but normal bleeding time (neonates have sterile intestines and are unable to synthesize vitamin K).
• Can also occur after prolonged use of broad-spectrum antibiotics.
• Not in breast milk; neonates are given vitamin K injection at birth to prevent hemorrhagic disease of the
newborn.
Zinc
• FUNCTION
• Mineral essential for the activity of 100+ enzymes. Important in the formation of zinc fingers(transcription
factor motif).
• DEFICIENCY
• Delayed wound healing, suppressed immunity, male hypogonadism, decrease adult hair
(axillary,facial,pubic), dysgeusia, anosmia. Associated with acrodermatitis enteropathica ( defect in intestinal
zinc absorption). May predispose to alcoholic cirrhosis.
•B
