nutrient

n.
A source of nourishment, especially a nourishing ingredient in a food.

adj.
Providing nourishment.

[Latin nūtriēns, nūtrient-, present participle of nūtrīre, to suckle.]

Essential dietary factors such as vitamins, minerals, amino acids and fatty acids. Metabolic fuels (sources of energy) are not termed nutrients so that a commonly used phrase is ‘energy and nutrients’.

A substance present in food and used by the body to promote normal growth, maintenance, and repair. The major nutrients needed to maintain health are carbohydrates, fats, proteins, minerals, vitamins, and water. Roughage (fibre), although not assimilated into the body and therefore not a nutrient, is also regarded as an essential component of a balanced diet.

adjective

Providing nourishment: alimentary, nourishing, nutritious, nutritive. See ingestion.

n

The beneficial chemical in foods and beverages. Classified as carbohydrates, fats, proteins, water, vitamins, and minerals.

A substance present in food that is used by the body to promote normal growth. maintenance, and repair. The major nutrients needed to maintain health are carbohydrates, lipids proteins, minerals vitamins and water. Roughage (fibre), although never assimilated into the body and therefore not a nutrient, is also regarded as an essential component of a balanced diet.

Nutrients are those organic and inorganic compounds that a living organism must acquire from the environment to support essential life processes, including basal metabolism, growth and maintenance of body tissues, activity, reproduction, and maintenance of general health. Nutrients are normally obtained by the ingestion of foods. Organic nutrients include carbohydrates, proteins or amino acids, lipids, and vitamins. Inorganic nutrients include minerals. Water is sometimes included in a listing of nutrients.

Classification of Nutrients

Nutrients often are classified as essential or nonessential. Essential nutrients are those that cannot be synthesized in the body at all or in sufficient amounts to meet needs and, thus, must be obtained preformed in the diet. These include the essential (indispensable) amino acids, the essential fatty acids, the vitamins, and the minerals. Two amino acids are classified as semi-essential because, although they can be synthesized in sufficient quantities in the body, their synthesis depends upon a supply of an essential amino acid. Other nutrients are considered conditionally essential, meaning that they are not normally required by a healthy adult but may be required in certain disease states or at certain stages of life because of increased demand or impaired synthesis. Nonessential nutrients include those that are oxidized as fuels and those that provide carbon skeletons and amino groups for endogenous synthesis of body constituents. The term "dispensable" is sometimes used to describe these nutrients, as the nutrients are not truly nonessential: an adequate amount of carbohydrate, protein, and fat must be taken in to supply the substrates required for maintenance of blood glucose, as fuel for oxidative metabolism and synthesis of ATP, and as substrate for synthesis of body components. They are "nonessential" only in the sense that carbohydrate, fat, or protein, as well as ethanol, can be used as fuels; in that either carbohydrate or protein or even the glycerol backbone of triacylglycerols (fat) can be a source of glucose; in that any fuel potentially can be used for synthesis of most lipids; and in that amino groups from most amino acids can be used for synthesis of indispensable amino acids. Also, some food components that have health benefits and are considered important parts of healthy diets, such as fiber and phytochemicals, are not required and are not considered nutrients per se.

The following table summarizes the nutrient classes, the essential compounds in each class, and the basic functions of these nutrients in the body.

Additional information about some of these nutrients can be found below. Additional information for the other nutrients can be found under separate entries in this volume.

Niacin

The term "niacin" is used to refer to either nicotinic acid (pyridine-3-carboxylic acid) or nicotinamide (pyridine-3-carboxamide). Niacin is widely distributed in foods of both plant and animal origin. Good sources of niacin include meats, poultry, fish, legumes, peanuts, some cereals (mainly in the bran), and enriched or whole grain products. Much of the niacin in cereals is not readily available because it is esterified to complex carbohydrates or peptides.

The amino acid tryptophan also is an important precursor for synthesis of pyridine nucleotide coenzymes (see below). The estimated conversion factor for adults is 60 mg of tryptophan to 1 mg of niacin. The term "niacin equivalent" (NE) is used for expression of niacin intakes and requirements, with either 1 mg of nicotinic acid, 1 mg of nicotinamide, or 60 mg of tryptophan equal to 1 NE.

The adult recommended daily (or dietary) allowance (RDA) for NEs is 14 mg per day for females and 16 mg per day for males (Institute of Medicine, 1998). Most mixed diets in the United States provide more than 5 mg of preformed niacin. However, for individuals consuming typical Western diets, most NEs are derived from tryptophan rather than from preformed niacin. The tryptophan content of proteins ranges from about 0.6 percent for corn to 1.5 percent for animal products. Assuming that the average tryptophan content of protein is about 1 percent, a diet for adults that contains 100 g or more of protein provides about 16 mg NEs and would by itself meet the RDA for niacin. One should note that food composition tables do not take into account the bioavailability of niacin (from plant foods) and do not include an estimate of the NE available from tryptophan in the food. The adult male RDA for NEs would be supplied by ¼ cup peanut butter, 3½ slices roast beef, 4½ cups green peas, or 15 slices enriched wheat bread.

Nicotinic acid and nicotinamide are actively absorbed from the small intestine as well as from the renal filtrate. Niacin metabolites are excreted in the urine. Defects in tryptophan absorption or reabsorption from the renal filtrate have been associated with cases of niacin deficiency (pellagra).

Niacin is essential for the formation of the pyridine nucleotide coenzymes, nicotinamide adenine dinucleotide (NAD), and nicotinamide adenine dinucleotide phosphate (NADP). Reduced forms of these coenzymes are indicated as NADH and NADPH. NAD and NADP function in oxidation-reduction reactions that are involved in the catabolism of glucose, fatty acids, ketone bodies, and amino acids. These coenzymes ultimately funnel electrons to electron-to-oxygen transfer systems, including the mitochondrial electron transport chain. These coenzymes also are essential for reductive biosynthetic reactions. In addition, NAD has a non-coenzyme function: NAD serves as the donor of adenosine diphosphate-ribose moieties for ADP-ribosylation reactions. Poly-ADP-ribosylated proteins appear to function in DNA repair, DNA replication, and cell differentiation.

Symptoms of pellagra, or niacin deficiency, include functional changes in the gastrointestinal tract and nonspecific lesions of the central nervous system. Early symptoms include weakness, lassitude, anorexia, and indigestion. Later symptoms include various gastrointestinal and mental symptoms and a bilaterally symmetrical dermatitis that affects parts of the body exposed to sunlight, heat, or mild trauma. Pharmaceutical doses of nicotinic acid cause vasodilation, and long-term use can cause gastrointestinal irritation and possibly liver damage. The tolerable upper intake level (UL) set by the Institute of Medicine (1997) is 35 mg of niacin per day for adults.

Riboflavin

Riboflavin is the common name for 7,8-dimethyl-10-(1′-D-ribityl)isoalloxazine, which also is known as vitamin B₂. Much of the riboflavin in the American diet is supplied by dairy products. Meats, especially organ meats, and vegetables such as broccoli, spinach, and mushrooms are also good sources. Enriched flour and enriched breakfast cereals also contribute significantly to riboflavin intakes. The RDA for riboflavin is 1.3 mg for men and 1.1 mg for women (Institute of Medicine, 1998). Some amounts of common foods that would need to be consumed to supply 1.3 mg of riboflavin (assuming they were the sole dietary source of this vitamin) are 3 cups milk, 1¼ pounds beef round, 8 large eggs, 4⅓ cups broccoli, or 65 slices whole wheat bread. Daily intakes of riboflavin in the United States average about 1.5 to 2 mg for adults (Institute of Medicine, 1998).

Table 1

Summary of nutrients and their functions (See Appendix for complete chart of vitamins.)
Nutrient class	Essential compounds in class	Function in body
Carbohydrates (composed of glucose, galactose, fructose, and other sugars)	None	Fuel—oxidation or storage as glycogen;
		Source of carbon skeletons for synthesis of various organic compounds
Proteins (composed of amino acids)	Histidine	Protein synthesis;
	Isoleucine	Substrate for synthesis of essential nonprotein compounds;
	Leucine
	Lysine	Source of amino groups for synthesis of nonessential amino acids;
	Methionine (and Cysteine)
	Phenylalanine (and Tyrosine)	Source of carbon skeletons for synthesis of various organic compounds including glucose and nonessential amino acids;
	Threonine
	Tryptophan
	Valine	Fuel—oxidation or conversion to carbohydrate or fat for storage
	Sufficient total amino acids to supply amino groups for synthesis of nonessential amino acids
Lipids	n-6 Essential fatty acids (e.g., linoleic acid)	Fuel—oxidation or storage;
	n-3 Essential fatty acids (e.g., α-linolenic acid)	Carbon skeletons for synthesis of various organic compounds in body;
	Sufficient dietary lipids to ensure adequate absorption of fat-soluble vitamins	Polyunsaturated (n-6 and n-3) fatty acids are required for synthesis of eicosanoids, inositol phosphoglycerides, sphingolipids, and membrane phospholipids
Vitamins
B vitamins	Niacin	Synthesis of coenzymes NAD(H) and NADP(H) that participate in oxidation-reduction reactions;
		Substrate for ADP-ribosylation of macromolecules
	Thiamin	Synthesis of coenzyme thiamin pyrophosphate (TPP) that is required by transketolase and α-ketoacid dehydrogenase complexes
	Riboflavin	Synthesis of coenzymes FAD and FMN that participate in oxidation-reduction reactions
	Vitamin B12	Synthesis of coenzymes deoxyadenosylcobalamin and methylcobalamin that participate in the metabolism of methionine and of propionyl/methylmalonyl CoA, respectively
	Folate	Synthesis of folate coenzymes, including tetrahydrofolate, methyl-tetrahydrofolate, methylene-tetrahydrofolate, and 10-formyl-tetrahydrofolate; the coenzymes are required for the metabolism of glycine, serine, methionine, and histidine, and the synthesis of purines and dTMP
	Vitamin B6	Synthesis of coenzymes pyridoxal 5'-phosphate (PLP) and pyridoximine 5'-phosphate (PMP) that are involved in amino acid metabolism
	Pantothenic Acid	Synthesis of coenzyme A;
		Synthesis of acyl carrier protein domain of fatty acid synthase
	Biotin	Coenzyme for synthesis of holocarboxylases
Other Vitamins
	Vitamin C	Electron donor for enzymatic and nonenzymatic reactions
	Vitamin A	Precursor of 11-cis-retinal required for visual function;
		Precursor of all-trans retinoic acid and other metabolites that bind retinoid nuclear receptors
	Vitamin D	Precursor of vitamin D hormone
	Vitamin E	Lipid-soluble antioxidant
	Vitamin K	Substrate for γ-glutamylcarboxylase
[continued]

Table 2

Summary of nutrients and their functions
Nutrient class	Essential compounds in class	Function in body
Minerals
Macroelements	Calcium	Regulation of cellular activities by intracellular Ca2+ (2d messenger function);
		Activation of certain proteins;
		Effects on excitability of nerve and muscle tissues;
		Component of mineralized tissue
	Phosphorus	Substrate for synthesis of nucleotides, DNA and RNA, phospholipids, signaling molecules, creatine phosphate, and other phosphoesters;
		Regulation of protein function via phosphorylation of tyrosyl, seryl, or threonyl residues of proteins;
		Substrate for oxidative phosphorylation (ATP synthesis);
		Component of mineralized tissue;
		Acid-base buffer system
	Magnesium	Anion charge neutralization (e.g., Mg2+.ATP4-);
		Essential for function of certain proteins;
		Stabilization of DNA and RNA structures
	Sodium	Membrane potentials of all cells and excitability of nerve and muscle tissues;
		Major extracellular cation;
		Generation and maintenance of electrical and osmotic gradients;
		Nutrient transport
	Potassium	Major intracellular cation;
		Membrane potential and excitability of nerve and muscle tissues
	Chloride	Major inorganic anion in body fluids
	(Sulfur)	Not essential as sulfur because sufficient inorganic sulfur is formed from catabolism of methionine and cysteine;
		Synthesis of Fe-S cluster proteins, various sulfoesters, including those in glycosaminoglycans
Microelements
	Iron	Synthesis of heme proteins, iron-sulfur cluster proteins, Fe-containing metalloenzymes
	Zinc	Conformation of zinc-finger proteins;
		Metalloenzymes—catalytic and noncatalytic roles
	Copper	Metalloenzymes—catalytic role
	Manganese	Metalloenzymes—catalytic and regulatory roles
	Iodine	Synthesis of thyroid hormone
	Molybdenum	Synthesis of Mo-containing coenyzme
	Selenium	Synthesis of selenocysteinyl residues of selenoproteins
	Boron and Chromium?	Probably are essential
	Nickel, Vanadium, Silicon, Arsenic, and Fluorine?	Possibly are essential
		(Although fluorine is not known to be nutritionally essential, its health benefits in prevention of dental caries are significant and fluoride intake, mainly from water, is recommended.)
	(Cobalt)	Vitamin B12 contains cobalt, but inorganic cobalt is not required

Following ingestion, flavin coenzymes are released from noncovalent attachment to proteins by gastric acidification and subsequent proteolysis. Nonspecific pyrophosphatases and phosphatases act on coenzyme forms to release riboflavin. Covalently bound flavin coenzymes make up about 5 percent to 10 percent of the riboflavin naturally occurring in foods, and the 8α-(amino acid)-riboflavins obtained from their digestion cannot by used for resynthesis of coenzymes. Free riboflavin is actively taken up from the small intestine. Riboflavin and small amounts of riboflavin catabolites are excreted in urine.

Riboflavin is required for synthesis of flavin mono-nucleotide (FMN), which is riboflavin 5′-phosphate, and flavin-adenine dinucleotide (FAD). Fully reduced forms of these coenzymes are indicated by FMNH₂ and FADH₂. Riboflavin coenzymes are involved in oxidationreduction reactions in which the ring portion of the coenzyme undergoes sequential addition or loss of hydrogens and electrons. Flavoproteins function in either one-or two-electron transfer reactions.

The flavin coenyzmes, FAD and FMN, function indispensably in oxidation-reduction reactions involved in the catabolism of glucose, fatty acids, ketone bodies, and amino acids, as well as in energy production via the respiratory chain and in reductive biosynthetic reactions.

Inadequate dietary intake of riboflavin can result in stunting of growth, a variety of lesions involving the skin and the epithelium of the gastrointestinal tract, anemia, and neuropathy. Riboflavin has a low toxicity, perhaps because of its low solubility or ready excretion in the urine. No tolerable upper intake level has been established because of a lack of suitable data.

Thiamin

Thiamin, also known as vitamin B₁, is 3-(2-methyl-4-aminopyrimidinyl)methyl-4-methyl-5-(β-hydroxyethyl)thiazole. Excellent sources of thiamin include unrefined cereal germs and whole grains, meats (especially pork), nuts, and legumes. Enriched flours and grain products in the United States contain thiamin, as well as niacin, riboflavin, iron, and folic acid.

The RDAs for thiamin are 1.2 mg of thiamin for men and 1.1 mg for women (Institute of Medicine, 1998). Typical intakes of thiamin in the United States average 1.2 to 2.0 mg per day for adults (Institute of Medicine, 1998). The recommended 1.2 mg of thiamin per day is provided by a 3½-ounce pork chop, 20 slices of whole wheat bread, 1⅔ cups of pecan halves, or 17 ounces of roasted peanuts.

Thiamin is released from its phosphate ester forms in which it is found in most natural foods by the action of pyrophosphatases and phosphatases in the small intestine. Free thiamin is absorbed by an active transport process that is probably carrier mediated. Trapping of thiamin as thiamin pyrophosphate in the mucosal cells appears to facilitate the uptake by metabolic trapping. Excess thiamin is excreted in the urine as various metabolites.

Raw fish may contain microbial thiaminases, which hydrolyze and, thus, destroy thiamin in the gastrointestinal tract. Certain thiamin antagonists that are found in coffee, tea, rice bran, and heme-containing animal products can impair thiamin uptake or utilization. Chronic alcoholism results in impaired thiamin absorption, which may be secondary to a folate deficiency. Thiamin requirements also appear to be elevated in individuals with high caloric intakes, especially when calories are derived primarily from carbohydrates, in renal patients undergoing long-term dialysis, in patients fed intravenously for long periods, and in patients with chronic febrile infections.

Thiamin is required for synthesis of thiamin pyrophosphate (TPP), which is also known as thiamin diphosphate (TDP); this may be the sole coenzyme form of thiamin. However, monophosphate and triphosphate esters occur naturally, and thiamin triphosphate has been implicated in nerve function. TPP functions in two general types of reactions in which TPP functions as a Mg²⁺-coordinated coenzyme for "active aldehyde transfers." First, TTP is a coenzyme for the oxidative decarboxylation of α-keto acids (catalyzed by the pyruvate, ketoglutarate, and branched-chain keto acid dehydrogenase complexes). Second, TPP is required as a coenzyme for transketolase, which catalyzes sugar rearrangements in the pentose phosphate pathway of glucose metabolism.

Thiamin deficiency, or beriberi, affects the nervous and cardiovascular systems. Clinical symptoms include mental confusion, anorexia, muscular weakness, ataxia, peripheral paralysis, paralysis of the motor nerves of the eye, edema, muscle wasting, tachycardia, and an enlarged heart. In Western countries, symptomatic thiamin deficiency is usually observed only in association with alcoholism.

No toxic effects of thiamin administered by mouth have been reported in humans, and thiamin is readily cleared by the kidneys. Injection of doses of thiamin that are more than 200 times those required for optimal nutrition produces a variety of pharmacological effects and can even induce death because of depression of the respiratory center. No tolerable upper intake level has been established for thiamin because of a lack of sufficient data.

Vitamin B₁₂

Vitamin B₁₂, or cobalamin, consists of a central cobalt atom coordinately linked to the four pyrrole nitrogens of a heme-like planar corrin ring structure. The 5^th coordinate bond of cobalt is to one of the nitrogens in a phosphoribo-5,6-dimethylbenzimidazolyl side group of the corrin ring structure, and the 6^th coordinate bond of cobalt can be occupied by a number of ligands. In vitamin B₁₂ preparations, this ligand is typically a cyano group that is formed by trace amounts of cyanide during purification of the vitamin from natural sources.

Vitamin B₁₂ is synthesized by some anaerobic microorganisms and by some algae, such as seaweed. Most plants and higher organisms do not use vitamin B₁₂ as a coenzyme, and they do not synthesize it. Vitamin B₁₂ is found in meat, dairy products, some seafoods, and in fortified cereals. A strictly vegetarian diet contains low levels of vitamin B₁₂, most of which come from algal sources or possibly microbial contamination associated with plant roots.

The RDA for vitamin B₁₂ is 2.4 micrograms for adults (Institute of Medicine, 1998). This amount of vitamin B₁₂ can be obtained from 1/10 ounce of beef liver, 1 egg, or 2⅔ ounces of canned tuna. Typical intake of vitamin B₁₂. in the United States averages 3.3 to 5.6 micrograms per day for adults (Institute of Medicine, 1998).

Absorption of vitamin B₁₂ is a complex process. Vitamin B₁₂ in food must be released from proteins to which it is naturally bound; this is accomplished in the stomach by the acid environment and by proteolysis of proteins by pepsin. The vitamin B₁₂ then binds to other proteins that have affinity for vitamin B₁₂, but these binding proteins are hydrolyzed by pancreatic proteases in the small intestine. The free vitamin B₁₂ then binds to an intrinsic factor, which is a high-affinity vitamin B₁₂-binding protein secreted by the gastric glands. The vitamin B₁₂-intrinsic factor complex binds to receptors located near the end of the small intestine, and the complex is taken up by endocytosis. The intrinsic factor is degraded by lysosomal enzymes, and free vitamin B₁₂ is released into the cytosol of the mucosal cells. The vitamin B₁₂ is released from the intestinal mucosal cells into the plasma as a complex with another protein, transcobalamin II. The transcobalamin II-B₁₂ complex is transported into tissues by receptor-mediated endocytosis; the complex is degraded in the lysosome, and the free vitamin B₁₂ is transported out of the lysosome into the cytosol.

Vitamin B₁₂ is excreted from the body in the urine. It is also secreted in the bile, but vitamin B₁₂ secreted in the bile is normally reabsorbed via the enterohepatic circulation. Vitamin B₁₂ is needed for synthesis of two coenzymes: methylcobalamin, which is a cofactor for cytosolic methionine synthase, and 5′-deoxyadenosylcobalamin, which is a cofactor for mitochondrial methylmalonyl CoA mutase.

Vitamin B₁₂ deficiency seldom is caused by a dietary lack of the vitamin and most commonly is because of a defect in vitamin B₁₂ absorption. Malabsorption of vitamin B₁₂ can result from a lack of intrinsic factor secretion, decreased gastric acid production, or pancreatic enzyme insufficiency. Food vitamin B₁₂ is malabsorbed by many elderly individuals, and it is recommended that adults older than 50 years ingest adequate vitamin B₁₂ from supplements or fortified foods. Symptoms of vitamin B₁₂ deficiency include megaloblastic anemia and a severe, and often irreversible, neurological disease called subacute combined degeneration.

No toxicity of vitamin B₁₂ has been reported. Absorption is limited by the amount of intrinsic factor secreted. No tolerable upper intake level has been established for vitamin B₁₂ because of lack of suitable data.

Vitamin B₆

Vitamin B₆ refers to several 4-substituted 2-methyl-3-hydroxyl-5-hydroxymethylpyridine compounds, which include pyridoxal, pyridoxine, pyridoxamine, and their respective 5′-phosphate derivatives. Good sources of vitamin B₆ include cereals, meat, especially organ meats, poultry, fish, starchy vegetables, and noncitrus fruits and juices.

The RDA for vitamin B₆ is 1.3 mg for adults (Institute of Medicine, 1998). The median intake of vitamin B₆ from food sources (i.e., not including supplements) is about 2 mg for men and about 1.5 mg for women. Amounts of some foods that would by themselves supply the daily RDA for vitamin B₆ include 1⅓ whole chicken breasts, 2 bananas, 1⅓ cups of oatmeal, 12 cups of milk, or 22 large eggs.

Phosphate derivatives of vitamin B ₆ are hydrolyzed by phosphatase prior to uptake from the small intestine. Some plants contain pyridoxine as a glucoside derivative; these normally are deconjugated by a mucosal glucosidase before the pyridoxine is absorbed. Vitamin B₆ in a mixed diet is about 75 percent bioavailable, whereas the vitamin B₆ in supplements is about 90 percent bioavailable. Vitamin B₆ is absorbed by a nonsaturable passive diffusion mechanism with metabolic trapping of the vitamers by formation of the phosphate derivatives. Excess vitamin B₆ is excreted in the urine. The major excretory form of vitamin B₆ is the 4-carboxylate derivative 4-pyridoxic acid, but unmetabolized vitamin also is excreted and may be the major excretory form when very high doses of vitamin B₆ are ingested.

Vitamin B₆ is used to form pyridoxal phosphate (PLP), this vitamin's major coenzyme form. PLP binds to proteins and PLP-dependent enzymes via Schiff base formation with the ε-amino group of specific lysyl residues in the proteins. PLP serves as a coenzyme for many enzymes involved in amino acid metabolism, including aminotransferases, decarboxylases, aldolases, racemases, and dehydratases. Aminotransferase reactions convert the coenzyme between the PLP and pyridoxamine phosphate forms.

Vitamin B₆ deficiency can result in seborrheic dermatitis, microcytic anemia (because of decreased hemoglobin synthesis), convulsions, depression, and confusion. Low vitamin B₆, folate, or vitamin B₁₂ intakes can lead to an elevated plasma homocysteine level. Alcoholics tend to have low vitamin B₆ status.

Some subjects taking very large pharmaceutical doses of pyridoxine have developed severe sensory neuropathy. There is some evidence for toxicity at daily doses of 500 mg or more, and a safe upper level of intake is thought to be 100 mg/day. The tolerable upper intake level set for vitamin B₆ by the Institute of Medicine (1998) is 100 mg/day for adults.

Pantothenic Acid

Pantothenic acid, also known as vitamin B₅, consists of β-alanine moiety condensed with pantoic acid. Pantothenic acid is distributed widely in plant and animal sources. Meat (especially liver), fish, poultry, milk, yogurt, legumes, and whole-grain cereals are good sources of pantothenic acid. Pantothenic acid is present in foods in the free form and in various bound forms, including coenzyme A, coenzyme A esters, acyl carrier protein, and glucosides.

The Adequate Intake established for pantothenic acid by the Institute of Medicine (1998) is 5 mg per day for adults. This amount of pantothenic acid can be obtained by eating 2½ cups of peanuts, 6 eggs, 3 whole chicken breasts, 6½ cups of milk, or 19 slices of whole wheat bread. The average dietary intake of pantothenic acid in the United States is about 5 to 6 mg, with somewhat lower average intakes in the elderly and young children.

Dietary coenzyme A, coenzyme A esters, and acyl carrier protein are degraded enzymatically in the small intestine to release free pantothenic acid. Pantothenic acid is taken up by active transport. Approximately 50 percent of dietary pantothenic acid is available. Pantothenic acid is excreted unchanged in the urine. The kidneys regulate excretion of pantothenic acid, secreting it when plasma concentrations are high and largely reabsorbing it when plasma concentrations are in the physiological range.

Cells use pantothenic acid to synthesize coenzyme A, which consists of pantothenate linked to cysteamine by a peptide bond and to a 3′-phospho-ADP moiety via a phosphoester linkage. Coenzyme A contains a reactive sulfhydryl group that is involved in the formation of thioesters with fatty acids and other carboxylic acids. Coenzyme A plays a major role in fatty acid metabolism and in the final oxidative steps in the catabolism of all fuels. Much of the metabolism of fatty acids and certain amino acid derivatives, as well as a numerous amphibolic steps in metabolism, use coenzyme A thioester substrates and produce coenzyme A thioester products. Coenzyme A also is used for the synthesis of the acyl carrier protein domain of fatty acid synthase, a multifunctional enzyme that catalyzes palmitate synthesis. Coenzyme A is involved in oxidative decarboxylation reactions catalyzed by α-keto acid dehydrogenase complexes, β-oxidation of fatty acids, ketone body synthesis, fatty acid and triacyl-glycerol synthesis, amino acid and organic acid catabolism, and in synthesis of isoprenoids, cholesterol, and steroids.

A naturally occurring deficiency of pantothenic acid has not been documented reliably and is undoubtedly rare because of the wide distribution of pantothenic acid in foods. Pantothenic acid deficiency has been produced experimentally in a small number of volunteers via a pantothenic acid-free diet; these volunteers appeared listless and complained of fatigue after nine weeks on the pantothenic acid-free diet. A "burning feet" syndrome that was observed among prisoners of war and among malnourished individuals in Asia may have been because of pantothenic acid deficiency, as symptoms appeared to be reduced by pantothenic acid.

Pantothenic acid is relatively nontoxic. Doses below 10 g of pantothenic acid per day do not seem to be associated with any toxic symptoms. No tolerable upper intake limit was set by the Institute of Medicine (1998) because of insufficient data.

Biotin

Biotin contains a ureido group attached to a tetrahydrothiophene ring and has a valeric acid side chain extending from the tetrahydrothiophene ring. Biotin is synthesized by bacteria, yeast, algae, and some plant species. Biotin is distributed widely in foods, existing both as free biotin and as biotin covalently bound to lysyl residues in biotinyl-proteins. Liver, whole-grain cereals, nuts, legumes, yeast, and egg yolks are relatively high in biotin. Biotin is synthesized by microflora in the large intestine, but biotin produced at that site appears to be excreted mainly in the feces.

The Adequate Intake for biotin, as set by the Institute of Medicine (1998), is 30 micrograms per day for adults. About 3 ounces roasted peanuts, 3 medium eggs, 5 cups of milk, ⅓ cup of peanut butter, or 1⅓ cups of oatmeal will provide 30 micrograms of biotin. The daily intake of biotin in Western countries is estimated to be about 60 micrograms per day.

Digestion of proteins releases biotinyl-lysine (biocytin) and small lysine-containing peptides with biotin attached covalently. These are hydrolyzed to release free biotin by a specific hydrolase called biotinidase that is present in the pancreatic digestive secretions. Free biotin is transported into the mucosal cells of the small intestine by a carrier-mediated, sodium-dependent process.

Biotin is excreted as such and as several degradation products. Degradation products include bisnorbiotin, in which the 5-carbon valerate side chain has been shortened by two carbons, and biotin sulfoxide, in which the thiophene ring sulfur has been oxidized to a sulfoxide.

The only known function of biotin in humans and other mammals is as a prosthetic group for four carboxylases: pyruvate carboxylase, acetyl CoA carboxylase, propionyl CoA carboxylase, and 3-methylcrotonyl CoA carboxylase (in the pathway of leucine catabolism). Holocarboxylase synthetase attaches biotin to the apocarboxylases in an ATP-requiring reaction; the biotin is attached by an amide bond to an ε-amino group of a specific lysyl residue in the enzyme protein. In the holocarboxylases, biotin serves as a CO₂ carrier and carboxyl donor to substrates.

A dietary deficiency of biotin is very rare because of the wide distribution of biotin in foods. Biotin deficiency with clinical symptoms of hair loss, dermatitis, and neurological symptoms has occurred in individuals consuming an abnormal diet that is low in biotin and high in raw egg white. Raw egg white contains avidin, a protein that binds biotin with a very high affinity and prevents its uptake from the intestine. Biotin deficiency may occur in individuals who routinely take certain anticonvulsants or in individuals with severe protein-energy malnutrition. 3-Hydroxyisovalerate is elevated in the urine of biotin-deficient subjects.

Intakes of biotin up to 10 mg per day have not been reported to be associated with toxicity. No tolerable upper intake level has been set for biotin because of lack of data. Inborn errors of biotin metabolism, biotinidase deficiency and holocarboxylase synthetase deficiency, can both be treated with pharmacological doses of biotin.

Vitamin C

Ascorbic acid or vitamin C is a 6-carbon lactone synthesized from glucose by plants and many animals. Humans, as well as nonhuman primates and several other species, are unable to synthesize ascorbic acid because of a lack of gulonolactone oxidase, the terminal enzyme in the biosynthetic pathway.

Ascorbic acid is found in many fruits and vegetables. Some dietary vitamin C is present as an oxidized form, dehydroascorbic acid. Cantaloupe, kiwi, oranges, lemons, strawberries, and watermelon are especially high in vitamin C. Vegetables that are rich sources of vitamin C include broccoli, red peppers, cauliflower, brussels sprouts, asparagus, potatoes, cabbage, spinach, collard greens, green peas, and carrots. Citrus juices and tomato juice are good sources of vitamin C. Many foods, such as fruit drinks and breakfast cereals, are fortified with vitamin C.

The current RDA for vitamin C is 75 mg for women and 90 mg for men (Institute of Medicine, 2000). An additional 35 mg per day is recommended for smokers. The adult female RDA is contained in ¾ cup orange juice, 1 orange, 1 kiwi, ⅓ cantaloupe, 1 small sweet pepper, 2 cups broccoli, or 3 baked potatoes. Typical intake of vitamin C by adults is 70 to 100 micrograms per day.

Ascorbic acid absorption probably occurs by a Na⁺-dependent system in the intestine. Bioavailability is close to 100 percent for vitamin C at doses between 15 and 200 mg but declines at higher doses. Ascorbic acid and its metabolites are excreted mainly in the urine.

Ascorbic acid acts as an electron donor, or reducing agent. Two electrons are lost, probably sequentially, with formation of semidehydroascorbic acid (free radical) and dehydroascorbic acid. Dehydroascorbic acid can be enzymatically or nonenzymatically reduced back to ascorbate or hydrolyzed irreversibly to 2,3-diketogulonic acid, which is converted to other products, including oxalate.

Vitamin C acts as an electron donor for eight mammalian enzymes: three dioxygenases that are involved in collagen hydroxylation (prolyl 4-hydroxylase, prolyl 3-hydroxylase, and lysyl hydroxylase), two dioxygenases that are involved in carnitine synthesis (6-N-trimethyl-L-lysine hydroxylase and γ-butyrobetaine hydroxylase), 4-hydroxyphenylpyruvate dioxygenase, dopamine β-hydroxylase, and peptidylglycine α-amidating monooxygenase. Ascorbic acid may also function in nonenzymatic reduction reactions and thus acts as a water-soluble antioxidant.

An early sign of vitamin C deficiency is fatigue. With more severe deficiency, petechial hemorrhage, coiled hairs, ecchymoses, bleeding and tenderness of the gums, hyperkeratosis, joint pain, and shortness of breath may occur.

Vitamin C is relatively nontoxic. Excess vitamin C may promote the formation of oxalate kidney stones. The tolerable upper intake level, or maximum intake level likely to pose no risk of adverse health effects in most individuals, was set at 2000 mg ascorbic acid per day from food plus supplements (Institute of Medicine, 1998).

Vitamin K

Vitamin K refers to a group of compounds that are 2-methyl-1,4-napthoquinones with a hydrophobic substituent at the 3-position. Phylloquinone (vitamin K₁), which is synthesized by plants, has a 20-carbon phytyl substituent at the 3-position of the napthoquinone ring. Menaquinones (vitamin K₂) are synthesized by bacteria and have an unsaturated side chain, made up of four to thirteen isoprenyl units, instead of the saturated phytyl chain present in phylloquinone. Animal tissues contain both phylloquinone and menaquinones. In addition to these naturally occurring compounds with vitamin K activity, a synthetic form of vitamin K called menadione can be alkylated to an active form in the liver and is used in animal feeds. Human vitamin K supplements are phylloquinone.

Green vegetables are the major dietary source of phylloquinone: kale, spinach, broccoli, brussels sprouts, cabbage, and lettuce are rich sources. Some vegetable oils, especially soybean oil and rapeseed (canola) oil, are good sources. Menaquinones, which are obtained especially from liver, provide only a minor portion of the vitamin K needed to meet the requirement. The nutritional significance of menaquinones synthesized by bacteria in the lower bowel is uncertain.

The RDA for vitamin K for adults who are age twenty-five years and older is 65 and 80 micrograms for women and men, respectively (National Research Council, 1989). The RDA for males is provided by ⅓ ounce of spinach or kale, ⅓ cup of broccoli, ⅔ cup of shredded cabbage, or 2¼ ounces of lettuce. Typical intake of vitamin K by adults is 70 to 100 micrograms per day.

Absorption of dietary vitamin K depends upon adequate lipid absorption. Vitamin K is incorporated into chylomicrons, along with other lipids, and ultimately is taken up by the liver as part of the chylomicron remnants. Vitamin K is stored in liver; the hepatic phylloquinone pool turns over more rapidly than that of menaquinones. Vitamin K is excreted predominantly as metabolites and glucuronides; these are excreted primarily in feces via the bile, but significant amounts are also excreted in urine.

The hydroquinone form of vitamin K is required for the posttranslational modification (γ-glutamylcarboxylation) of a group of proteins (referred to as Gla proteins or vitamin K-dependent proteins) during their synthesis. Vitamin K serves as substrate, or coenzyme, for an enzyme that converts targeted glutamyl residues to carboxyglutamyl (Gla) residues in these proteins. This posttranslational modification of glutamyl residues is essential for the normal physiological function of vitamin K-dependent proteins. Continued function of vitamin K in γ-glutamylcarboxylation reactions is dependent upon the recycling of oxidized vitamin K (vitamin K epoxide) back to the hydroquinone form (vitamin KH₂).

Vitamin K-dependent proteins include four plasma clotting proteins (prothrombin, factor VII, Factor IX, and factor X), two plasma proteins involved in thrombin-initiated inactivation of factor V (protein C and protein S), plasma protein Z of uncertain function, and two bone proteins (osteocalcin, or bone Gla protein, and matrix Gla protein). At physiological pH, both carboxyl groups of each Gla residue are negatively charged, and these anionic residues are involved in the association of Gla proteins with Ca²⁺.

Primary vitamin K deficiency is rare. Vitamin K-responsive hemorrhagic disease of the newborn can occur because of low vitamin K stores in the liver of the newborn and the low vitamin K content of human milk, along with other factors. In developed countries, commercial infant formulas are supplemented routinely with phylloquinone, and the practice of oral or intramuscular administration of phylloquinone to the newborn is almost universal. Vitamin K deficiency also has been reported in adults with low intakes of vitamin K who are receiving antibiotics and in patients subjected to long-term total parenteral nutrition without vitamin K supplementation. Vitamin K status should be of concern in disorders of lipid digestion or absorption and in persons treated with anticoagulant drugs that act by blocking reduction of oxidized vitamin K.

Toxic manifestations from ingestion of large amounts of vitamin K have not been reported. Menadione administration to infants has been associated with hemolytic anemia and liver toxicity, and should not be used for human supplements.

Vitamin E

Vitamin E is the term used for all tocopherols and tocotrienols and their derivatives that exhibit vitamin E activity. Tocopherols are more important sources of vitamin E. Both the tocopherols and tocotrienols consist of a chromanol head and a phytyl tail. The side chain of tocopherols is saturated, whereas that of tocotrienols contains double bonds at the 3′, 7′, and 11′ positions. Four tocopherols and four tocotrienols occur naturally; they differ in the number and position of the methyl groups on the chromanol ring. The naturally occurring isomer of α-tocopherol is the 2′R, 4′R, 8′R isomer, whereas synthetic tocopherols are mixtures of all eight possible stereoisomers.

Tocopherols in foods exist primarily as the free or unesterified forms. Ester forms (e.g., α-tocopheryl acetate or α-tocopheryl succinate) are less susceptible to oxidation and are used for food fortification and for supplements. The 6-hydroxyl group on the phenolic ring is the site for esterification of fatty acids.

A variety of naturally occurring RRR-α-tocopherols and tocotrienols are supplied by foods. Tocopherols differ in their antioxidant and biological activities. Currently, the biological activity of various forms of vitamin E are expressed as units of activity in relation to that of all-rac-α-tocopheryl acetate, which is a common pharmaceutical or synthetic form of vitamin E. The unit used to express vitamin E activity is the α-tocopherol equivalent (α-TE) with 1 equivalent equal to 1.49 mg of all-rac-α-tocopheryl acetate or 1.0 mg of RRR-α-tocopherol. The majority of the tocopherols consumed in the diet are not α-tocopherol, and γ-tocopherol accounts for more than half the estimated total tocopherol intake. Rich sources of vitamin E include vegetable oils, vegetable shortenings, margarines, mayonnaise, salad dressings, wheat germ, rice bran, nuts, seeds, peanut butter, eggs, potato chips, whole milk, and tomato products.

The RDA for vitamin E is 15 mg α-TEs for adults. This amount of vitamin E could be provided by 4 teaspoons of soybean oil, ⅔ cup of margarine, 2 cups of whole milk, 4½ cups of green peas, or 2 pounds of salmon. The average intake of vitamin E from American diets is 11 to 13 mg α-TEs daily in adults not taking vitamin E supplements.

Tocopheryl esters are hydrolyzed to free tocopherol in the small intestinal lumen, presumably by pancreatic esterases. Vitamin E is absorbed with other lipids, and the majority of the vitamin E is incorporated into chylomicrons in the mucosal cells of the small intestine. The chylomicrons are secreted into the lymph and then enter the circulation. Vitamin E is taken up by the liver in the chylomicron remnants and is then either stored in the parenchymal cells of the liver, incorporated into nascent very low density lipoproteins (VLDL) that are secreted into the blood stream, or excreted via the bile. Both vitamin E and its metabolites are primarily excreted in the feces via biliary secretion from the liver. Some metabolites are excreted in the urine.

Vitamin E is the major lipid-soluble, chain-breaking antioxidant found in plasma, red cells, and tissues, and it plays an essential role in maintaining the integrity of biological membranes. Among the biological functions proposed for vitamin E, the reaction of α-tocopherol with lipid peroxyl radicals to prevent uncontrolled free radical-initiated lipid peroxidaion is the best understood. Whether other tocopherols have other roles is uncertain.

Patients with familial isolated vitamin E deficiency have clear signs of vitamin E deficiency (extremely low plasma vitamin E levels and neurological abnormalities—spinocerebellar dysfunction with progressive ataxia) but do not have fat malabsorption or lipoprotein abnormalities. Absence of hepatic α-tocopherol transfer protein impairs secretion of α-tocopherol into hepatic lipoproteins (VLDL) and appears to be responsible for the low plasma vitamin E status of patients with familial isolated vitamin E deficiency and the low delivery of vitamin E to tissues. In humans, low plasma levels of vitamin E are associated with shorter lifespans of red blood cells because of their increased susceptibility to hemolysis. Vitamin E deficiency is rarely associated with lipid malabsorption syndromes or lipoprotein abnormalities. Neurological symptoms occur in individuals with malabsorption syndromes as well as in individuals with familial isolated vitamin E deficiency.

Vitamin E is relatively nontoxic when taken by mouth. The upper tolerable intake level set by the Institute of Medicine (2000) is 1000 mg of α-TEs per day from vitamin E supplements in addition to dietary intake. Consumption of more than this increases risk of hemorrhagic damage because vitamin E can act as an anticoagulant.

Potassium

Potassium (K⁺) is distributed widely in the body and is the principal cation in intracellular fluids. Like sodium and chloride ions, potassium ions exist as free hydrated ions that bind only weakly to organic molecules. Potassium functions in the maintenance of electrolytic and osmotic balances or gradients. The distribution of potassium between the intracellular and extracellular fluids is the result of ion pumps and of the permeability characteristics of cell membranes. The Na⁺, K⁺-ATPase pump, which moves 3 Na⁺ out of the cell in exchange for 2 K⁺ that are moved into the cell, is of particular importance.

Potassium is widely distributed in foods, especially in fruits and vegetables. Rich sources of potassium include fruits such as avocado, banana, cantaloupe, orange juice, and watermelon; vegetables such as lima beans, potatoes, tomatoes, spinach, and winter squash; and fresh meats.

Obligatory losses of potassium, which must be replaced, average about 800 mg of potassium per day. The estimated minimum requirement for potassium established by the National Research Council (1989) is 2 g per day for adults. Two grams of potassium are provided by 4 cups of fresh orange juice, 5½ small bananas, 5 medium potatoes, or 9/10 pound of beef chuck. Typical Western diets provide about 3 g of potassium per day.

Over 90 percent of the potassium in the diet is absorbed from the gut into the circulation. However, although nearly all of the dietary K⁺ is absorbed in the small intestine, there is normally some net secretion of K⁺ in the colon that results in loss of potassium in the feces. Absorption of dietary K⁺ causes a rise in the concentration of K⁺ in the plasma, and this immediately stimulates physiological mechanisms to promote rapid entry of K⁺ into cells so that a rapid rise in the plasma K⁺ concentration is prevented. Uptake of K⁺ by cells is essential in preventing life-threatening hyperkalemia. Nevertheless, in the long-term, to maintain K⁺ balance, the excess K⁺ from the diet must be excreted by the kidneys.

At typical potassium intakes, renal tubular secretion of K⁺ is required to maintain potassium balance. Renal secretion of K⁺ is under the control of various homeostatic regulatory mechanisms. The most important hormone regulating secretion of K⁺ is aldosterone, the release of which is triggered by a high concentration of K⁺ in plasma (or a low concentration of Na⁺ or by angiotensin II). When potassium intake is high, secretion of K⁺ by the colon as well as the kidney is increased to eliminate the excess potassium.

During potassium depletion, the kidney reabsorbs most of the filtered K⁺, and essentially no K⁺ is secreted. The small amount of K⁺ excreted in the urine under these circumstances comes from the filtered K⁺ that escaped reabsorption.

The high concentration gradient of K⁺ between the intracellular fluid and the extracellular fluid is important for generation and maintenance of the normal resting membrane potentials across cell membranes and for excitability of nerves and muscles. Higher intakes of potassium may have beneficial effects in preventing hypertension.

Dietary deficiency of potassium does not occur under normal circumstances. Large losses can occur, by either gastrointestinal or renal routes, in cases of prolonged vomiting, chronic diarrhea, use of diuretic agents, some forms of chronic renal disease, and in some metabolic disturbances such as metabolic acidosis. Hypokalemia causes membrane hyperpolarization, and this can interfere with the normal functioning of nerves and muscles, resulting in muscle weakness and decreased smooth muscle contractility. Deficiency symptoms include weakness, anorexia, nausea, drowsiness, and irrational behavior.

Acute hyperkalemia can result from sudden enteral or parenteral increases in potassium intake to amounts of about 18 g per day for an adult. Hyperkalemia causes membrane depolarization, causing muscular weakness, flaccid paralysis, and cardiac arrhythmias. Severe hyperkalemia can cause cardiac arrest and death.

Chloride

Chloride is the principal inorganic anion in the extracellular fluids of the body. Dietary chloride comes almost entirely from sodium chloride, and a small amount comes from potassium chloride. Thus, table salt and foods or beverages that contain NaCl added during food processing or preparation are the major sources of chloride in the diet. The amount of chloride contributed by water is low compared to that contributed by salt.

The estimated minimum requirement for chloride is 750 mg/day for adults, which corresponds to about 1.3 g of sodium chloride per ¼ teaspoon of table salt). Typical salt intake in the United States is higher than this. It is recommended that daily salt intake should not exceed 6 g because of the association of high intake with hypertension.

Loss of fluids through the skin, feces, and urine cause loss of both sodium and chloride. Chloride movement tends to parallel that of sodium, and loss of sodium usually is accompanied by a similar molar loss of chloride. Thus, conditions that cause loss of sodium (e.g., heavy losses through sweating, chronic diarrhea or vomiting, trauma, or renal disease) also cause loss of chloride and can result in hypochloremic metabolic alkalosis.

Chloride is essential for maintenance of fluid and electrolyte balance. Hydrochloric acid is an essential component of the gastric juice secreted by the stomach.

Deficiency of chloride does not occur under normal circumstances. Toxicity from excess intake of chloride is not known to occur, but water-deficiency dehydration can cause hyperchloremia.

Bibliography

Chow, Ching K. "Vitamin E." In Biochemical and Physiological Aspects of Human Nutrition, edited by Martha H. Stipanuk. Philadelphia: Saunders, 2000.

Church, Charles F., and Helen N. Church. Food Values of Portions Commonly Used—Bowes and Church, 11th ed. Philadelphia: Lippincott, 1970.

Institute of Medicine. Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B₆, Folate, Vitamin B₁₂, Pantothenic Acid, Biotin, and Choline. Washington, D.C.: National Academy Press, 1998.

Institute of Medicine. Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. Washington, D.C.: National Academy Press, 2000.

Levine, Mark, et al. "Vitamin C." In Biochemical and Physiological Aspects of Human Nutrition, edited by Martha H. Stipanuk. Philadelphia: Saunders, 2000.

Mahan, L. Kathleen, and Sylvia Escott-Stump. Krause's Food, Nutrition, and Diet Therapy, 9th ed. Philadelphia: Saunders, 1996.

McCormick, Donald B. "Niacin, Riboflavin, and Thiamin." In Biochemical and Physiological Aspects of Human Nutrition, edited by Martha H. Stipanuk. Philadelphia: Saunders, 2000.

National Research Council. Recommended Dietary Allowances, 10th ed. Washington, D.C.: National Academy Press, 1989.

Shane, Barry. "Folic Acid, Vitamin B₁₂, and Vitamin B₆." In Biochemical and Physiological Aspects of Human Nutrition, edited by Martha H. Stipanuk. Philadelphia: Saunders, 2000.

Sheng, Hwai-Ping. "Sodium, Chloride, and Potassium." In Biochemical and Physiological Aspects of Human Nutrition, edited by Martha H. Stipanuk. Philadelphia: Saunders, 2000.

Suttie, John W. "Vitamin K." In Biochemical and Physiological Aspects of Human Nutrition, edited by Martha H. Stipanuk. Philadelphia: Saunders, 2000.

Sweetman, Lawrence. "Pantothenic Acid and Biotin." In Biochemical and Physiological Aspects of Human Nutrition, edited by Martha H. Stipanuk. Philadelphia: Saunders, 2000.

—Martha H. Stipanuk

1. nourishing; aiding nutrition.
2. a nourishing substance, food or component of food. Includes minerals, vitamins, fats, protein, carbohydrate and water.

• n. allowance — the total feed provided to an animal for a day. Includes its basic nutritional requirements plus allowances for waste in the feeding process, special allowances for special states and activities, and for special qualities of the feed being used.
• n. analysis — chemical analysis of feedstuff with measurement of fiber, protein, fat, carbohydrate, individual minerals and vitamins.
• n. artery — one of the arterial blood supplies to a typical long bone; enters the bone via an oblique canal. Other blood supply routes to bone include metaphyseal, epiphyseal and periosteal arteries.
• n. content — the proportion of a feed or diet that is digestible and assimilable. See also total digestible nutrients.
• n. profile — a listing of the optimal level of each nutrient in dog and cat foods; published by the Association of American Feed Control Officials.
• n. requirements — daily requirement for each nutrient for each animal species at the recognized stages of life and production; usually presented in feeding tables.
• n. veins — mimics the nutrient artery.

IN BRIEF: Nourishing ingredient in food.

She took care that her diet included a full array of nutrients.

This entry is from Wikipedia, the leading user-contributed encyclopedia. It may not have been reviewed by professional editors (see full disclaimer)

Common misspelling(s) of nutrient

• nutritent

Dansk (Danish)
n. - næringsstof
adj. - nærende

Nederlands (Dutch)
voedings-/bouwstof, voedingswaarde bevattend

Français (French)
n. - élément nutritif
adj. - nutritif

Deutsch (German)
n. - Nährstoff, Baustoff
adj. - nahrhaft, Ernährungs-, Nähr-

Ελληνική (Greek)
n. - θρεπτική ουσία
adj. - θρεπτικός, τροφικός

Italiano (Italian)
nutriente

Português (Portuguese)
n. - substância (f) nutritiva
adj. - nutriente

Русский (Russian)
питательное вещество

Español (Spanish)
n. - alimento, sustancia nutritiva
adj. - nutriente

Svenska (Swedish)
n. - näringsämne
adj. - näringsrik, närande

中文（简体）(Chinese (Simplified))
营养物, 滋养物, 营养的, 滋养的

中文（繁體）(Chinese (Traditional))
n. - 營養物, 滋養物
adj. - 營養的, 滋養的

한국어 (Korean)
n. - 영양물[제]
adj. - 영양에 도움이 되는

日本語 (Japanese)
adj. - 栄養のある
n. - 栄養素, 栄養分

العربيه (Arabic)
‏(الاسم) مادة مغذيه (صفه) مغذي‏

עברית (Hebrew)
n. - ‮חומר מזין‬
adj. - ‮מזין, מספק מזון מבריא‬

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Gatorade Endurance Drink Nutrient Data