Thirteen vitamins are necessary for health; four—A, D, E, and K—are fat-soluble, and the remainder are water-soluble. The distinction between fat- and water-soluble vitamins is
important, because although fat-soluble vitamins are more readily stored in the body, they are likely to be poorly absorbed in gastrointestinal disorders of fat malabsorption ( Chapter 17 ).
Small amounts of some vitamins can be synthesized endogenously—vitamin D from precursor steroids; vitamin K and biotin by the intestinal microflora; and niacin from tryptophan, an
essential amino acid—but the rest must be supplied in the diet. A deficiency of vitamins may be primary (dietary in origin) or secondary (because of disturbances in intestinal absorption,
transport in the blood, tissue storage, or metabolic conversion). In the following sections, the major vitamins, together with their well-defined deficiency states, are discussed individually
(with the exception of vitamin B12 and folate, which are discussed in Chapter 13 ) beginning with the fat-soluble vitamins. However, deficiencies of a single vitamin are uncommon, and
the expression of a deficiency of a combination of vitamins may be submerged in concurrent PEM. A summary of all the essential vitamins, along with their functions and deficiency
syndromes, is presented in Table 9-22 .
Vitamin A is actually a group of related natural and synthetic chemicals that exert a hormone-like activity or function. The relationship of some important members of this
TABLE 9-22-- Vitamins: Major Functions and Deficiency Syndromes
Vitamin Functions Deficiency Syndromes
Vitamin A A component of visual pigment Night blindness, xerophthalmia, blindness
Maintenance of specialized epithelia Squamous metaplasia
Maintenance of resistance to infection Vulnerability to infection, particularly measles
Vitamin D Facilitates intestinal absorption of calcium and phosphorus and mineralization of bone Rickets in children
Osteomalacia in adults
Vitamin E Major antioxidant; scavenges free radicals Spinocerebellar degeneration
Vitamin K Cofactor in hepatic carboxylation of procoagulants—factors II (prothrombin), VII, IX,
and X; and protein C and protein S
Vitamin B1 (thiamine) As pyrophosphate, is coenzyme in decarboxylation reactions Dry and wet beriberi, Wernicke syndrome, ?Korsakoff
Vitamin B2 (riboflavin) Converted to coenzymes flavin mononucleotide and flavin adenine dinucleotide,
cofactors for many enzymes in intermediary metabolism
Ariboflavinosis, cheilosis, stomatitis, glossitis, dermatitis,
Niacin Incorporated into nicotinamide adenine dinucleotide (NAD) and NAD phosphate,
involved in a variety of redox reactions
Pellagra—three "D's": dementia, dermatitis, diarrhea
Vitamin B6 (pyridoxine) Derivatives serve as coenzymes in many intermediary reactions Cheilosis, glossitis, dermatitis, peripheral neuropathy
Vitamin B12 Required for normal folate metabolism and DNA synthesis Combined system disease (megaloblastic pernicious anemia
and degeneration of posterolateral spinal cord tracts)
Maintenance of myelinization of spinal cord tracts
Vitamin C Serves in many oxidation-reduction (redox) reactions and hydroxylation of collagen Scurvy
Folate Essential for transfer and use of 1-carbon units in DNA synthesis Megaloblastic anemia, neural tube defects
Pantothenic acid Incorporated in coenzyme A No nonexperimental syndrome recognized
Biotin Cofactor in carboxylation reactions No clearly defined clinical syndrome
group is presented in Figure 9-22 . Retinol, perhaps the most important form of vitamin A, is the transport form and, as the retinol ester, also the storage form. It is oxidized in vivo to the
aldehyde retinal (the form used in visual pigment) and the acid retinoic acid. Important dietary sources of vitamin A are animal derived (e.g., liver, fish, eggs, milk, butter). Yellow and
leafy green vegetables such as carrots, squash, and spinach supply large amounts of carotenoids, many of which are provitamins that can be metabolized to active vitamin A in vivo; the
most important of these is beta-carotene. A widely used term, retinoids, refers to both natural and synthetic chemicals that are structurally related to vitamin A but do not necessarily have
vitamin A activity.
As with all fats, the digestion and absorption of carotenes and retinoids require bile, pancreatic enzymes, and some level of antioxidant activity in the food. Retinol, whether derived from
ingested esters or from beta-carotene (through an intermediate oxidation step involving retinal), is transported in chylomicrons to the liver for esterification and storage. More than 90% of
the body's vitamin A reserves are stored in the liver, predominantly in the perisinusoidal stellate (Ito) cells. In normal persons who consume an adequate diet, these reserves are sufficient
for at least 6 months' deprivation. Retinoic acid, on the other hand, can be absorbed unchanged; it represents a small fraction of vitamin A in the blood and is active in epithelial
differentiation and growth but not in the maintenance of vision.
Figure 9-22Interrelationships of retinoids and their major functions.
Figure 9-23Vitamin A deficiency: its major consequences in the eye and in the production of keratinizing metaplasia of specialized epithelial surfaces, and its possible role in potentiating
Figure 9-24 A, Schema of normal vitamin D metabolism. B, Vitamin D deficiency. There is inadequate substrate for the renal hydroxylase (1), yielding a deficiency of 1,25(OH)2 D (2),
and deficient absorption of calcium and phosphorus from the gut (3), with consequent depressed serum levels of both (4). The hypocalcemia activates the parathyroid glands (5), causing
mobilization of calcium and phosphorus from bone (6a). Simultaneously, the parathyroid hormone (PTH) induces wasting of phosphate in the urine (6b) and calcium retention.
Consequently, the serum levels of calcium are normal or nearly normal, but the phosphate is low; hence, mineralization is impaired (7).
TABLE 9-23-- Predisposing Conditions for Rickets or Osteomalacia
Date: 2016-04-22; view: 436