Vitamin Metabolism - an overview (2022)

METABOLISM VITAMINS AND HORMONES | Structure and Regulation of Pyruvate Dehydrogenases.

From: Encyclopedia of Biological Chemistry (Second Edition), 2013

Hormones and Disorders of Mineral Metabolism

Shlomo Melmed MB ChB, MACP, in Williams Textbook of Endocrinology, 2020

Metabolism of Vitamin D

Vitamin D is not a true vitamin, because nutritional supplementation is not required in humans who have adequate sun exposure. When exposed to ultraviolet irradiation, the cutaneous precursorof vitamin D, 7-dehydrocholesterol, undergoes photochemical cleavage of the carbon bond between carbons 9 and 10 of the steroid ring (Fig. 29.15). The resultant product, previtamin D, is thermally labile and over a period of 48 hours undergoes a temperature-dependent molecular rearrangement that results in the production of vitamin D. Alternatively, this thermally labile product can isomerize to two biologically inert products, luminosterol and tachysterol. This alternative photoisomerization prevents production of excessive amounts of vitamin D with prolonged sun exposure. The degree of skin pigmentation, which increases in response to solar exposure, also regulates the conversion of 7-dehydrocholesterol to vitamin D by blocking the penetration of ultraviolet rays.

The alternative source of vitamin D is dietary. The elderly, the institutionalized, and those living in northern climates likely obtain most of their vitamin D from dietary sources. However, with increasing avoidance of sun exposure by the general population, ensuring adequate dietary intake of vitamin D has become important for the population at large. Vitamin D deficiency is prevalent and has been shown to contribute significantly to osteopenia and fracture risk. The major dietary sources of vitamin D are fortified dairy products, although the lack of monitoring of this supplementation results in marked variation in the amount of vitamin D provided.183 Other dietary sources include egg yolks, fish oils, and fortified cereal products. Vitamin D provided by plant sources is in the form of vitamin D2, whereas that provided by animal sources is in the form of vitamin D3 (seeFig. 29.15). These two forms have equivalent biologic potencies and are activated equally efficiently by the hydroxylases in humans. While vitamin D3 has been shown to be more effective at increasing 25-hydroxyvitamin D levels,184 this effect is dependent upon vitamin D–binding protein (VDBP) genotype and concentration.185

Vitamin D is absorbed into the lymphatics and enters the circulation bound primarily to VDBP, although a fraction of vitamin D circulates bound to albumin. The human VDBP is a 52-KDa α-globulin synthesized in the liver. The protein has a high affinity for 25(OH)D but also binds vitamin D and 1,25(OH)2D. Approximately 88% of 25(OH)D circulates bound to the VDBP, 0.03% is free, and the rest circulates bound to albumin. In contrast, 85% of the circulating 1,25(OH)2D3 binds to the VDBP, 0.4% is free, and the rest binds to albumin. Mice lacking VDBP have increased susceptibility to 1,25(OH)2D3 toxicity as well as to dietary vitamin D deficiency.186 Vitamin D–binding protein polymorphisms have been postulated to be the basis for difference in vitamin D levels in several groups, including African Americans and Finns.187 Measurements of free 25(OH) vitamin D across multiple populations, however, suggest that the monoclonal antibody used in the former study can bring misleading results.188

Vitamin Metabolism

N.V. Bhagavan, Chung-Eun Ha, in Essentials of Medical Biochemistry (Second Edition), 2015


The word vitamin is used to describe any of a heterogeneous group of organic molecules that are needed in small quantities for normal growth, reproduction, and homeostasis, but that the human body is unable to synthesize in adequate amounts. The group includes the fat-soluble vitamins (A, D, E, and K) and the water-soluble vitamins (B-complex and C). Vitamins are generally needed in catalytic quantities and do not function as structural elements in the cell. Other organic compounds are not synthesized in the body but are required for maintenance of normal metabolism, such as essential fatty acids (Chapter 16) and essential amino acids (Chapter 3). These substances are needed in relatively large quantities, serve as nonregenerated substrates in metabolic reactions, and are used primarily as structural components in lipids and proteins. Vitamins discussed in other chapters include vitamin D (Chapter 35) and vitamin K (Chapter 34). All the B vitamins function as cofactors or precursors for cofactors in enzyme-catalyzed reactions and are discussed in appropriate chapters. Additional properties and less-well-defined actions are reviewed here.

Vitamin deficiency is caused by nutritional inadequacy, or may result from malabsorption, effects of pharmacological agents, and abnormalities of vitamin metabolism or utilization in the metabolic pathways. Thus, in biliary obstruction or pancreatic disease, the fat-soluble vitamins are poorly absorbed despite adequate dietary intake, because of steatorrhea. Absorption, transport, activation, and utilization of vitamins require the participation of enzymes or other proteins whose synthesis is under genetic control. Dysfunction or absence of one of these proteins can produce a disease that is clinically indistinguishable from one caused by dietary deficiency. In vitamin-dependent or vitamin-responsive disorders, use of pharmacological doses of the vitamin can overcome the blockage sufficiently for normal function to occur.

Vitamin deficiency can result from treatment with certain drugs. Thus, destruction of intestinal microorganisms by antibiotic therapy can produce symptoms of vitamin K deficiency. Isoniazid, used to treat tuberculosis, is a competitive inhibitor of pyridoxal kinase, which is needed to produce pyridoxal phosphate. Isoniazid can produce symptoms of pyridoxine deficiency. To prevent this, pyridoxine is often incorporated into isoniazid tablets. Methotrexate and related folate antagonists act by competitively inhibiting dihydrofolate reductase (Chapter 25).

Excessive intake of vitamins A and D produces hypervitaminosis. Vitamin D toxicosis was discussed in Chapter 35; vitamin A toxicosis is discussed later in this chapter. The toxicity of high doses of vitamin B6 is also covered later in the chapter.

Certain vitamins can be synthesized by humans in limited quantities. Niacin (also known as nicotinic acid or vitamin B3) can be formed from tryptophan (Chapter 15). This pathway is not active enough to satisfy all the body’s needs; however, when one is calculating the RDA for niacin, 60mg of dietary tryptophan is considered equivalent to 1mg of dietary niacin. In Hartnup’s disease (Chapter 15), a rare hereditary disorder in the transport of monoaminomonocarboxylic acids (e.g., tryptophan), a pellagra-like rash may appear, suggesting that over a long period of time dietary intake of niacin is insufficient for metabolic needs. This pattern also occurs in carcinoid syndrome, in which much tryptophan is shunted into the synthesis of 5-hydroxytryptamine. Vitamin D is synthesized in the skin, provided radiant energy is available for the conversion (Chapter 35):

7-Dehydrocholesterolphotonscholecalciferol(vitamin D3)

Physiological age-related changes in the elderly can affect nutritional status. Decreased active intestinal transport and atrophic gastritis impair the absorption of vitamins and other nutrients. Reduced exposure to sunlight can lead to decreased vitamin D synthesis. Many drugs may impair both appetite and absorption of nutrients. Some examples of unfavorable drug–nutrient interactions are drugs that inhibit stomach acid production (e.g., omeprazole); drugs that reduce vitamin B12 absorption; anticonvulsant drugs (e.g., barbiturates, phenytoin, primidone) that act by inducing hepatic microsomal enzymes which accelerate inactivation of vitamin D metabolites and aggravate osteoporosis (Chapter 35); interference with folate metabolism by antifolate drugs (methotrexate) used in the treatment of some neoplastic diseases; and vitamin B6 metabolism affected by isoniazid, hydralazine, and D-penicillamine. Examples of negative impacts of vitamins on drug action are vitamin B6-dependent action of peripheral conversion of L-3,4-dihydroxyphenylalanine (L-dopa) to L-dopamine, which is mediated by aromatic L-amino acid decarboxylase and prevents L-dopa’s transport across the blood–brain barrier; also, ingestion of large amounts of vitamin K-rich foods or supplements, and action of warfarin on anticoagulation (Chapter 34). L-dopa is the metabolic precursor of L-dopamine and is used in the treatment of Parkinson’s disease (Chapter 30). Thus, L-dopa is administered along with a peripherally acting inhibitor of aromatic L-amino acid decarboxylase (e.g., carbidopa).

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(Video) Metabolism & Nutrition, Part 1: Crash Course Anatomy & Physiology #36

Bone Metabolism and Osteoporosis

H. Richard Winn MD, in Youmans and Winn Neurological Surgery, 2017

Vitamin D Metabolism

Vitamin D has become a focus of nutritional interest because of its importance not only as a major determinant of bone health but also as an important factor in other biologic processes.4 Vitamin D exists in two forms: vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol). Vitamin D3, the naturally occurring form, is a normal by-product of cholesterol synthesis when 7-dehydrocholesterol is exposed to ultraviolet light. This process depends on exposure to sunshine and thus is subject to limitations. In northern climates or in individuals who are not exposed to 30 minutes per day of direct sunlight, vitamin D synthesis will likely be inadequate to sustain metabolic needs. Such individuals would include large sections of the adult population, who work indoors under fluorescent lighting.

After synthesis in the skin, vitamin D3 is converted to 25-hydroxyvitamin D, which is abbreviated 25(OH)D, in the liver. This substance is then subsequently converted into 1,25-dihydroxyvitamin D—abbreviated 1,25(OH)2D—which is the biologically active metabolite. Normal production of 1,25(OH)2 D is stimulated by low circulating serum of calcium or phosphate or by increased PTH levels. This rise in 1,25(OH)2D increases calcium absorption from the intestinal tract, thus raising serum calcium levels. In addition, 1,25(OH)2 D increases reabsorption in the distal tubules of the kidney, again resulting in increased serum calcium levels.5

Inadequate vitamin D levels during skeletal development result in osteomalacia or rickets. In the skeletally mature individual, vitamin D deficiency is associated with osteoporosis. This deficient state is a common cause of osteoporosis in adults. For those with severe deficiency, 50,000 IU weekly of vitamin D for 3 months may be given.4 Otherwise, 1000 IU daily should be sufficient.5 The effect of vitamin D and calcium supplementation on bone is to substantially reduce the risk of osteoporotic fracture by up to 40%.4 These effects, which are noted only in the elderly or postmenopausal patient, are associated with an increase in bone mineral density of 1% to 2%. For the surgeon commonly treating elderly patients, knowledge of the patient's bone health is critical for optimizing outcomes, particularly in patients undergoing spinal fusion procedures. When a patient's candidacy for elective spinal fusion is being considered, procedures determining the patient's vitamin D [1,25(OH)2D] level should be considered as part of a thorough preoperative work-up. Changes in bone density occur slowly, even with aggressive supplementation therapy, a fact that should be kept in mind by the physician or surgeon treating an osteoporotic patient who may be a candidate for surgery.

Drug–Nutrient Interactions in Renal Failure

Raimund Hirschberg, in Nutritional Management of Renal Disease (Third Edition), 2013

Drug-Induced Vitamin Deficiencies

Vitamin metabolism and requirements in renal disease and renal failure are described in Chapter 24. Thiamine deficiency may be aggravated or caused by chronic alcoholism. The literature, at present, does not suggest that specific short-term or long-term drug therapies may cause vitamin B1 deficiency. However, thiamine deficiency may occur in severely ill patients who undergo parenteral nutrition [36,37]. Thiamine is a co-enzyme for pyruvate dehydrogenase, and thiamine deficiency may cause the acute onset of unexplained, severe lactic acidosis [36–38]. Riboflavin deficiency can be caused or aggravated by long-term administration of chlorpromazine or amitriptyline. Pyridoxine deficiency may be caused by long-term treatment with isoniazid. It is recommended that vitamin B6 supplements (10–15 mg/day) should be prescribed for the entire period of time that isoniazid is taken. Vitamin B6 deficiency may also be caused by hydralazine and penicillamine [23]. High doses of pyridoxine hydrochloride reduce the serum levels of anticonvulsants and may reduce the clinical seizure control. Chronic vitamin B12 deficiency may develop during long-term treatment with colchicine or cimetidine [39,40].

Several drugs antagonize folic acid and may cause megaloblastic anemia. These include phenytoin, phenobarbital, sulphasalazine, triamterene, trimethoprim, trimetrexate and methotrexate [41–43]. On the other hand, folate supplementation may interact with these medicines and reduce their clinical efficacy. Daily dosages of folate of more than 5 mg reduces the plasma levels of phenytoin and phenobarbital and may reduce their therapeutic efficacy [44]. A risk for the development of niacin deficiency may exist when treatment with isoniazid is prescribed. During such treatment, concurrent administration of niacin (100 mg/day) may be advisable. Retinoids and possibly retinol increase the blood cyclosporine levels [45]. Vitamin A supplements should be avoided in renal patients. In addition to Coumadin anticoagulants, there are a number of drugs that can cause vitamin K deficiency and that may induce or enhance severe bleeding. This has been described particularly with the administration of moxalactam, cefotetan, cefamandole, cefoperazone and other cephalosporins that contain the methylthiotetrazole side chain. Vitamin K supplements should be administered concurrently with these antibiotics [46,47]. Weaker anti-vitamin K effects have been shown with tetracycline and cholestyramine [48]. Ingestion of megadoses of vitamin E can cause vitamin K deficiency and should be avoided [31].

Drug-induced osteomalacia can be due to chronic intake of anticonvulsants, isoniazid and possibly cimetidine. Anticonvulsant therapy with phenytoin, phenobarbital, or carbamazepine results in reduced levels of 24,25-dihydroxyvitamin D3, and this may play a role in the anticonvulsant-induced osteomalacia [49]. In patients with CKD this drug-induced risk for osteomalacia may be additive to the increased risk of renal bone disease. Patients undergoing chronic dialysis therapy are often supplemented with 1,25-dihydroxycholecalciferol or analogues. However, in patients with moderate CKD not receiving 1,25-dihydroxycholecalciferol, vitamin D supplements should be given concurrently with the above drug treatments.

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The Liver

Courtney M. Townsend JR., MD, in Sabiston Textbook of Surgery, 2022

(Video) Carbohydrate Structure and Metabolism, an Overview, Animation.

Vitamin Metabolism

Along with the intestine, the liver is responsible for the metabolism of the fat-soluble vitamins A, D, E, and K. These vitamins are obtained exogenously and absorbed in the intestine. Their adequate intestinal absorption is critically dependent on adequate fatty acid micellization, which requires bile acids.

Vitamin A is from the retinoid family and is involved in normal vision, embryonic development, and adult gene regulation. Storage of vitamin A is solely in the liver and occurs in the hepatic stellate cells. Overingestion of vitamin A can result in hepatic toxicity. Vitamin D is involved in calcium and phosphorus homeostasis. One of vitamin D’s activation steps (25-hydroxylation) occurs in the liver. Vitamin E is a potent antioxidant and protects membranes from lipid peroxidation and free radical formation. Finally, vitamin K is a critical cofactor in the posttranslational γ-carboxylation of the hepatically synthesized coagulation factors II, VII, IX, and X, as well as of protein C and protein S, the so-called vitamin K–dependent cofactors. Cholestasis syndromes can result in the inadequate absorption of these vitamins secondary to poor micellization in the intestine. The associated vitamin deficiency syndromes, such as metabolic bone disease (vitamin D deficiency), neurologic disorders (vitamin E deficiency), and coagulopathy (vitamin K deficiency), can subsequently occur.

The liver is also involved in the uptake, storage, and metabolism of a number of water-soluble vitamins, including thiamine, riboflavin, vitamin B6, vitamin B12, folate, biotin, and pantothenic acid. The liver is responsible for converting some of these water-soluble vitamins to active coenzymes, transforming some to storage metabolites and using some for enterohepatic circulation (e.g., vitamin B12).


KOSIN AMATAYAKUL, in Hormonal Steroids: Proceedings of the Fifth International Congress on Hormonal Steroids, 1979


Several articles have described significant alterations in vitamin metabolism in the users of hormonal contraceptives, in particular the combined oral contraceptive preparations [24, 25]. Markedly disturbed tryptophan metabolism mentioned earlier has also been observed in these women [18]. This latter change appears to be identical to the altered excretion of intermediate tryptophan metabolites in vitamin B6 deficient individuals, which can be reversed by treatment with a large pharmacological dose of peridoxine hydrochloride. These findings prompted us to include vitamin studies in the protocol design. A total of eight vitamins were included in the in-house study, but only six in the field study. These were: vitamin A, vitamins B1, B2, B6, B12 and folates. The other additional assessments of vitamin status, carried out only in the in-house study, were vitamin E, β-carotene and oral tryptophan loading test. For the assessment of the vitamin B-complex series, we adopted methodologies based on red cell enzymes, namely (a) erythrocytic transketolase activities both in the absence and presence of added thiamine co-factor for vitamin B1, (b) erythrocytic glutathione reductase activities both in the absence and presence of added flavine adenine dinucleotide for vitamin B2, and (c) erythrocytic aspartate amino-transferase activities both in the absence and presence of added pyridoxine-5-phosphate for vitamin B6. The following two Tables (8, 9) indicate quite clearly that none of these vitamins changed significantly as a result of DMPA treatment in this series of Thai subjects.

Table 8. DMPA and vitamins

ControlsDMPA Administration
A µg%)47.07 ± 14.4345.83 ± 23.4446.96 ± 7.0245.97 ± 8.2346.30 ± 13.4743.28 ± 10.8340.94 ± 10.60
B µg% Carotene64.17 ± 22.2452.64 ± 16.8348.00 ± 13.3578.70 ± 37.7256.08 ± 26.2465.36 ± 34.8049.75 ± 23.99
E mg%0.389 ± 0.1950.538 ± 0.2220.610 ± 0.1830.412 ± 0.1560.520 ± 0.2300.470 ± 0.1200.440 ± 0.240
Serum ng/ml Folate12.13 ± 6.2613.21 ± 5.0920.35 ± 7.4715.95 ± 7.4317.22 ± 6.2412.34 ± 5.1015.01 ± 6.47
Rbc's ng/ml Folate378.41 ± 121.45336.40 ± 76.49421.74 ± 65.64468.29 ± 82.53352.97 ± 55.19395.13 ± 86.96312.86 ± 70.75

Table 9. DMPA and vitamins (B's)

ControlsDMPA Administration
B1 µmol-7-P/h/ml rbc8.55 ± 0.7710.96 ± 3.1811.38 ± 2.899.28 ± 1.2110.04 ± 0.598.46 ± 3.088.37 ± 1.04Basal act
11.67 ± 10.194.48 ± 3.812.13 ± 3.9919.56 ± 9.046.12 ± 3.4337.44 ± 15.099.05 ± 1.61% Stim. act.
B2 µmol NADPH/h/ml rbc59.00 ± 24.80122.00 ± 42.30149.50 ± 32.8059.60 ± 11.65124.71 ± 24.5191.90 ± 43.09126.50 ± 39.08Basal act.
164.00 ± 65.5942.25 ± 37.8117.25 ± 6.55112.00 ± 42.9717.57 ± 8.6670.90 ± 53.8614.50 ± 6.65% Stim. act.
B6 µmol NADPH/h/ml rbc73.83 ± 25.2896.67 ± 27.81105.86 ± 20.0675.71 ± 21.7282.71 ± 16.9481.00 ± 37.0876.75 ± 18.37Basal act.
78.33 ± 42.4569.00 ± 12.8251.00 ± 10.8996.28 ± 38.1471.00 ± 9.5076.91 ± 23.1671.83 ± 18.06% Stim. act.
B12373.28 ± 114.69487.60 ± 155.37446.26 ± 148.95396.82 ± 156.90496.37 ± 214.13413.12 ± 155.00459.85 ± 194.20

It is true that the percentage stimulated activities in the case of transketolase on days 90 and 270, and the glutathione reductase on admission and on days 90 and 270, were higher than normal. This indicated a possible mild degree of sub-clinical deficiency, which we believe to be typical of the subjects' vitamin status while living in their rural home villages. We take this view because subsequent estimations were entirely normal. None of the eight vitamins studied was altered by DMPA usage.

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Enteral Nutrition for the High-Risk Neonate

Tarah T. Colaizy, ... Brenda B. Poindexter, in Avery's Diseases of the Newborn (Tenth Edition), 2018

(Video) 087-Vitamins; Complexity of Metabolism

Vitamin D

Conflicting guidelines are proposed by different professional organizations regarding the optimal dosing of vitamin D. The AAP Committee on Nutrition issued guidelines establishing the amount of recommended vitamin D as 400 IU/day for infants. The recommendation applies to infants receiving human milk and those who are consuming less than 1 quart of infant formula per day and is based in part on the risk of rickets in exclusively breastfed infants who do not receive supplementation with 400 IU of vitamin D per day. This level of supplementation is sufficient to meet a target plasma 25-hydroxyvitamin D concentration of 50 mmol/L in most infants (Abrams and Committee on Nutrition, 2013; McCarthy et al., 2013). However, the Endocrine Society recommends that infants may require up to 1000 IU/day to meet a target plasma 25-hydroxyvitamin D concentration of 75 mmol/L for nonskeletal health benefits (Nehra et al., 2013).

Antiepileptic drugs such as phenytoin and phenobarbital may affect vitamin metabolism. Ethnicity has a role in serum 25-hydroxyvitamin D levels, with Hispanic infants having a lower umbilical cord blood level (Abrams et al., 2012). Preterm infants are at higher risk of being born with lower 25-hydroxyvitamin D umbilical cord serum levels (Burris et al., 2014).

Controversy Box

Certain vitamin D receptor polymorphisms are associated with increased frequency of BPD (Koroglu et al., 2014). Lower maternal and neonatal serum 25-hydroxyvitamin D levels are associated with BPD in preterm infants (Cetinkaya et al., 2015; Fettah et al., 2015). Recent studies have revealed that vitamin D supplementation in black preterm infants is associated with more recurrent wheezing (Hibbs et al., 2015). A randomized clinical trial of different vitamin D dosing strategies for black preterm infants is under way.

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TOM BRODY, in Nutritional Biochemistry (Second Edition), 1999

Enzymes Have a Three-Dimensional Structure

Figure 1.23 shows the overall structures of two enzymes, chymotrypsin and dihydrofolate reductase. Chymotrypsin catalyzes the digestion of dietary proteins, while dihydrofolate reductase catalyzes a step in vitamin metabolism. In these diagrams, a ribbon is a form of shorthand that represents a linear polymer of amino acids. The enzymes in Figure 1.23 are roughly spherical, not long and filamentous. Such spherical proteins have an inside core and an outer surface. The amino acids in parts of the peptide chain near the inner core tend to have lipophilic R groups. Those with hydrophilic R groups tend to occur on the outer surface.

Vitamin Metabolism - an overview (1)

FIGURE 1.23. Three-dimensional structures of two proteins, chymotrypsin (top) and dihydrofolate reductase (bottom). Dihydrofolate reductase is shown not in its natural state, but with a drug molecule bound to its surface.

[Reprinted by permission from Nature 214, 652–656 (copyright © 1967 Macmillan Magazines Limited) and Science 197, 452 (copyright © 1977 by the AAAS (London)).]

As a polypeptide is synthesized in a cell, its amino acid sequence might appear random (i.e., a few hydrophilic acids, followed by several lipophilic acids, then a number of hydrophilic ones, and so on). However, as the polypeptide folds and coils into a three-dimensional shape, it becomes apparent that this structure is controlled by the sequence of R groups. The polypeptide chain folds so that the lipophilic amino acid R groups associate with one another in the core and the hydrophilic groups remain on the outer surface, where they associate with the surrounding water. Compare this configuration with those of vesicles and micelles.

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Cytochrome P450 Function and Pharmacological Roles in Inflammation and Cancer

Byoung-Joon Song, ... Mohamed A. Abdelmegeed, in Advances in Pharmacology, 2015

3.7 Role and Regulation of CYP2A5, CYP3A, and CYP4 Isozymes in Liver Disease

CYP4 enzyme family members have multiple functions in human biochemistry and physiology through not only the metabolism of potent signaling eicosanoids, but also their functional role in peroxisome-mediated fatty acids oxidation, vitamin, and steroid metabolism. These CYP4A enzymes also play pathophysiological roles in liver disease, hypertension, shock and sepsis, ischemic stroke adrenoleukodystrophy, Refsum disease, Bietti's crystalline dystrophy, and hyperkeratotic skin disease (See chapter “Cytochrome P450 ω-hydroxylases in inflammation and cancer” by Johnson et al.). For instance, CYP4A isozyme can be important in producing ROS and NASH, as shown in mice exposed to MCD, which was shown to elevate CYP2E1 mRNA and activity along with NASH-like inflammation (Chalasani et al., 2003; Weltman et al., 1996). In this case, CYP2E1 may be important in promoting NASH-related inflammatory changes in the pericentral regions. However, MCD-exposed Cyp2e1-null mice still developed NASH with lipid peroxidation, despite the absence of CYP2E1 (Leclercq et al., 2000; Robertson, Leclercq, Farrell, & Robertson, 2001). In this model, CYP4A becomes a major player in producing ROS and NADPH-dependent lipid peroxidation, which can cause liver injury. In fact, treatment with a specific antibody to CYP4A in Cyp2e1-null mice prevented the ROS production and lipid peroxidation, although treatment with the same CYP4A antibody did not prevent lipid peroxidation in wild-type mice. Similar to CYP2E1, CYP4A can metabolize various long-chain fatty acids at ω and ω-1 positions to produce shorter chain fatty acids (Hardwick, 2008). Through uncoupling during its catalytic cycle, CYP4A-mediated metabolism can produce ROS (Hardwick et al., 2013). In addition, it can produce dicarboxylic acids of long-chain fatty acids, which can inhibit the mitochondrial ETC, increased oxidative stress, and toxicity (Hardwick, 2008; Hardwick et al., 2013). One recent study showed that CYP4A, elevated in db/db mice, seems to play a major role in promoting high-fat-induced insulin resistance, ER stress, and apoptosis since inhibition of CYP4A with a specific inhibitor (HET0016) or intravenous injection of a small hairpin RNA specific to CYP4A mRNA efficiently blocked insulin resistance, ER stress, and apoptosis in diabetic db/db mice (Park et al., 2014).

Compared to CYP2E1, there are few studies on the role of human CYP4 family members in either NAFLD or AFLD. In humans with NAFLD, a fourfold increase in CYP4A11, which metabolizes arachidonic acid to 20-hydroxyeicosatetraenoic acid (HETE) (Nakamura et al., 2008), was observed with a slight increase in CYP2E1 during steatosis and a decrease of CYP2E1 in patients with NASH (Fisher et al., 2009). Because vitamin E improves liver histology in patients with NAFLD and that CYP4F2 is the major enzyme metabolizing vitamin E, participants in PIVENS and TONIC clinical trials were genotyped for CYP4F2 variants (V433M and W12G) (Athinarayanan et al., 2014). The results showed a significant decrease in plasma α-tocopherol in patients with CYP4F2 V433M genotype, but CYP4F2 polymorphisms likely play a minor or moderate role in the overall pharmacokinetics of vitamin E used as a therapeutic agent. A recent publication indicated that 20-HETE impairs endothelial insulin signaling by inducing the phosphorylation of IRS-1 (Li, Wong, et al., 2014; Li, Zhao, et al., 2014) with activation of SREBP-1α that induces the expression of mouse hepatic CYP4A genes, possibly leading to increased production of 20-HETE (Horton et al., 2003). These data indicate an important role of CYP4A/CYP4F produced 20-HETE in the regulation of insulin signaling in mice. However, the interplay of CYP4A11 and CYP4F2 P450s in the regulation of the fasting and feeding response in the progression of NAFLD needs further studies to identify the precise role of 20-HETE in insulin resistance and activation of AMPK by cellular stress.

Several reports indicated the differential expression of cytochrome P450 omega-hydroxylase isoforms in the clinic-pathological features of liver cirrhosis and cancer. The human CYP4F2 metabolizes the potent chemotactic eicosanoid leukotriene B4 to 20-hydroxy-leukotriene B4, which has less potent capabilities in recruiting immune cells. The induction of mouse CYP4A during hepatic steatosis along with fatty acid-induced uncoupling of the catalytic cycle can produce ROS. Increased ROS production and decreased levels of 20-hydroxy-leukotriene B4 due to suppressed CYP4F may be an important mechanism for providing the third hit, which promotes the progression of steatosis to steatohepatitis and eventually liver fibrosis, cirrhosis, and hepatocarcinogenesis. Decreased activity of CYP4F2 in the metabolism of arachidonic acid to 20-HETE due to Val433Met (1297C/T) substitution was strongly associated with rapid hepatic cirrhosis development (OR=6.0, CI=0.28, p=0.222) (Vavilin et al., 2013). In contrast, the potent vasoconstrictive 20-HETE, which has strong mitogenic and angiogenic properties, is increased in tumors of liver, brain, kidney, and ovary with increased expression of CYP4A/4F genes compared to those in normal tissues (Alexanian, Miller, Roman, & Sorokin, 2012). Similarly, increased expression of CYP4A11, CYP4F2, and CYP4F3 isoforms were significantly expressed in pancreatic ductal adenocarcinoma (Gandhi et al., 2013), suggesting that 20-HETE, which increases expression of HIF and its downstream target vascular endothelial growth factor (VEGF), promotes blood vessel sprouting and metastasis by activation of metalloproteinases (MMPs) (Yu et al., 2011). Thus, selective inhibitors of 20-HETE synthesis by CYP4 omega hydroxylase have been demonstrated to reduce proliferation, angiogenesis, and invasion in lung, renal, and brain cancers (Edson & Rettie, 2013). Consistently, other reports indicated the utility of selective inhibitors of 20-HETE formation as potential therapeutic agents to inhibit tumor progression. In fact, the administration of HET0016 inhibited both 9L gliosarcoma and U251 glioma cell proliferation and tumor growth in a dose-dependent manner (Guo, Roman, Falck, Edwards, & Scicli, 2005), leading to increased mean survival time of the animals (Guo et al., 2006). Although these results and other reports suggest a promising role of 20-HETE antagonist as a therapeutic agent in the treatment of cancer, the development of isoform-selective antagonist may show increased efficacy without adverse drug reactions that may be present. Many of the presently used antagonists inhibit CYP4-mediated formation of 20-HETE in human microsomes with an IC50 value of less than 100nM (Sato et al., 2001) although various CYP4A/4F isoforms can be differentially inhibited by broad-spectrum pan-CYP4 inhibitors (Miyata et al., 2001; Nakano, Kelly, & Rettie, 2009). These results suggest that careful cautions should be considered when using these pan-CYP4A inhibitors to define the role of 20-HETE CYP4A isoforms in the pathophysiological progression of disease. Thus, future efforts need to focus on the development of selective inducers and inhibitors of specific CYP4 subfamily members, and identification of major CYP4 isoforms in these widely diverse diseases.

Alcohol intake or nonalcoholic molecules can increase the levels of CYP3A and CYP2B, although the degree of their elevation is lower than that of CYP2E1 (Johansson et al., 1988; Niemelä et al., 2000). Since CYP3A is responsible for the metabolism of many drugs, it is likely that metabolic activation of some drugs by CYP3A may be directly related to drug disposition (Yin, Tomlinson, & Chow, 2010) or drug-induced cytotoxicity (Hosomi, Fukami, Iwamura, Nakajima, & Yokoi, 2011; Hosomi et al., 2010), especially after alcohol intake, as reported (Wolf et al., 2007). Examples of fat accumulation and DILI include APAP, isoniazid, valproate, tamoxifene, troglitazone, tacrin, rifampicin, and many others. The reactive metabolites of these drugs may be responsible for stimulating DILI (Jaeschke et al., 2012; Pessayre et al., 2012; Stachlewitz et al., 1997; Yuan & Kaplowitz, 2013). Alternatively, metabolism of these substrates may increase oxidative stress, which can activate the cell-death-associated JNK and/or p38K, leading to mitochondria-dependent apoptosis, as demonstrated with APAP (Bae et al., 2001) and troglitazone (Bae & Song, 2003). Furthermore, the levels of acetaldehyde and lipid peroxidation-protein adducts seem to correlate with the induced levels of CYP3A and CYP2E1 in alcohol or high-fat exposed rats, suggesting an important role of CYP3A in protein adducts formation (Niemelä et al., 1998).

Additive or synergistic interactions between alcohol and smoking can lead to increased hepatotoxicity and carcinogenesis in experimental animal models and human cases (Kuper et al., 2000; Purohit et al., 2013; Seitz & Cho, 2009). Chronic alcohol intake is known to increase the levels of CYP2A5, which can metabolize nicotine, a major ingredient of tobacco (Lu, Zhuge, Wu, & Cederbaum, 2011; Niemelä et al., 2000). In mice, alcohol feeding induces CYP2A5 in a CYP2E1-dependent manner (Lu et al., 2011), possibly through the CYP2E1-ROS-Nrf2 axis (Lu, Zhang, & Cederbaum, 2012). Elevated levels of hepatic CYP2A6 (the human ortholog of the mouse CYP2A5) were also observed in some patients with ALD or cirrhosis than the control, despite the small sample size (Lu et al., 2011). In the mouse model, ethanol-mediated CYP2A5 induction was dependent on the presence of CYP2E1, while ethanol induction of CYP2E1 was not CYP2A5 dependent. Ethanol-mediated CYP2A5 induction was not observed in Cyp2e1-null mice despite ethanol feeding. However, CYP2A5 induction was markedly elevated in the Cyp2e1 knockin mice after treatment with ethanol but not with the dextrose-control. Furthermore, CYP2E1-dependent ROS was needed for CYP2A5 induction through activation of the NRF2 (Lu et al., 2012). Since CYP2A5 can also metabolize many cancer causing agents, such as aflatoxin B1 and nitrosamines, the induction of CYP2A5 in rodents by alcohol (Lu et al., 2011) or HFD (Choi et al., 2013) and CYP2A6 in alcoholic individuals is likely to contribute to increased oxidative stress and hepatic injury in ALD and NALD.

(Video) Vitamin A- Biochemical functions, Deficiency manifestations, RDA, Sources

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Water-Soluble Vitamins and Nonnutrients

Martin Kohlmeier, in Nutrient Metabolism (Second Edition), 2015

Nutritional Summary

Function: Riboflavin is the precursor of FMN and FAD, which serve both as prosthetic groups and as cofactors for a wide range of enzymes important for beta-oxidation and oxidative phosphorylation, antioxidant defense, vitamin metabolism (folate, niacin, vitamins A, C, B6, and B12), amino acid utilization, hormone synthesis, and many other functions.

Food sources: Milk and dairy products, meat, poultry and fish, cereals and bread, and green vegetables each can provide at least one-sixth of recommended intake per serving.

Requirements: The current RDA for women is 1.1mg/day, and for men, it is 1.3mg/day (Food and Nutrition Board, Institute of Medicine, 1998). Pregnancy, lactation, and increased energy intake and expenditure all increase requirements. Since only 1–2 weeks’ requirement of riboflavin is stored, regular adequate intake is important.

Deficiency: Prolonged low intake causes cracking and swelling of the lips (cheilosis), cracking and inflammation of the angles of the mouth (angular stomatitis), dark-red tongue (glossitis), skin changes at other sites (seborrheic dermatitis), and normocytic anemia. Deficiency during infancy and childhood impairs growth.

Excessive intake: There is little danger even when intake exceeds the RDA many times. Since excess riboflavin is lost rapidly, there is no additional benefit over recommended intake levels and stores will not increase.

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What is the metabolism of vitamins? ›

Metabolic pathways for water-soluble B group and C vitamins, and for fat-soluble vitamins A, D and K are annotated in Reactome, covering processes that convert dietary forms of these molecules into active forms, and that regenerate active forms of vitamin cofactors consumed in other metabolic processes.

Why are vitamins important in metabolism? ›

Vitamins and minerals play a different kind of role in energy metabolism; they are required as functional parts of enzymes involved in energy release and storage. The water-soluble B vitamins are involved as coenzymes in the breakdown of nutrients and in the building of macromolecules, such as protein, RNA, and DNA.

What is vitamin short answer? ›

Vitamins are substances that our bodies need to develop and function normally. They include vitamins A, C, D, E, and K, choline, and the B vitamins (thiamin, riboflavin, niacin, pantothenic acid, biotin, vitamin B6, vitamin B12, and folate/folic acid).

What are the 13 vitamins your body needs? ›

There are 13 essential vitamins — vitamins A, C, D, E, K, and the B vitamins (thiamine, riboflavin, niacin, pantothenic acid, biotin, B6, B12, and folate). Vitamins have different jobs to help keep the body working properly.

How do vitamins affect metabolism? ›

Supplements to increase metabolism

B-complex vitamins: These help metabolize carbohydrates, fats, and proteins, activating stored energy instead of letting it turn to fat. Niacin, vitamin B-6, and iron: This impressive trio increases your body's production of the amino acid L-carnitine to help burn fat.

Which vitamin is most important in energy metabolism? ›

The B vitamins play many essential roles in energy metabolism in the body. The B vitamins include: B-12.
Deficiency in one of the B vitamins can affect other B vitamins, which can disrupt a person's metabolism.
  • B-12 is essential for the metabolism of proteins and fats . ...
  • B-6 also helps metabolize protein.
Jul 31, 2018

Where are vitamins metabolized? ›

The liver is importantly involved in vitamin metabolism. The liver produces bile for absorption of fat-soluble vitamins (A, D, E, K), and the liver is an important site for vitamin storage.

Do vitamins regulate metabolism? ›

The vitamins regulate reactions that occur in metabolism, in contrast to other dietary components known as macronutrients (e.g., fats, carbohydrates, proteins), which are the compounds utilized in the reactions regulated by the vitamins.

Which vitamin is stored in the body? ›

The fat-soluble vitamins — A, D, E, and K — dissolve in fat and are stored in your body. The water-soluble vitamins — C and the B-complex vitamins (such as vitamins B6, B12, niacin, riboflavin, and folate) — dissolve in water. Your body can't store these vitamins.

What vitamin is most important? ›

The role it plays in so many bodily functions and the staggering amount of people who are deficient in it makes Vitamin D the most important vitamin for your body overall, and there's a good chance that you are not getting enough.

What is vitamin function? ›

Vitamins are vital for good health, but needed in much smaller amounts than macro-nutrients, like carbs and fats. They're important for many daily bodily functions, such as cell reproduction and growth, but most importantly for the processing of energy in cells.

How do vitamins work in the body? ›

How do vitamins work? - Ginnie Trinh Nguyen - YouTube

Which vitamin should not be stored? ›

Vitamin C is cannot be stored in our body because it is a water-soluble vitamin and gets excreted from the body with sweat or urine.

Which vitamin helps your eyes adjust in the dark? ›

Research has concluded that vitamin A deficiency is a rare cause of night blindness and a more frequent cause of vision problems for children in developing countries. The vitamin helps the eyes to adjust between the light and dark.

What vitamins do you need daily to survive? ›

The 13 Vitamins Essential for Survival
  • Vitamin A. Vitamin A helps to maintain healthy teeth, bones, skin, and mucous membrane. ...
  • Vitamin B1. Also called thiamine, this converts carbohydrates into energy and helps regulate proper heart function. ...
  • Vitamin B2. ...
  • Vitamin B3. ...
  • Vitamin B5. ...
  • Vitamin B6. ...
  • Vitamin B7. ...
  • Vitamin B12.
Jul 11, 2018

How do vitamins play in fat metabolism? ›

Other vitamins, like vitamin B12, folic acid, vitamin C, and essential fatty acids influence lipid metabolism by different mechanisms. Coenzyme B12 and folate coenzyme provide to balance, by methionine synthesis, the pool of methyl radicals necessary for phospholipid biosynthesis.

What vitamin is best for tiredness? ›

Vitamin B is recommended as one of the top vitamins to help with tiredness, so you can also opt for a supplement if you're struggling to stay topped up through your diet. Vitamins should be used alongside a balanced diet.

What is the use of metabolism? ›

Metabolism is the process by which your body converts what you eat and drink into energy. During this complex process, calories in food and beverages are combined with oxygen to release the energy your body needs to function.

Which vitamin helps in weight loss? ›

Vitamins are meant to be a support to weight loss, not the only cause. Vitamin B, D, iron, and magnesium are 4 popular supplements for weight loss.

Which vitamin is stored in liver? ›

Any leftover or excess amounts of these leave the body through the urine. They have to be consumed on a regular basis to prevent shortages or deficiencies in the body. The exception to this is vitamin B12, which can be stored in the liver for many years.

What vitamins are metabolized by the liver? ›

The liver stores vitamin A, D, E, K and B12. The first four of these are all fat soluble. This means that the bile secreted during digestion is essential for absorbing them so that the body can use them. If bile production is compromised by liver damage, the proper absorption of these vitamins may be affected.

Which vitamin is not stored in liver? ›

After that we introduce the vitamins that are not stored in the liv‌er. These vitamins include vitamins C, fatty acids, and some B vitamins. Finally, we talk about supplements that can be taken along with normal nutrition to provide these vitamins for the body.

What are the main sources of vitamins? ›

Good sources include:
  • citrus fruit - including oranges and grapefruit.
  • red and green peppers.
  • potatoes.
  • strawberries, blueberries and blackberries.
  • green leafy vegetables - such as broccoli and brussels sprouts.

What are vitamins made from? ›

Vitamins are made by living things, while minerals are found in the earth. For example, carrots produce beta carotene, which the body turns into vitamin A; minerals, such as iron and copper, can be found in soil and rock.

Which vitamin is good for eyes and skin? ›

1. Vitamin A
Vitamin AUses
How does vitamin A protect the eyes from future diseases and keeps them healthy?It reduces the risk for age-related macular degeneration and vision loss, Retinol helps to strengthen immunity and prevent eye infections
2 more rows

What vitamin makes your hair grow? ›

Biotin. Biotin, also known as vitamin B7, is a complex B vitamin that is often touted for having hair growth benefits. And some of that hype may actually be worth it. Biotin has functions in “creating red blood cells, which carry oxygen and nutrients to the scalp and hair follicles,” says Dr.

Which vitamin is best for hairs? ›

Biotin. Biotin (vitamin B7) is important for cells inside your body. Low levels of it can cause hair loss, skin rashes, and brittle nails.

What are the 3 main functions of vitamins? ›

Vitamins and minerals are considered essential nutrients—because acting in concert, they perform hundreds of roles in the body. They help shore up bones, heal wounds, and bolster your immune system. They also convert food into energy, and repair cellular damage.

What is vitamin classification? ›

Vitamins are generally classified as water-soluble vitamins and fat-soluble vitamins.

How many vitamins do we have? ›

In humans there are 13 vitamins: 4 fat-soluble (A, D, E, and K) and 9 water-soluble (8 B vitamins and vitamin C).

How long do vitamins stay in your system? ›

With all of that said, the exact time that water-soluble vitamins circulate in your body will depend on factors like age, nutrient status, diet, and the like. However, most are depleted within 1-2 days, which means replenishing them daily to ensure sufficient levels if critical for optimal health and performance 7.

What are the 6 functions of vitamins? ›

Vitamins are micronutrients that offer a range of health benefits, including:
  • boosting the immune system.
  • helping prevent or delay certain cancers, such as prostate cancer.
  • strengthening teeth and bones.
  • aiding calcium absorption.
  • maintaining healthy skin.
  • helping the body metabolize proteins and carbs.
Aug 22, 2019

What vitamins can you overdose on? ›

Watch out for these fat-soluble vitamins: A, E and K

Vitamin A is a fat-soluble nutrient that is naturally present in many foods, like beef, eggs and many fruits and vegetables. An overdose of this vitamin can lead to problems with confusion, hair loss, liver damage and bone loss.

What vitamins can you take too much of? ›

Dwyer says vitamin D, calcium, and folic acid are three nutrients you may get too much of, especially through supplements. Adults who regularly far exceed the 4,000 international units (IUs) daily safe upper limit for vitamin D might may end up with serious heart problems.

What vitamins Cannot be taken together? ›

Large doses of minerals can compete with each other to be absorbed. Don't use calcium, zinc, or magnesium supplements at the same time. Also, these three minerals are easier on your tummy when you take them with food, so if your doctor recommends them, have them at different meals or snacks.

Which fruit is best for eyesight? ›

Look to Fruits and Vegetables for Good Eye Health
Foods Rich in Antioxidants for Eye HealthAntioxidants Related to Eye Health
Red berries, kiwi, red and green bell peppers, tomatoes, broccoli, spinach, and juices made from guava, grapefruit, and orange.Vitamin C (ascorbic acid)
5 more rows

What foods make your eyes whiter? ›

Make sure that you include fresh vegetables and fruits in your diet such as carrots, pumpkins, lemons and oranges. The fruits and vegetable rich in vitamins and antioxidants will keep your eyes white. Also eating green, leafy foods such as spinach and nuts like almonds, walnuts and peanuts will promote eye health.

Which oil is best for eyesight? ›

Castor oil has antimicrobial and anti-inflammatory properties that make it safe for your eyes and boost tear film lipids. Lasting effects. Another benefit to castor oil eye drops is how long they last. Studies show that they may stay in your eyes up to 4 hours.

Which vitamins body Cannot produce? ›

Vitamin C. Dietary intake of vitamin C (from food and drinks) is essential, because the human body cannot make this vitamin from other compounds.

Which vitamins pose the greatest risk of toxicity? ›

The fat-soluble vitamins A and D are the most likely to cause toxicity symptoms if you consume them in high amounts.

What happens to the body without vitamins? ›

Without these nutrients, the body produces red blood cells that are too large and don't work properly. This reduces their ability to carry oxygen. Symptoms can include fatigue, shortness of breath and dizziness. Vitamin supplements, taken by pill or injection, can correct the deficiencies.

How are vitamins processed in the body? ›

They are absorbed directly into the bloodstream as food is broken down during digestion or as a supplement dissolves. Because much of your body consists of water, many of the water-soluble vitamins circulate easily in your body.

What is this metabolism? ›

Metabolism is the process by which your body converts what you eat and drink into energy. During this complex process, calories in food and beverages are combined with oxygen to release the energy your body needs to function.

What is the metabolism of minerals? ›

Mineral metabolism disorders are abnormal levels of minerals -- either too much or too little -- in the blood. Minerals are very important for the human body. They have various roles in metabolism and body functions. They are essential for the proper function of cells, tissues, and organs.

How are vitamins and minerals metabolized in the body? ›

The liver acts as a storage site for some vitamins, minerals and glucose. These provide a vital source of energy for the body which the liver transforms into glycogen for more efficient storage (see 'metabolism'). The liver stores vitamins and minerals for the times when they may be lacking in the diet.

Where are vitamins stored in the body? ›

Fat-soluble vitamins are stored in the body's liver, fatty tissue, and muscles. The four fat-soluble vitamins are vitamins A, D, E, and K. These vitamins are absorbed more easily by the body in the presence of dietary fat. Water-soluble vitamins are not stored in the body.

Where are most vitamins absorbed in the body? ›

Most of the vitamins and minerals you consume are also absorbed in the small intestine, but each one requires its own unique mechanism to cross the intestinal cell lining.

What part of the body absorbs vitamins? ›

The small intestine is where vitamin absorption happens (along with most other types of absorption). Water-soluble vitamins, such as vitamin C, have "active transports" for absorption -- molecules that pick them up in the small intestine, in a section called the jejunum, which is located about midway through.

What are the 3 types of metabolism? ›

There are three basic metabolism types: ectomorph, mesomorph, and endomorph – definitely words you probably don't use in your normal, day-to-day conversations. But learning the types of body you were born with will help your fitness plan in the long run.

What are the 3 stages of metabolism? ›

Catabolism: The Breakdown
  • Stage 1: Glycolysis for glucose, β-oxidation for fatty acids, or amino acid catabolism.
  • Stage 2: Citric Acid Cycle (or Kreb cycle)
  • Stage 3: Electron Transport Chain and ATP synthesis.
May 2, 2022

What are the 2 types of metabolism? ›

Metabolism can be conveniently divided into two categories: Catabolism - the breakdown of molecules to obtain energy. Anabolism - the synthesis of all compounds needed by the cells.

What hormone controls mineral metabolism? ›

Calcium-Regulating Hormones

PTH regulates calcium homeostasis by acting on the major calcium reservoir of the body, the skeleton. It stimulates osteoclastic activity and thereby bone resorption.

What vitamins or minerals boost metabolism? ›

Vitamin B Complex

"B vitamins—thiamine, riboflavin, niacin, pantothenic acid, vitamin B6, biotin, and folic acid—are all necessary for energy metabolism, including the digestion, breakdown, and storage of nutrients such as carbohydrates, proteins, and fats, which help the body turn nutrients into energy."

Are vitamins metabolized in the liver? ›

Even in high doses, most vitamins have few adverse events and do not harm the liver. Many vitamins are normally concentrated in, metabolized by and actually stored in the liver, particularly the fat soluble vitamins.

Which vitamin is not stored in liver? ›

After that we introduce the vitamins that are not stored in the liv‌er. These vitamins include vitamins C, fatty acids, and some B vitamins. Finally, we talk about supplements that can be taken along with normal nutrition to provide these vitamins for the body.


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