Introduction to Human Nutrition

The Vitamins 179

other fatty acyl) moieties in a variety of biosynthetic
and catabolic reactions, including:

● cholesterol and steroid hormone synthesis
● long-chain fatty acid synthesis from palmitate and
elongation of PUFAs in mitochondria
● acylation of serine, threonine and cysteine residues
on proteolipids, and acetylation of neuraminic
acid.

Fatty acid synthesis is catalyzed by a cytosolic multi-
enzyme complex in which the growing fatty acyl
chain is bound by thioester linkage to an enzyme-
bound 4′-phosphopantetheine residue, rather than to
free CoA, as in β-oxidation. This component of the
fatty acid synthetase complex is the acyl carrier
protein.

Pantothenic acid defi ciency and safe and
adequate levels of intake

Prisoners of war in the Far East in the 1940s, who
were severely malnourished, showed, among other
signs and symptoms of vitamin defi ciency diseases, a
new condition of paresthesia and severe pain in the
feet and toes, which was called the “burning foot syn-
drome” or nutritional melalgia. Although it was ten-
tatively attributed to pantothenic acid defi ciency, no
specifi c trials of pantothenic acid were conducted,

rather the subjects were given yeast extract and other

rich sources of all vitamins as part of an urgent

program of nutritional rehabilitation.

Experimental pantothenic acid depletion, together

with the administration of ω-methyl-pantothenic

acid, results in the following signs and symptoms after

2–3 weeks:

● neuromotor disorders, including paresthesia of the

hands and feet, hyperactive deep tendon refl exes,

and muscle weakness. These can be explained

by the role of acetyl-CoA in the synthesis of the

neurotransmitter acetylcholine, and impaired

formation of threonine acyl esters in myelin.

Dysmyelination may explain the persistence and

recurrence of neurological problems many years

after nutritional rehabilitation in people who had

suffered from burning foot syndrome

● mental depression, which again may be related to

either acetylcholine defi cit or impaired myelin

synthesis

● gastrointestinal complaints, including severe vom-

iting and pain, with depressed gastric acid secretion

in response to gastrin

● increased insulin sensitivity and a fl attened glucose

tolerance curve, which may refl ect decreased antag-

onism by glucocorticoids

CNH

H 2

C

H 2

C SH

CH 2

CH 2

NH

C

CHOH

C

O

O

CH 2

H 3 C

POP

O-

O O

O

N

N N

N

NH 2

O

O OH

CH 2

P

O-

• O O

Coenzyme A (CoASH)

-SH group forms thioesters

with fatty acids

O

CH 3

• O

C

CH 2

CH 2

NH

C

CHOH

C

O

O

CH 2

H 3 C

OH

CH 3

OH

Pantothenic acid

Figure 8.18 Pantothenic acid

and coenzyme A.