All B vitamins and vitamin C are {{c1::water-soluble}}.
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All B vitamins and vitamin C are water-soluble.
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All B vitamins and vitamin C are {{c1::water-soluble}}.
All B vitamins and vitamin C are water-soluble.
Vitamin K is required for {{c1::posttranslational gamma-carboxylation}} of proteins.
Vitamin K is required for posttranslational gamma-carboxylation of proteins.
Vitamin K is necessary for formation of clotting factors {{c1::II, VII, IX, and X}}.
Vitamin K is necessary for formation of clotting factors II, VII, IX, and X.
Dietary sources of vitamin K include {{c1::cabbage, kale, spinach, egg yolk, and liver}}.
Dietary sources of vitamin K include cabbage, kale, spinach, egg yolk, and liver.
A common cause of vitamin K deficiency is decreased {{c1::intestinal microbiota}} (e.g., after antibiotic use).
A common cause of vitamin K deficiency is decreased intestinal microbiota (e.g., after antibiotic use).
Newborns are given a single injection of {{c1::vitamin K}} to prevent hemorrhagic disease because they lack intestinal flora.
Newborns are given a single injection of vitamin K to prevent hemorrhagic disease because they lack intestinal flora.
Warfarin inhibits {{c1::vitamin K epoxide reductase (VKOR)}}.
Warfarin inhibits vitamin K epoxide reductase (VKOR).
Vitamin A is stored in the {{c1::liver}} and provides about a {{c2::6-month}} supply.
Vitamin A is stored in the liver and provides about a 6-month supply.
Vitamin A acts via conversion to {{c1::retinoic acid}} which functions as a {{c2::transcription factor}}.
Vitamin A acts via conversion to retinoic acid which functions as a transcription factor.
Earliest sign of vitamin A deficiency is {{c1::impaired vision}}.
Earliest sign of vitamin A deficiency is impaired vision.
The fat-soluble vitamins are {{c1::K, A, D, and E}}.
The fat-soluble vitamins are K, A, D, and E.
Chronic vitamin A deficiency causes epithelial {{c1::metaplasia and keratinization}} and immune deficiency.
Chronic vitamin A deficiency causes epithelial metaplasia and keratinization and immune deficiency.
Acute vitamin A toxicity symptoms include {{c1::headache, dizziness, vomiting, and blurred vision}}.
Acute vitamin A toxicity symptoms include headache, dizziness, vomiting, and blurred vision.
Thiamine (B1) functions as {{c1::thiamine pyrophosphate (TPP)}}, a coenzyme for pyruvate dehydrogenase and {{c2::transketolase}}.
Thiamine (B1) functions as thiamine pyrophosphate (TPP), a coenzyme for pyruvate dehydrogenase and transketolase.
Severe thiamine deficiency (beriberi) can cause impaired myocardial contractility and {{c1::muscle weakness/wasting}}.
Severe thiamine deficiency (beriberi) can cause impaired myocardial contractility and muscle weakness/wasting.
Wernicke-Korsakoff syndrome symptoms include {{c1::confusion, ataxia, nystagmus, and ophthalmoplegia}}.
Wernicke-Korsakoff syndrome symptoms include confusion, ataxia, nystagmus, and ophthalmoplegia.
Riboflavin (B2) active forms are {{c1::FMN}} and {{c2::FAD}}.
Riboflavin (B2) active forms are FMN and FAD.
Riboflavin deficiency causes {{c1::cheilosis, glossitis, dermatitis}}, and {{c2::photophobia}}/eye burning.
Riboflavin deficiency causes cheilosis, glossitis, dermatitis, and photophobia/eye burning.
Niacin is required to form {{c1::NAD+ and NADP+}} and can be synthesized from {{c2::tryptophan}}.
Niacin is required to form NAD+ and NADP+ and can be synthesized from tryptophan.
Niacin deficiency causes {{c1::pellagra}} characterized by {{c2::dermatitis, diarrhea, and dementia}}.
Niacin deficiency causes pellagra characterized by dermatitis, diarrhea, and dementia.
High-dose niacin causes prostaglandin-mediated {{c1::flushing}} that is reduced by {{c2::aspirin}}.
High-dose niacin causes prostaglandin-mediated flushing that is reduced by aspirin.
Pantothenic acid (B5) is a component of {{c1::coenzyme A}} which transfers {{c2::acyl groups}}.
Pantothenic acid (B5) is a component of coenzyme A which transfers acyl groups.
Pyridoxal phosphate (PLP), the active form of vitamin B6, is a cofactor for {{c1::transaminase reactions}}.
Pyridoxal phosphate (PLP), the active form of vitamin B6, is a cofactor for transaminase reactions.
Vitamin B6 deficiency can cause {{c1::hypochromic microcytic anemia}} because PLP is required for {{c2::heme biosynthesis}}.
Vitamin B6 deficiency can cause hypochromic microcytic anemia because PLP is required for heme biosynthesis.
Biotin functions as a coenzyme for {{c1::carboxylation reactions}} and is bound to {{c2::lysine residues}} on carboxylase enzymes.
Biotin functions as a coenzyme for carboxylation reactions and is bound to lysine residues on carboxylase enzymes.
Avidin, found in {{c1::raw egg whites}}, binds biotin and prevents its absorption.
Avidin, found in raw egg whites, binds biotin and prevents its absorption.
Folic acid is converted to {{c1::tetrahydrofolate (THF)}}, which transfers {{c2::one-carbon units}} for nucleotide synthesis.
Folic acid is converted to tetrahydrofolate (THF), which transfers one-carbon units for nucleotide synthesis.
Chronic vitamin A toxicity can cause {{c1::hepatosplenomegaly}} and {{c2::bone and joint pain}} with increased fracture risk.
Chronic vitamin A toxicity can cause hepatosplenomegaly and bone and joint pain with increased fracture risk.
Vitamin D is converted to the active form {{c1::calcitriol (1,25-(OH)2D)}}.
Vitamin D is converted to the active form calcitriol (1,25-(OH)2D).
Vitamin D increases {{c1::intestinal calcium absorption}}.
Vitamin D increases intestinal calcium absorption.
Skin synthesis of vitamin D converts {{c1::7-dehydrocholesterol}} to cholecalciferol under {{c2::UVB sunlight}}.
Skin synthesis of vitamin D converts 7-dehydrocholesterol to cholecalciferol under UVB sunlight.
Vitamin D deficiency in children causes {{c1::rickets}}; in adults it causes {{c2::osteomalacia}}.
Vitamin D deficiency in children causes rickets; in adults it causes osteomalacia.
Vitamin E functions primarily as an {{c1::antioxidant}}.
Vitamin E functions primarily as an antioxidant.
Vitamin C is required as a coenzyme for {{c1::hydroxylation reactions}} in {{c2::collagen}} synthesis.
Vitamin C is required as a coenzyme for hydroxylation reactions in collagen synthesis.
Vitamin C deficiency (scurvy) presents with {{c1::sore/spongy gums}} and {{c2::perifollicular hemorrhages}}.
Vitamin C deficiency (scurvy) presents with sore/spongy gums and perifollicular hemorrhages.
Folic acid deficiency during pregnancy increases the risk of {{c1::neural tube defects}} such as spina bifida and anencephaly.
Folic acid deficiency during pregnancy increases the risk of neural tube defects such as spina bifida and anencephaly.
Vitamin B12 is required for conversion of methylmalonyl-CoA to {{c1::succinyl-CoA}} and for remethylation of {{c2::homocysteine to methionine}}.
Vitamin B12 is required for conversion of methylmalonyl-CoA to succinyl-CoA and for remethylation of homocysteine to methionine.
Dietary vitamin B12 is obtained from {{c1::animal-derived foods}} because it is produced only by {{c2::microorganisms}}.
Dietary vitamin B12 is obtained from animal-derived foods because it is produced only by microorganisms.
In B12 deficiency, THF becomes trapped as {{c1::N5-methyl-THF}} (the "folate trap"), causing {{c2::megaloblastic anemia}}.
In B12 deficiency, THF becomes trapped as N5-methyl-THF (the "folate trap"), causing megaloblastic anemia.
Pernicious anemia results from loss of {{c1::gastric parietal cells}} leading to decreased {{c2::intrinsic factor}} and impaired B12 absorption.
Pernicious anemia results from loss of gastric parietal cells leading to decreased intrinsic factor and impaired B12 absorption.
