The American Journal of Clinical Nutrition 36: NOVEM BER 1982, pp 950-962.

Printed in USA
1982 American Society for Clinical Nutrition
Medium-chain triglycerides: an 2
Andr#{233}C Bach, ScD and Vigen K Babayan, PhD
ABSTRACT A review of the literature on the medical and nutritional use of medium-chain
triglycerides (M CTs) since 1970 is presented with additional discussions on the various modifica-
tions and applications of the M CTs in the synthesis of certain structured lipids. The metabolism of
M CTs in the liver and extrahepatic tissues is discussed along with further documentation of the use
of M CTs in malabsorption and hyperlipidemia cases. Recent applications of M CTs and modified
M CTs in hyperahimentation, deficiency in the carnitine system, epilepsy, obesity, and other special
areas of application are cited. The use of medium-chain monodiglycendes for dissolving cholesterol
gallstones is presented. The contraindications for the use of M CTs in ketosis, acidosis, and cirrhosis
are also discussed. Suggestions for use of M CTs in a variety of medical and nutritional applications
are presented. Am J Clin Nutr 1982;36:950-962.
KEY W ORDS M edium-chain triglycerides, hong-chain triglycerides, medium-chain fatty acid
(C6:0-Cl2:0), long-chain fatty acid (C 14:0 and longer), medium-chain monodiglycerides (mono-
diglycerides of caprylic and capric acids)
Introduction
M edium-chain triglycerides (M CTs) were
first introduced in 1950 for the treatment of
disorders of lipid absorption. Since then a
great deal has been learned about the metab-
olism and clinical use of M CTs and of their
fatty acids.
Herein, we have tried to evaluate the cur-
rent state of the art of M CTs emphasizing,
particularly, what has been learned since
1970. References 1 to 4 supply earlier biblio-
graphical information.
Physicochemical properties
M CTs are made up of a mixture of C6:0
(1 to 2% ), C8:0 (65 to 75% ), ClO:0 (25 to
35% ), and C12:0 (1 to 2% ) medium-chain
fatty acids (M CFAs) obtained by the hydrol-
ysis of coconut oil followed by the fractiona-
tion of the fatty acids. The M CFAs are ester-
ified with glycerol with or without a catalyst
to form the triacylglycerols (5). The melting
point of the M CFAs is much lower (C8:0,
16.7#{176}C; C 10:0, 31.3#{176}C)than that of the long-
chain fatty acids (LCFAs) (C 16:0, 63.1#{176}C).
Thus M CFAs, but also medium-chain triac-
ylglycerols, are liquid at room temperature.
By virtue of their smaller molecular size
M CFAs are relatively soluble in water: the
water solubility at 20#{176}Cis 68 mg/lOO ml for
950
C8:0 versus 0.72 mg for C 16:0. The fact that
M CFAs are weak electrolytes and are highly
ionized at neutral pH, increases even more
their solubility in biological fluids. As we
shall see, the greater water solubility and the
smaller molecular size of the M CFAs have
consequences in all levels of their metabo-
lism.
Absorption and metabolism
Absorption
The molecular weight of M CTs is smaller
than the molecular size of long-chain triglyc-
erides (LCTs). This facilitates the action of
pancreatic lipase. Consequently, M CTs are
hydrolyzed both faster and more completely
than LCTs. In the case of mixed triacylglyc-
erols the M CFAs are liberated preferentially.
M ott et a! (6) showed that in man, M CTs did
not produce any change in pancreatic secre-
tion, whereas with LCTs, there was a signifi-
cant overall increase.
I From the Laboratoire de Pathologic G#{233}n#{232}rahe, 5cr-
vice de M #{233}decine Interne A, Clinique M #{233}dicale A, Hos-
pices Civils, Strasbourg, France; and Nutritional Labo-
ratories, Stokely-Van Camp, Inc, Indianapolis, IN.
2 Address reprint requests to: Vigen K Babayan, PhD
Stokehy-Van Camp, Inc, 941 N M eridian St, Indianap-
olis, IN 46206.
Received December 4, 1981.
Accepted for publication M ay 4, 1982.

b
y

g
u
e
s
t

o
n

S
e
p
t
e
m
b
e
r

1
1
,

2
0
1
2
a
j
c
n
.
n
u
t
r
i
t
i
o
n
.
o
r
g
D
o
w
n
l
o
a
d
e
d

f
r
o
m

M EDI UM -CHA I N TRI GL Y CERI DES: UPDA TE 951
FI G. 1. Di gesti on, absorpti on, and transport of f ats. M G , monoacyl gl ycerol : C /n i. chyl omi crons: gp, ca-gl ycero-
phosphate; G CI RC, general ci rcul ati on.
The products of M CTs hydrol ysi s are ab-
sorbed f aster than those of L CTs, and as f ast
as gl ucose (7). Si nce thei r i ntral umi nal hy-
drol ysi s i s rapi d and rel ati vel y compl ete, the
M CTs-unl i ke L CTs- are absorbed mai nl y
as f ree f atty aci ds, and onl y rarel y as mono-
di acyl gl ycerol s (Fi g 1). I n cases where bi l e
sal ts or pancreati c l i pase def i ci ency or both
occur (8), a l arge f racti on of M CTs can be
absorbed as tri acyl gl ycerol s, whereas L CTs
cannot be absorbed. I n enterocytes, these
M CTs are then hydrol yzed by an i ntesti nal
l i pase.
I n the mucosa, L CFA are converted i nto
acyl -CoA s i n the presence of an acyl -CoA
synthetase. The acyl -CoA s are then i ncorpo-
rated i nto tri acyl gl ycerol s, whi ch are a maj or
component of chyl omi crons. Si nce thi s en-
zyme i s speci f i c f or f atty aci ds wi th more than
12 carbon atoms, the M CFA s are not si gni f i -
cantl y i ncorporated i nto chyl omi crons; there-
f ore, M CFA s l eave the i ntesti ne f aster than
the L CFA s. The tendency of f atty aci ds to be
esteri f i ed i s di rectl y proporti onal to thei r abi l -
i ty to bi nd to f atty-aci d-bi ndi ng protei n (9,
10). M CFA s are not easi l y bound to thi s
protei n and are not easi l y esteri f i ed, whi l e
L CFA s are easi l y bound to thi s protei n and
i ncorporated abundantl y i nto l i pi ds.
M CFA s f ol l ow the portal venous system
(Fi g 1), whereas L CFA s f ol l ow the l ymphati c
system. Thus, M CTs do not sti mul ate the
f l ow of l ymph, whi l e L CTs sti mul ate i t si g-
ni f i cantl y. The L CFA s are transported as
chyl omi crons, whi ch are i nsol ubl e parti cl es.
The M CFA s, however, are transported i n the
sol ubl e f orm of f atty aci ds, bound to serum
al bumi n. Thi s bond between M CFA s and
al bumi n, however, i s not as easi l y f ormed as
that between L CFA s and al bumi n (1 1).
Because M CFA s l eave the i ntesti nal mu-
cosa by the portal venous system, they reach
the l i ver more rapi dl y than the l onger mol e-
cul es. The l atter move vi a the extrahepati c
ti ssues, where they may be parti al l y retai ned.
Thus, M CFA s reachthe l i ver i n greater abun-
dance than do exogenous L CFA s. The ma-
j ori ty of the M CFA s i s retai ned i n the l i ver,
and onl y a smal l amount appears i n the pe-
ri pheral bl ood f or a short peri od of ti me.
W hen L CTs and M CTs are i ngested si -
mul taneousl y, the l atter parti al l y i nhi bi t the
absorpti on of the f ormer. Neverthel ess, the
total number of cal ori es absorbed i n thi s si t-

b
y

g
u
e
s
t

o
n

S
e
p
t
e
m
b
e
r

1
1
,

2
0
1
2
a
j
c
n
.
n
u
t
r
i
t
i
o
n
.
o
r
g
D
o
w
n
l
o
a
d
e
d

f
r
o
m

952 BA CH A ND BA BA Y A N
I
I
2 k
. T
- Ho p a t O c y t e -. -
1 - # {1 4 9 }-- # {1 4 9 }# {1 4 9 }.
- i _ __..= -- -
Te lI L
L YR J
FI G. 2. Hepati c metabol i sm of f atty aci ds. TG, tri acyl gl ycerol s; PL, phosphol i pi ds; CE, esteri f i ed chol esterol :
CPT, carni ti ne pal mi tyl transf erase.
uati on i s greater than the cal ori es absorbed
when ei ther f at i s i ngested al one (12).
The mode of transport of M CFA s resul ts
i n reduced sterol absorpti on (13). To be ab-
sorbed, sterol s must be i ncorporated i nto mi -
cel l es; and to be transported they must be
bound to L CFA s, and i ncorporated i nto chy-
l omi crons (14). These two processes do not
take pl ace wi th M CFA s and consequentl y
the absorpti on of sterol s i s di mi ni shed.
The absorpti on of cal ci um (15) and mag-
nesi um appears to be enhanced when the di et
contai ns M CTs, parti cul arl y i n i nf ants (16).
The absorpti on of ami no aci ds al so appears
to be i mproved (17, 18).
Hepati c metabol i sm
I n the endopl asmi c reti cul um of the hepa-
tocyte, the L CFA s are acti vel y f i xed on the
f atty-aci d-bi ndi ng protei n (9) and acti vated
i nto acyl -CoA s under the i nf l uence of a l ong-
chai n-acyl -CoA synthetase (Fi g 2). These
acyl -CoA s then pref erenti al l y esteri f y a-gl yc-
erophosphate to gi ve tri acyl gl ycerol s and
phosphol i pi ds; and esteri f y chol esterol , to
gi ve chol esterol esters. Because M CFA s do
# {1 4 9 } - # {1 4 9 }-- : -
L ONG C HA IN : - -
hCV tCo SY NThI TA SE
# {1 4 9 } - oA S
- - . - -s _ _ !_ :
. L C IA
DEN C I Y NTHESI St -
: . ..y::;c ;
- ACETYL CoA
#{ 163}
I
not bi nd easi l y to the f atty-aci d-bi ndi ng pro-
tei n (19), and the acyl -CoA synthetase spe-
ci f i c f or these f atty aci ds i s l ocated i n the
mi tochondri al matri x, M CFA s are al most
never acti vated i n the extrami tochondri al
space. Consequentl y, M CFA s are not si gni f i -
cantl y i ncorporated i nto the l i pi ds synthe-
si zed by the hepati c ti ssue (20).
M CFA s cross the doubl e mi tochondri al
membrane very rapi dl y and, unl i ke the
L CFA s, they do not requi re the presence of
carni ti ne (Fi g 2) (21). I n the mi tochondri al
matri x M CFA s are acyl ated by means of
an octanoyl -CoA synthetase. I n contrast,
L CFA s or thei r acyl -CoA deri vati ves cannot
cross the mi tochondri al wal l . I n the presence
of a carni ti ne pal mi tyl transf erase-I , L CFA s
are transf ormed i nto acyl -carni ti nes that cross
the membrane and regenerate l ong-chai n-
acyl -CoA s i n the matri x, by the acti on of a
carni ti ne pal mi tyl transf erase-I l .
The mi tochondri al acyl -CoA s, of whatever
chai n l ength, then undergo f l -oxi dati on, wi th
producti on of acetyl -CoA . I n a heal thy, wel l -
nouri shed organi sm, rel ati vel y f ew L CFA s
reach thi s stage at the same ti me, si nce these

b
y

g
u
e
s
t

o
n

S
e
p
t
e
m
b
e
r

1
1
,

2
0
1
2
a
j
c
n
.
n
u
t
r
i
t
i
o
n
.
o
r
g
D
o
w
n
l
o
a
d
e
d

f
r
o
m

M EDI UM -CHA I N TRI GL Y CERI DES: UPDA TE 953
f atty aci ds tend to be i ncorporated i nto the
l i pi ds synthesi zed by the l i ver. The carni ti ne
pal mi tyl transf erase compl ex i s rather mac-
ti ve under these condi ti ons. The M CTs, how-
ever, are avai l abl e and are rapi dl y oxi di zed.
The resul t i s an excess of acetyl -CoA (22),
whi ch then f ol l ows vari ous metabol i c path-
ways, both i n the mi tochondri a (K rebs cycl e,
ketogenesi s, el ongati on of f atty aci ds) and i n
the cytosol (de novo synthesi s of f atty aci ds
and chol esterol ). Duri ng thi s accel erated /9-
oxi dati on of M CFA s, many hydrogen atoms
are rel eased, and thus the cel l medi um i s
noti ceabl y reduced (22). Recentl y, i t has been
demonstrated that f atty aci ds can al so un-
dergo f l -oxi dati on i n the peroxi somes. But
the amount of peroxi somal oxi dati on of
M CFA s i s negl i gi bl e, because the key enzyme
i n thi s metabol i c pathway, acyl -CoA oxi dase,
i s not very acti ve wi th acyl -CoA s that have
f ewer than 12 carbon atoms (23).
A f racti on of the acetyl -CoA suppl i ed en-
ters i nto the K rebs cycl e and i s oxi di zed i nto
CO2. The l i ver produces about 10 ti mes more
CO2 f rom C8:0 than f rom Cl 6:0 (24); but the
capaci ty of the K rebs cycl e i s l i mi ted (25).
Furthermore, because of both the excess of
acetyl -CoA produced f rom M CTs and the
reducti on i n the cel l medi um, oxal oacetate
wi l l be i n short suppl y (26) (Fi g 2). A l arge
part of the acetyl -CoA i s then redi rected to-
ward the synthesi s of ketone bodi es.
M CTs are ketogeni c (27, 28), much more
so than L CTs. W i el and and M atschi nsky (29)
and M cGarry and Foster (25, 30) f ound that
the cl assi c anti ketogeni c substances-f ruc-
tose, gl ucose pl us i nsul i n, gl ycerol , and l ac-
tate-had l i ttl e ef f ect on the ketogenesi s i n-
duced i n the rat by octanoi c aci d. Freund and
W ei nsi er (3 1 ), however, f ound that sucrose
greatl y decreased the amount of acetone i n
the ai r exhal ed by subj ects who had i ngested
M CTs. The si mul taneous admi ni strati on of
M CTs and oxal oaceti c aci d donors noti ceabl y
reduces the producti on of ketone bodi es f rom
M CTs i n the rat (26).
The mi tochondri a have a system that don-
gates f atty aci ds that have 12 or more carbon
atoms. A smal l f racti on of the acetyl -CoA
produced duri ng the oxi dati on of M CFA s
serves to l engthen endogenous f atty aci ds.
The rel ati ve i mportance of thi s metabol i c
pathway i ncreases when L CTs are repl aced
by M CTs i n the di et (32).
By compl i cated transf er mechani sms i n-
vol vi ng ci trate and acetyl carni ti ne, acetyl -
CoA i s transported to the cytosol and can be
used i n the producti on of f atty aci ds and
chol esterol . A carbohydrate-ri ch di et i n-
creases the de novo synthesi s of f atty aci ds
and chol esterol by the l i ver. The synthesi s
decreases when some of the carbohydrate i s
repl aced by f ats. The decrease i s even smal l er
when M CTs, rather than L CTs, are provi ded
i n the di et (33-35). The sl i ght chol esterol -
l oweri ng ef f ect of M CTs i denti f i ed by many
i nvesti gators can be accounted f or by a de-
crease i n the i ntesti nal absorpti on of chol es-
terol and a sl owi ng of i ts synthesi s f rom ace-
tyl -CoA i n the l i ver (34, 36). L ess chol esterol
i s synthesi zed because the acetyl -CoA i s used
i n the de novo synthesi s of f atty aci ds (37);
and because the acti vi ty of f i -hydroxy-f i -
methyl gl utaryl -CoA reductase, the key en-
zyme i n chol esterol synthesi s, i s reduced (34).
A f ter a si ngl e oral dose of M CTs a sl i ght
hypogl ycemi a devel ops (27, 38). I t i s caused,
apparentl y, by a decrease i n the hepati c out-
put of gl ucose and not by an i ncrease i n the
peri pheral uti l i zati on of gl ucose. I nteresti ngl y
enough, the concentrati on of i nsul i n i n the
bl ood i ncreases at the same ti me, because the
i sl ets of L angerhans are sti mul ated ei ther by
the ketone bodi es or by the M CFA s them-
sel ves or by both. But, i n general , i t appears
that M CTs i mprove carbohydrate tol erance
(39, 40).
Extr a hepa tic meta bolism
Gi ven the magni tude of the hepati c uptake
of M CFA s, the rol e of the extrahepati c ti ssues
i n the metabol i sm of M CTs i s smal l , except
f or the uti l i zati on of ketone bodi es. The
M CFA s, however, pl ay an i mportant rol e i n
the human f etus. Pi l z (41) reported that 15 to
20% of the f atty aci ds i n cord bl ood have
ei ght or f ewer carbon atoms.
A s i n the l i ver, the extrahepati c ti ssues do
not i ncorporate much M CFA s i n the l i pi ds
they synthesi ze (24). I n addi ti on, L CFA s di -
mi ni sh the capaci ty of f at cel l s to esteri f y
C8:0 (42). A s i n the l i ver, i t appears that
M CFA s do not need carni ti ne to cross the
mi tochondri al membrane of extrahepati c ti s-
sues. Thi s, however, has been questi oned by
Groot and H#{ 252} l smann (43). M CFA s are oxi -
di zed i nto CO2 i n the extrahepati c ti ssues
more rapi dl y than are L CFA s (24). A l so, as

b
y

g
u
e
s
t

o
n

S
e
p
t
e
m
b
e
r

1
1
,

2
0
1
2
a
j
c
n
.
n
u
t
r
i
t
i
o
n
.
o
r
g
D
o
w
n
l
o
a
d
e
d

f
r
o
m

954 BA CH A ND BA BA Y A N
i n the l i ver, M CFA s i nhi bi t, onl y sl i ghtl y, the
de novo synthesi s of f atty aci ds i n adi pose
ti ssue (35).
Cl i ni cal use
F a t ma la bsor ption
For 30 yr the speci al properti es of M CTs
have been appl i ed i n human therapy, parti c-
ul arl y i n cases where the di gesti on, absorp-
ti on, or transport of usual di etary f ats are
di sturbed. I n such cases steatorrhea i s present
and i s of ten f ol l owed by a progressi ve 5cc-
ondary mal nutri ti on caused by the l oss of
ni trogen, water, and el ectrol ytes i n the f eces.
I n general , the steatorrhea subsi des when di -
etary L CTs are repl aced by M CTs, and the
number and wei ght of the stool s are reduced.
The l ow concentrati on of l i pi ds i n the serum
remai ns unchanged, but the dyspepsi a and
the nutri ti onal state i mproves. Pati ents gai n
wei ght and chi l dren start to grow agai n. Thus
M CTs have been used successf ul l y i n adul ts,
chi l dren, and newborns wi th the f ol l owi ng
di sorders:
1 ) I n di sorders of l i pi d di gesti on, as wi th
maj or or total resecti on of the esophagus or
of the stomach; bi l i ary atresi a, obstructi ve
j aundi ce, pri mary bi l i ary ci rrhosi s (44), and
bl i nd-l oop syndrome; and pancreati ti s (45),
cysti c f i brosi s (46-48), and pancreatectomy.
2) I n di sorders of l i pi d absorpti on, as when
there i s massi ve resecti on of the smal l i ntes-
ti ne (49, 50), cei ac di sease, W hi ppl e s di sease,
Crohn s di sease, enteri ti s, gl uten enteropathy,
tropi cal or i di opathi c sprues, and mal absorp-
ti on i n neonates (18, 51).
3) I n di sorders of l i pi d transport, as i n
def i ci ency of chyl omi cron synthesi s (eg, con-
geni tal /9-l i poprotei n def i ci ency); and i n l ym-
phati c di sorder due to engorgement (eg, i n-
testi nal l ymphangi ectasi a) or l eakage [ eg,
chyl uri a (52, 53), chyl ous asci tes, and chyl o-
thorax (54, 55)] . I n the case of an abnormal
exchange between the l ymphati c system and
another system or a cavi ty, M CTs decreases
l i pi d and protei n l osses. Si nce M CTs, unl i ke
L CTs, do not sti mul ate the f l ow of l ymph,
they f avor the heal i ng of f i stul as.
I n cases of mal di gesti on and/or mal ab-
sorpti on where L CTs are not wel l tol erated,
M CT-contai ni ng di ets have a great advantage
over l ow-f at di ets. The advantage i s that
M CTs are a f at and thus can be used i n
cooki ng. I n addi ti on, M CTs are a concen-
trated source of cal ori es (8.3 kcal /g compared
to 3 to 4 kcal /g f or carbohydrates and pro-
tei ns), and a good source of acetyl groups
whi ch are usef ul i n l i pi d synthesi s.
The i ngesti on of l abel ed f ats f ol l owed by
the detecti on of the tracer i n the expi red CO2
i s a method of ten used to measure the amount
of f at absorbed. Si nce M CTs are oxi di zed
much more rapi dl y than L CTs, l abel ed tri oc-
tanoyl gl ycerol has been pref erred to tri ol ei n
by Schwabe et a! (56) ( 4C tracer) and by
W atki ns et a! (57) ( 3C tracer) to detect ma! -
absorpti on of f ats.
Ga llbla dder disea se
The medi um-chai n monodi gl yceri des of
capryl i c and capri c aci d can be sol ubi l i zed i n
aqueous sol uti ons, oi l s, and other organi c
compounds. The medi um-chai n monodi gl y-
ceri des have been i nvesti gated i n i n vi tro (58)
and i n vi vo studi es f or thei r use i n di ssol uti on
of gal l stones. A product contai ni ng these me-
di um-chai n monodi gl yceri des i s under an i n-
vesti gati onal new drug status i n the USA
(Capmul 8210, Stokel y-V an Camp, I nc, I n-
di anapol i s, I N; US patent 4,205,086, M ay 27,
1980). I t has been used successf ul l y i n the
treatment of chol esterol -rel ated chol ei thi asi s
(59, 60) by perf usi ng i t i nto the common bi l e
duct. Recentl y, f urther advances have been
reported i n both percutaneous and endo-
scopi c entry techni ques conf i rmi ng the saf ety,
ef f i cacy, and rapi d di ssol uti on of gal l stones
wi th thi s product (61, 62).
Applica tion of the ener gy-pr oviding a nd
ketogenic pr oper ties of MCTs
W hen M CTs are suppl i ed i n the di et, they
are rapi dl y oxi di zed, renderi ng many ketone
bodi es and suppl yi ng a qui ck source of en-
ergy. The energy i s del i vered to the whol e
body, both the l i ver (duri ng the oxi dati on of
f atty aci ds), and the extrahepati c ti ssues
(mai nl y duri ng the uti l i zati on of ketone bod-
i es). A modest el evati on of the concentrati on
of ketone bodi es i n the bl ood i s known not to
be dangerous: al l the extrahepati c ti ssues can
use the ketone bodi es suppl i ed by the bl ood.
W hen the bl ood l evel of f i -hydroxybutyrate
and acetoacetate i ncreases, the uti l i zati on of
ketone bodi es i s enhanced (63). These ti ssues

b
y

g
u
e
s
t

o
n

S
e
p
t
e
m
b
e
r

1
1
,

2
0
1
2
a
j
c
n
.
n
u
t
r
i
t
i
o
n
.
o
r
g
D
o
w
n
l
o
a
d
e
d

f
r
o
m

M EDI UM -CHA I N TRI GL Y CERI DES: UPDA TE 955
are enzymati cal l y equi pped to produce ace-
tyl -CoA f rom ketone bodi es. The acti vated
acetate i s then used accordi ng to l ocal needs,
ei ther as a source of energy, or as a basi c
i ngredi ent i n the de novo synthesi s of l i pi ds.
Sour ces of ener gy
The M CTs are, theref ore, a f ood of choi ce
f or any organi sm that has i ncreased energy
needs, as af ter maj or surgery (64), or duri ng
normal or retarded growth (16, 18, 65). I t i s
general l y bel i eved that M CTs shoul d be i n-
cl uded i n the nutri ti onal management of the
severe undernouri shed pati ent.
A nother maj or consumer of ketone bodi es
i s the f etus. Rubal tel l i et al (66) have sug-
gested that the perf usi on of L CTs i nto cx-
pectant mothers coul d hel p the treatment of
the f etus wi th sl ow i ntrauteri ne growth. From
what i s known about M CTs, i t al l ows us to
thi nk that i n thi s i nstance, i t woul d be pref -
erabl e to use M CTs rather than L CTs.
Lipid pr ecur sor s
The acetyl -CoA produced i n the peri pheral
ti ssues f rom M CTs can al so enter i nto ana-
bol i c pathways. I n the brai n, l arge synthesi s
of l i pi ds-mai nl y phosphol i pi ds-f rom ke-
tone bodi es have been demonstrated (67).
Thi s synthesi s appears to be very ef f ecti ve
duri ng the peri od of mycl i ni zati on of the
brai n. The use of M CTs as a source of energy
and l i pi d precursors i n compl i cated pregnan-
ci es shoul d be f urther expl ored.
A nticonvulsive pr oper ties
K etone bodi es al so have a narcoti c and
anti convul si ve property that has not yet been
expl ai ned (68). Thi s property has l ong been
used i n the treatment of epi l epsy. A l though
many drugs are now avai l abl e, a ketogeni c
di et (69) remai ns a val uabl e al ternati ve i n
anti convul si ve therapy i n at l east two cases:
when there i s resi stance to the usual drugs
(eg, epi l epti c myocl oni a of chi l dhood) and i n
i ntol erance to the medi cati on, or both.
I n addi ti on to provi di ng an i nsuf f i ci ent
amount of carbohydrates, a ketogeni c di et
has the di sadvantages of bei ng unpal atabl e
and di f f i cul t to prepare and admi ni ster. These
di sadvantages are parti al l y overcome wi th the
M CT-based ketogeni c di et i ntroduced by
Huttenl ocher et al (70) and used wi th com-
pl ete success by some authors (7 1-73). The
di et provi des 70% of the cal ori es f rom M CTs,
as compared to 87% cal ori es f rom f at i n the
L CT-based ketogeni c di et. However, some
setbacks i n the treatment of epi l epsy wi th
M CTs have recentl y been reported (74-77).
Hyper a limenta tion
M CTs arc a pref erabl e f ood f or any orga-
ni sm that has i ncreased energy needs, such as
undernouri shed pati ents af ter maj or surgery
(64) or chi l dren duri ng normal or retarded
growth (16, 18, 65).
The metabol i sm of M CFA s by the extra-
hepati c ti ssues i s i ncreased consi derabl y when
M CTs are suppl i ed i ntravenousl y. M CTs are,
consequentl y, suppl i ed i n abundance to the
vari ous ti ssues where they are hydrol yzed. I n
these ti ssues, part of the rel eased f atty aci ds
are i ncorporated i nto l i pi ds (42), but most of
them are oxi di zed. The resul ti ng acetyl -CoA
generates energy i n si tu and contri butes to
l i pi d synthesi s. The cal ori c demands of the
stressed pati ent are di f f i cul t to meet wi thout
i ncorporati ng f at i nto the parenteral regi men.
L i pi d emul si ons contai ni ng L CFA s, whi ch
f or the most part are stored i n the hepati c
and adi pose ti ssues, are not capabl e of sup-
pl yi ng qui ck energy i n l arge quanti ti es.
Theref ore, repl acement of L CTs wi th M CTs
coul d be val uabl e. Sai l er and Berg (64)
showed that emul si ons of L CTs contai ni ng
25 or 50% M CTs were very usef ul i n pati ents
requi ri ng i ntensi ve nutri ti onal therapy. The
M CTs were rapi dl y removed f rom the ci rcu-
l ati on, the i ncrease i n ketonemi a was wi thi n
acceptabl e l evel s, and the tol erance to these
f ats was excel l ent, even i n protracted therapy.
I n chroni cal l y i l l pati ents i n cri ti cal condi ti on,
M CTs not onl y cover the energy needs, but
al so contri bute a spari ng acti on f or the l ow-
ered muscul ar carni ti ne l evel s (78) and cor-
rect the depressi on i n ketonemi a (79) rel ated
to septi cemi a or trauma.
I n recent years wi th the i ntroducti on of
structured l i pi ds based on the M CTs as the
mai n backbone of the l i pi d, we are seei ng
modi f i cati ons of M CTs whi ch i mprove thei r
uti l i ty and nutri ti onal sui tabi l i ty i n hyperal i -
mentati on. A l though physi cal mi xtures of
M CTs and L CTs have been tri ed i n paren-
teral nutri ti on (64, 80, 81), such mi xes dem-
onstrate the dual pattern of cl earance and

b
y

g
u
e
s
t

o
n

S
e
p
t
e
m
b
e
r

1
1
,

2
0
1
2
a
j
c
n
.
n
u
t
r
i
t
i
o
n
.
o
r
g
D
o
w
n
l
o
a
d
e
d

f
r
o
m

BA CH A ND BA BA Y A N
geni c. 4) The l i f e span i s l onger when the
di et i s ri cher i n M CTs than i n L CTs (92).
956
energy uti l i zati on of M CTs and L CTs. W i th
the advent of structured l i pi ds of M CTs and
L CTs at random di stri buti on i n the same
tri gl yceri de mol ecul e, there i s now the poten-
ti al f or tai l or-maki ng of l i pi ds to meet the
physi cal and nutri ti onal needs of pati ents
recei vi ng parenteral or enteral nutri ti on. Ba-
bayan (82) has proj ected the types of struc-
tured l i pi ds that are avai l abl e f or cl i ni cal
i nvesti gati ons. Such structured l i pi ds promi se
real progress i n the hyperal i mentati on f i el d
where l i pi ds and hi gh-densi ty cal ori e requi re-
ments are sought by the physi ci an.
Hyper hpidemia s
Because M CFA s are i ncorporated i nto l i p-
i ds onl y i n smal l amounts, many studi es have
been perf ormed to f i nd out whether M CTs
can be usef ul i n the treatment of hyperl i pi -
demi as.
A l though some authors (32, 34, 36, 83, 84)
have reported thei r observati ons on the de-
crease i n bl ood and l i ver chol esterol l evel s
wi th an M CT di et, we do not have a cl ear
pi cture of the rol e M CT can pl ay i n the
treatment of hyperchol esterol emi a. Thi s area
deserves f urther study.
I n vi ew of present knowl edge of the causes
of hyperl i pi demi as, i t i s cl ear that M CTs have
no rol e i n thei r treatment, except i n type I
(l i poprotei n l i pase def i ci ency, mast-cel l def i -
ci ency) and i n type V (di mi ni shed acti vi ty of
l i poprotei n l i pase) hyperl i poprotei nemi as.
Si nce i n these cases the cl eari ng enzyme, or
i ts coenzyme are absent or i nsuf f i ci ent, the
repl acement of di etary L CTs wi th M CTs (85)
has been very usef ul i n the treatment of these
di sorders. I n studi es done i n rats, M CTs,
unl i ke L CTs, sl owed down the appearance of
al cohol i c steatosi s (86) and speeded up the
regressi on of establ i shed atheroscl eroti c l e-
si ons, when al cohol was wi thdrawn f rom the
di et (87).
M al mros et a! (88) f ound that an M CT-
based di et f ed to rabbi ts i nduced atheroma-
tous changes i n the aorta and coronary arter-
i es. The di et, however, was probabl y def i ci ent
i n pol yunsaturated f atty aci ds. I n contrast,
the f ol l owi ng observati ons have been made
i n the rat. 1) The aorta al most compl etel y
oxi di zes M CFA s i nto Co2 (89). 2) M CTs
l i mi t the deposi ti on of chol esterol i n al l ti ssues
(84, 90). 3) M CFA s are not thrombogeni c,
whi l e saturated L CFA s are (91) thrombo-
Deficiency of the ca r nitine system
I n skel etal muscl e, the transport of L CFA s
f rom the sarcopl asm i nto the mi tochondri a i s
dependent on the carni ti ne system. Theref ore,
a def i ci ency of carni ti ne or carni ti ne pal mi tyl
transf erase (I or I I , or both) resul ts i n a
di mi ni shed capaci ty to oxi di ze L CFA s (93).
The l oweri ng of thi s energy catabol i sm,
whi ch i s essenti al f or the worki ng muscl e, i s
mani f ested by vari ous symptoms: muscul ar
weakness, pai n af ter exerti on, myogl obi nuri a,
l i pi d-f i l l ed vacuol es wi thi n muscl e f i bers, and
epi sodes of metabol i c encephal opathy. A s the
f atty aci ds conti nue to reach the muscl e, they
are i ncorporated i nto tri acyl gl ycerol s, whi ch
accumul ate. I n the myopathi c f orm of carni -
ti ne def i ci ency, the pathol ogy i s l i mi ted to the
skel etal muscl es, but i n the systemi c f orm the
heart, l i ver, and ki dneys are af f ected.
I n vi ew of the parti cul ar i ntrami tochon-
dri al transf er of the M CFA s, pati ents suf f er-
i ng f rom a def i ci ency of muscul ar carni ti ne
have been treated rather successf ul l y wi th an
M CT-based di et (93-97). I n some i nstances,
carni ti ne was added. However, the di sorders
observed i n pati ents wi th carni ti ne pal mi tyl
transf erase def i ci ency di d not al ways regress
when treated wi th a di et provi di ng M CTs
(98, 99). The more or l ess marked success of
treatment wi th M CTs i s probabl y due to the
f act that onl y a smal l amount of M CFA s
reach the muscl e. Undoubtedl y, more studi es
i n thi s area are necessary. Studi es on the
ef f ect of i ntravenous M CT i nf usi on woul d be
of speci al i nterest i n thi s regard.
Obesity
A ni mal studi es on the ef f ect of the i ncor-
porati on M CFA s i nto the adi pose ti ssue have
shown that M CTs can produce a sl i ght re-
ducti on (not al ways stati sti cal l y si gni f i cant)
i n body wei ght, and i n the wei ght of the
adi pose ti ssues (33, 35, 100- 105, Gel i ebter A ,
Torbay N, Bracco EF, V an I tal l i e TB,
Hashi m SA , unpubl i shed data). The f ood
ef f i ci ency rati o i s di mi ni shed i n rats f ed
M CTs (104, 107): the ani mal s need to con-
sume 20.3 kcal /g of wei ght gai n when f ed
M CTs as compared to 16.6 kcal /g of wei ght
gai n wi th L CTs. The reason f or the l owered
f ood ef f i ci ency rati o seems to be an enhanced

b
y

g
u
e
s
t

o
n

S
e
p
t
e
m
b
e
r

1
1
,

2
0
1
2
a
j
c
n
.
n
u
t
r
i
t
i
o
n
.
o
r
g
D
o
w
n
l
o
a
d
e
d

f
r
o
m

M EDI UM -CHA I N TRI GL Y CERI DES: UPDA TE 957
thermogenesi s i nduced by M CTs (105).
K auni tz et al (108) f ound that the wei ght of
normal and obese subj ects di mi ni shed when
L CTs were repl aced wi th M CTs i n thei r di et.
The val ue of M CTs i n obesi ty i s not as yet
wel l understood. The resul ts of Rath et a!
(83) f ai l ed to provi de any evi dence i n f avor
of M CTs. I n thei r study, obese women gi ven
a 550 kcal di et contai ni ng 30 g of M CTs l ost
as much wei ght as when M CTs were repl aced
by sugars. K auni tz et al (109) f ound that
obese subj ects consumi ng a 1200 kcal di et
l ost the same amount of wei ght whether the
di etary f at was ol i ve oi l or M CTs. I n the
geneti cal l y obese Zucker rat (1 10) and the
BHE rat (1 1 1), an M CT di et di d not reduce
body wei ght.
Neverthel ess, several reports i ndi cate that
M CTs may be a usef ul tool i n the control of
obesi ty. L avau and Hashi m (35), Schemmel
(104), Travi s et a! (105), Turkenkopf et a!
(1 12), Gel i ebter et al (106), Baba et a! (1 13),
Bray et a! ( 1 14), and Bach et a! ( 1 1 5) i ndi cate
a reducti on of carcass mass wi th the use of
M CTs. I n vi ew of these conf l i cti ng resul ts i n
the l i terature, addi ti onal studi es are needed
to understand the rol e of M CTs i n the treat-
ment of obesi ty. One expl anati on f or these
resul ts coul d be that the noni ncorporati on of
M CFA s i nto the adi pose ti ssue i s more or l ess
compensated f or by the weak i nhi bi ti on of de
novo synthesi s of f atty aci ds by the l i ver and
adi pose ti ssue (35).
The monoesters and di esters of pol ygl ycer-
ol s contai ni ng M CFA s can be consi dered as
repl acements f or natural f ats. These pol ygl y-
cerol esters appear to have the abi l i ty to
i mpart a f eel i ng of sati ety whi l e el i mi nati ng
and/or reduci ng the l i pi d l evel i n a f ood
product, whi l e sti l l mai ntai ni ng the desi red
appearance and physi cal f orm. Thei r energy
val ue i s onl y 6 to 8.5 kcal /g. The use of these
esters i n f oods wi l l be a conveni ent way to
reduce cal ori es, parti cul arl y f at cal ori es (116).
Contrai ndi cati ons
Ketosis a nd a cidosis
M CTs are ketogeni c i n the normal subj ect
and even more i n the pati ent wi th hyperos-
mol ar di abeti c syndrome (117). Hence, M CTs
shoul d not be gi ven to pati ents wi th di abetes.
They shoul d al so not be gi ven to pati ents
wi th ketosi s or aci dosi s. I n these condi ti ons,
the capaci ty of the extrahepati c ti ssues to use
ketone bodi es i s saturated. Theref ore, the
addi ti onal suppl y of such substrates i s not
onl y wasted as an energy source, but i t al so
aggravates the metabol i c aci dosi s and accel -
crates the breakdown of the homeostati c
mechani sms. The sol uti on to thi s probl em
may be usi ng M CTs wi th odd carbon chai n
f atty aci ds i nstead of the even carbon chai n
f atty aci ds. I ndeed Guy and Tul ey (118)
showed that tri pel argoni n i s l ess ketogeni c
than usual M CTs i n rats.
Cir r hosis
Si nce M CFA s are metabol i zed mostl y i n
the l i ver, the i ntesti nal perf usi on of octanoate
i n heal thy subj ects resul ts i n the appearance
of onl y smal l amounts of thi s f atty aci d i n the
ci rcul ati ng bl ood (1 19). However, when the
f uncti onal cel l mass of the l i ver i s reduced, as
i n ci rrhosi s, the C8:0 concentrati on i n the
bl ood i ncreases due to the reduced hepati c
cl earance. I n the case of a portacaval shunt,
f or exampl e, C8:0 reaches very hi gh amounts
(1 19). I t i s general l y bel i eved that f atty aci ds
are somewhat toxi c when gi ven i n l arge
amounts. I ntravenous i nf usi on of C8:0, f or
exampl e, resul ts i n a syndrome resembl i ng
hepati c encephal opathy: hyperventi l ati on,
hyperammoni emi a, hyperl actaci demi a, and
di sturbed el ectroencephal ogram ( 1 20, 121).
I n heal thy subj ects, the bi ndi ng of f atty aci ds
to al bumi n i n the serum rel i eves thi s toxi ci ty.
But, i n ci rrhosi s, the al bumi nemi a drops. I n
addi ti on, the af f i ni ty of M CFA s f or al bumi n
i s weak, because L CFA s and M CFA s com-
Pete f or the al bumi n bi ndi ng si tes (122). Un-
der these ci rcumstances, f ree f atty aci ds, not
bound to protei n, di f f use passi vel y across the
capi l l ary membranes. Thus, f ree octanoi c
aci d has been f ound, not onl y i n the bl ood,
but al so i n the asci ti c f l ui d, and the cerebro-
spi nal f l ui d of persons wi th ci rrhosi s who
were gi ven thi s f atty aci d by i ntesti nal per-
f usi on (123). I t appears that, i n ci rrhosi s, there
i s the danger that the energy metabol i sm of
the brai n may be al tered.
A vai l abi l i ty and suggesti ons f or use
I ni ti al l y, M CTs were avai l abl e onl y i n the
f orm of oi l or margari ne. M CTs are now
avai l abl e i n l i qui d or sol i d preparati ons and
i n si mpl e or compl ex combi nati ons wi th pro-

b
y

g
u
e
s
t

o
n

S
e
p
t
e
m
b
e
r

1
1
,

2
0
1
2
a
j
c
n
.
n
u
t
r
i
t
i
o
n
.
o
r
g
D
o
w
n
l
o
a
d
e
d

f
r
o
m

958 BA CH A ND BA BA Y A N
tei ns, sugars, vi tami ns, essenti al f atty aci ds,
and mi neral s. These vari ous f orms make i t
possi bl e to provi de the i nf ant or the adul t
wi th the amounts of M CTs needed f or par-
enteral , oral , or tube f eedi ng (124).
I t i s i ndi spensabl e to determi ne f or each
pati ent the threshol d dose that must not be
exceeded i f probl ems are to be prevented
f rom ari si ng, eg, osmoti c di arrhea i n i l ei ti s
and i n extensi ve resecti on of the smal l i ntes-
ti ne, or i n dumpi ng syndrome i n pati ents wi th
gastrectomy.
I n enteral f eedi ng, M CTs shoul d f i rst be
i ntroduced i n smal l amounts and gradual l y
i ncreased to the prescri bed dose. I n general ,
M CTs are wel l tol erated when the dai l y dose
i s di vi ded proporti onal l y i nto meal s of a wel l -
bal anced di et. M CTs di ets seem to be better
tol erated by chi l dren than by adul ts (90). A
nutri ti onal l y bal anced di et i s the best way of
avoi di ng ketosi s. A dai l y suppl y of 50 or even
100 g i s easi l y tol erated. Obvi ousl y, when
M CTs are gi ven f or thei r ketogeni c properti es
the procedure wi l l be di f f erent (68, 75).
M CTs are not a panacea. Onl y rarel y do
M CTs al one provi de the best therapeuti c so-
l uti on. V ery of ten, i t i s advi sabl e to combi ne
M CTs wi th the standard therapy of the par-
ti cul ar i l l ness: a reducti on i n the suppl y of
L CTs, or the provi si on of bi l e sal ts (i n bi l i ary
def i ci ency), enzyme therapy (i n pancreati c
def i ci ency), a gl uten-f ree di et (i n cel i ac di s-
ease), anti bi oti cs (i n tropi cal sprue), or car-
ni ti ne (i n carni ti ne def i ci ency).
I t must be remembered that when the
di gesti on or absorpti on of L CTs i s perturbed,
a smal l er amount of M CTs i s absorbed than
i n the heal thy organi sm; but i n any case more
M CTs are absorbed than L CTs. A s di scussed
previ ousl y, the i ngesti on of l arge amounts of
M CTs decreases the absorpti on of L CTs, and
i ncreases the l osses of L CFA s i n the f eces.
Neverthel ess, extrapol ati ng the resul ts ob-
tai ned i n rats to pati ents wi th reduced l i pi d
absorpti on, Cl ark and Hol t (12) suggested
that the amount of L CTs normal l y tol erated
coul d be doubl ed, by means of an M CT
suppl ement, wi thout i nduci ng steatorrhea.
W hen M CTs are i nf used parenteral l y, the
dose shoul d be caref ul l y cal cul ated and the
pati ent cl osel y moni tored. I f the dose i s i n
excess, there i s danger of aci dosi s due to
hyperketonemi a and hyperl acti caci demi a
(125).
I n total parenteral nutri ti on, the essenti al
f atty aci ds shoul d be i ncl uded i n the regi men.
W hi l e K auni tz et a! (126) showed i n the rat
that M CTs l owered the need f or l i nol ei c aci d
more than L CTs, Hi rono et a! (127) reported
that the need f or thi s f atty aci d was i ncreased
i n newborn babi es gi ven an M CT-based mi l k.
W i l l i ams and Oski (128) f ound no change i n
the vi tami n E status of newborn babi es f ed
M CT-based mi l k. I t i s, theref ore, i mportant
that when M CTs are gi ven i ntravenousl y or
enteral l y as the sol e source of f at, that the
needs f or essenti al f atty aci ds are met. There
are now avai l abl e tai l or-made M CTs wi th
varyi ng amounts of l i nol ei c aci d (Captex 810,
Stokel y-V an Camp, I nc) These products are
f aci l i tati ng the desi gn of regi mens that meet
the essenti al f atty aci d requi rements of pa-
ti ents.
W hen M CTs are used f or cooki ng or
f ryi ng, they shoul d not be heated to temper-
atures above 150 to 160#{ 176} C. A bove thi s tem-
perature, i t wi l l resul t i n oxi dati on and ther-
ma! breakdown whi ch wi l l af f ect the pal ata-
bi l i ty and acceptabi l i ty of the product.
Concl usi ons
The parti cul ar physi cochemi cal properti es
of M CFA s make M CTs a val uabl e tool i n the
di eteti c management of a number of di sorders
of l i pi d metabol i sm. M ost f at mal di gesti on
and mal absorpti on condi ti ons, and some di s-
orders of the l ymphati c f at transport and of
the f at removal f rom the bl ood, can be com-
pl etel y or parti al l y corrected by repl aci ng
di etary L CTs wi th M CTs. The cruci al needs
f or energy or f or acetyl -CoA as precursors of
l i pi ds, can be met by a suppl y of M CTs,
whether the need i s transi ent or l ong l asti ng.
A l though M CTs are f ats, they tend some-
ti mes, to behave l i ke carbohydrates. A l -
though M CTs are oxi di zed rapi dl y and have
l ow tendency to be stored i n the adi pose
ti ssue, M CTs are not hyperl i pi demi c, but they
are ketogeni c. A l though M CTs are not hy-
pergl ycemi c, they sl i ghtl y sti mul ate i nsul i n
producti on, but do not l ower l i pogenesi s si g-
ni f i cantl y. M CTs are not drugs-they have
no pharmacol ogi cal ef f ect.
I n summary, the benef i ci al ef f ects of M CTs
are: 1) M CTs are di gested, absorbed, and
transported easi l y and rapi dl y i n di sorders
where the di gesti on, absorpti on, or transport

b
y

g
u
e
s
t

o
n

S
e
p
t
e
m
b
e
r

1
1
,

2
0
1
2
a
j
c
n
.
n
u
t
r
i
t
i
o
n
.
o
r
g
D
o
w
n
l
o
a
d
e
d

f
r
o
m

M EDI UM -CHA I N TRI GL Y CERI DES: UPDA TE 959
of L CTs are not opti mal . 2) M CTs are oxi -
di zed rapi dl y i n the organi sm and they have
a very l ow tendency to deposi t as body f at. 3)
M CTs are a source of abundant and rapi dl y
avai l abl e energy. 4) M CTs are ketogeni c. 5)
M CTs are donors of hydrogen i ons and pre-
cursors of acetyl -CoA .
M CTs do not behave as conventi onal f ats.
Thus, M CTs must be treated separatel y and
di f f erentl y f rom our understandi ng of f ats
and oi l s. The uni que physi cal , chemi cal , and
structural characteri sti cs of M CTs and thei r
modi f i cati ons (structured l i pi ds) makes such
speci al l i pi ds tool s f or sol vi ng certai n medi cal
probl ems. a
The authors acknowl edge the assi stance and contri -
buti on of M argari ta Nagy f or edi ti ng the manuscri pt.
Ref erences
1. Seni or I R, ed. M edi um chai n tri gl yceri des. Phi l a-
del phi a, PA : Uni versi ty of Pennsyl vani a Press,
1968.
2. K al ser M H. M edi um chai n tri gl yceri des. A dv I n-
tern M ed 197 1;17:301-32.
3. Si cki nger K . Cl i ni cal aspects and therapy of f at
mal assi mi l ati on wi th parti cul ar ref erence to the use
of medi um-chai n tri gl yceri des. I n: V ergroesen A l ,
ed. The rol e of f ats i n human nutri ti on. L ondon:
A cademi c Press, 1975: 1 15-209.
4. Bach A , M #{ 233} tai sP. Grai sses a chal nes courtes et
moyennes. A spects physi ol ogi ques, bi ochi mi ques,
nutri ti onnel s et therapeuti ques. A nn Nutr A hi ment
1970;24:74-144.
5. Babayan V K . M edi um-chai n tri gl yceri des-thei r
composi ti on, preparati on, and appl i cati on. I A m
Oi l Chem Soc l 968;45:23-5.
6. M ott CB, Sarl es H, Ti scorni a 0. A cti on di f f #{ 233} rente
des tri gl yceri des a chal nes courtes, moyennes ou
l ongues, sur l a s#{ 233} cr#{ 233} ti on pancr#{ 233} ati que exocri ne de
l homme. Bi ol Gastro-ent#{ 233} rol 1972;5:79-84.
7. I ber F. Rel ati ve rates of metabol i sm M CT, L CT
and ethanol i n man. I n: K auni tz H, L ang K , Fekl
W , eds. M i ttel ketti ge Tri gl yceri de i n der Di nt. Z
Ern#{ 228} hrungswi ss 1974; 17(suppl ):9- 16.
8. V al di vi eso V . A bsorpti on of medi um-chai n tri gl yc-
eri des i n ani mal s wi th pancreati c atrophy. A m I
Di g Di s 1972;17:129-36.
9. M i shki n S. Stei n L , Gatmai tan Z, A ri as I M . The
bi ndi ng of f atty aci ds to cytopl asmi c protei ns: bi nd-
i ng to Z protei n i n l i ver and other ti ssues of the rat.
Bi ochem Bi ophys Res Commun l 972;47:997-1003.
10. Ockner RK , M anni ng I A , Poppenhausen RB, Ho
W K L . A bi ndi ng protei n f or f atty aci ds i n cytosol
of i ntesti nal mucosa, l i ver, myocardi um and other
ti ssues. Sci ence 1972; 177:56-8.
11. Spector A A . Fatty aci d bi ndi ng to pl asma al bumi n.
I L i pi d Res 1975;16:165-79.
12. Cl ark SB, Hol t P. I nhi bi ti on of steady-state i ntes-
ti nal absorpti on of l ong-chai n tri gl yceri de by me-
di um-chai n tri gl yceri de i n the unanestheti zed rat.
I Chi n I nvest 1969;48:2235-43.
13. Takahashi Y l , Underwood BA . Ef f ect of l ong and
medi um chai n l ength l i pi ds upon aqueous sol ubi l i ty
of a-tocopherol . L i pi ds l 974;9:855-9.
14. Roel s OA , Hashi m SA . I nf l uence of f atty aci ds on
serum chol esterol . Fed Proc 1962;21:71-6.
15. A gnew I E, Hol dsworth CD. The ef f ect of f at on
cal ci um absorpti on f rom a mi xed meal i n normal
subj ects, pati ents wi th mal absorpti ve di sease,
and pati ents wi th a parti al gastrectomy. Gut
197 1; 12:973-7.
16. Tanti bhedhyangkul P, Hashi m SA . M edi um-chai n
tri gl yceri de f eedi ng i n premature i nf ants: ef f ects on
cal ci um and magnesi um absorpti on. Pedi atri cs
1978;6 1:537-45.
17. Hol tzappl e P. Berman W , Segal S. Enhancement of
non-el ectrol yte transport i n j ej unal mucosa by f atty
aci ds. Gastroenterol ogy 1972;62:849.
18. Tanti bhedhyangkul P, Hashi m SA . M edi um-chai n
tri gl yceri de f eedi ng i n premature i nf ants: ef f ects of
f at and ni trogen absorpti on. Pedi atri cs 1975;
55:359-69.
19. W u-Ri deout M Y C, El son C, Shrago E. The rol e of
f atty aci d bi ndi ng protei n on the metabol i sm of
f atty aci ds i n i sol ated rat hepatocytes. Bi ochem
Bi ophys Res Commun 1976;71:809-16.
20. M cGarry I D, Foster DW . Regul ati on of hepati c
f atty aci d oxi dati on and ketone body producti on.
A nn Rev Bi ochem l 980;49:395-420.
2 1. Bremer I . Carni ti ne and i ts rol e i n f atty aci d me-
tabohi sm. Trends Bi ochem Sci 1980;2:207-9.
22. Bach A , Phan T, M #{ 233} tai sP. Ef f ect of the f atty aci d
composi ti on of i ngested f ats on rat l i ver i nterme-
di ary metabol i sm. Horm M etab Res 1976;8:375-9.
23. Osumi T, Hashi moto T. A cyl -CoA oxi dase of rat
l i ver: a new enzyme f or f atty aci d oxi dati on. Bi o-
chem Bi ophys Res Commun 1978;83:479-85.
24 Schei g R. Hepati c metabol i sm of medi um chai n
f atty aci ds. I n: Seni or I R, ed. M edi um chai n tri -
gl yceri des. Phi l adel phi a, PA : Uni versi ty of Penn-
syl vani a Press, 1968:39-49.
25. M cGarry I D, Foster DW . The regul ati on of keto-
genesi s f rom ol ei c aci d and the i nf l uence of anti -
ketogeni c agents. I Bi ol Chem 197 l ;246:6247-53.
26. Bach A . Oxahoacetate def i ci ency i n M CT-i nduced
ketogenesi s. A rch I nt Physi ol Bi ochi m 1978;
86:1133-42.
27. Y eh Y Y , Zee P. Rel ati on of ketosi s to metabol i c
changes i nduced by acute medi um-chai n tri gl ycer-
i de f eedi ng i n rats. I Nutr 1976; 106:58-67.
28. Bach A , Schi rardi n H, Bauer M , W eryha A . K eto-
geni e response to medi um-chai n tri gl yceri de l oad
i n the rat. I Nutr 1977;107:1863-70.
29. W i el and 0, M atschi nsky F. Zur Natur der anti ke-
togenen W i rkung von Gl yceri n und Fruktose. L i f e
Sci 1962;2:49-54.
30. M cGarry I D, Foster DW . The regul ati on of keto-
genesi s f rom octanoi c aci d. The rol e of the tri car-
boxyl i c aci d cycl e and f atty aci d synthesi s. I Bi ol
Chem 171246:1149-59.
31. Freund G, W ei nsi er RL . Standardi zed ketosi s i n
man f ol l owi ng medi um chai n tri gl yceri de i ngesti on.
M etabol i sm 1966; 15:980-91.
32. L evei l l e GA , Pardi ni RS, Ti l l otson I A . I nf l uence
of medi um chai n tri gl yceri des on l i pi d metabol i sm
i n rat. L i pi ds 1967;2:287-94.

b
y

g
u
e
s
t

o
n

S
e
p
t
e
m
b
e
r

1
1
,

2
0
1
2
a
j
c
n
.
n
u
t
r
i
t
i
o
n
.
o
r
g
D
o
w
n
l
o
a
d
e
d

f
r
o
m

960
33. A l i ce GL , Romsos DR. L evei hl e GA , Baker DH.
M etabol i c consequences of di etary medi um chai n
tri gl yceri des i n the pi g. Proc Soc Exp Bi ol M ed
1972; 139:422-7.
34. Takase 5, M ori moto A , Nakani shi M , M uto Y .
L ong-term ef f ect of medi um-chai n tri gl yceri de i n
hepati c enzymes catal yzi ng hi pogenesi s and chol es-
terogenesi s i n rats. I Nutr Sci V i tami nol 1977;
23:43-51.
35. L avau M M , Hashi m SA . Ef f ect of medi um chai n
tri gl yceri de on hi pogenesi s and body f at i n the rat.
I Nutr 1978;108:613-20.
36. K ri tchevsky D, Tepper SA . I nf l uence of medi um-
chai n tri gl yceri des on chol esterol metabol i sm i n
rats. I Nutr 1965;86:67-72.
37. K ri tchevsky D, Rabi nowi tz I L . l nf l uence of di etary
f at on f atty aci d bi osynthesi s i n rat. Bi ochi m Bi o-
phys A cta 1966;1 16:185-8.
38. Bach A , W eryha A , Schi rardi n H. I nf l uence of an
oral M CT or L CT l oad on gl ycemi a i n W i star and
Zucker rats and i n gui nea pi gs. A nn Bi ol A ni m
Bi ochi m Bi ophys l 979;l 9:625-35.
39. Tanti bhedhyangkul P. Hashi m SA , V an I tal l i e TB.
Ef f ects of i ngesti on of l ong-chai n and medi um-
chai n tri gl yceri des on gl ucose tol erance i n man.
Di abetes 1967; 16:769-9.
40. L ederer I , L ambert A E, Henqui n I C, Potti er-A r-
noul d A M , Bettendorf B. I nf l uence des tri gl yceri des
a chamnes moyennes sur l a tol erance au gl ucose et
I a producti on d i nsuhi ne chez l e rat. Di ab#{ 233} te
1972;20:201-7.
4 1 . Pi l z W . Untersuchungen #{ 252} ber Fermente des men-
schl i chen Bl utes. I X . Di e A ryl esterasen des men-
schl i chen Nabel schnurserums. Z Physi ol Chem
1964;338:238-50.
42. M aragoudaki s M E, K al i nsky HI , L ennane J. M e-
tabohi sm of octanoate and i ts ef f ect on gl ucose and
pal mi tate uti l i zati on by i sol ated f at cel l s. Proc Soc
Exp Bi ol M ed 1975;148:606-l 0.
43. Groot PHE, H#{ 252} l smann W C. The acti vati on and
oxi dati on of octanoate and pal mi tate by rat skel etal
muscl e mi tochondri a. Bi ochi m Bi ophys A cta
1973;3 16:124-35.
44. K ehayogl ou K , Hadzi yanni s 5, K ostami s P, M al a-
mos B. The ef f ect of medi um-chai n tri gl yceri de on
47 cal ci um absorpti on i n pati ents wi th pri mary
bi l i ary ci rrhosi s. Gut 1973;14:653-6.
45. Harri son I E, M cHatti e JD, L i gon hR. Jeej eebhoy
K N, Fi nl ay I M . Ef f ect of medi um chai n tri gl ycer-
i de on f ecal cal ci um l osses i n pancreati c i nsuf f i -
ci ency. Cl i n. Bi ochem 1973;6: 136-40.
46. Gal abert C, Fi l hi at M , Chazal ette I P, M endy F,
Del haye N. A bsorpti on i ntesti nal e des tri gl yceri des
a chamnes moyennes dans l a f i brose kysti que du
pancreas. A nn PCdi atr 1975;22:745-53.
47. Gracey M , Burke U, A nderson CM . A ssessment of
medi um-chai n tri gl yceri de f eedi ng i n i nf ants wi th
cysti c f i brosi s. A rch Di s Chi l d 1969;44:401-3.
48. Dune PR, Newth CI , Forstner GG, Gal l DO.
M al absorpti on of medi um chai n tri gl yceri des i n
i nf ants wi th cysti c f i brosi s. Correcti on wi th pan-
creati c enzyme suppl ements. I Pedi atr 1980;96:862-
4.
49. Hof mann A F, Pol ey I R. Rol e of bi l e aci d mal ab-
sorpti on i n pathogenesi s of di arrhea and steator-
BA CH A ND BA BA Y A N
rhea i n pati ents wi th i l eal resecti on. Gastroenter-
ol ogy l 972;62:918-34.
50. Tandon RK , Rodgers JB, Bahi nt I A . The ef f ects of
medi um-chai n tri gl yceri des i n the short bowel syn-
drome. I ncreased gl ucose and water transport. A m
I Di g Di s 1972;17:233-8.
51. Roy CC, Ste-M ari e M , Chartrand L , W eber A ,
Bard H, Doray B. Correcti on of the mal absorpti on
of the preterm i nf ant wi th a medi um-chai n tri gl yc-
eri de f ormul a. I Pedi atr 1975;86:446-50.
52. V an Devenne A , Brogard I M , I ahn H, V i vi l l e C.
Communi cati on l ympho-py#{ 233} hi que avec chyl uri e.
I nf l uence f avorabl e du trai tement di #{ 233} t#{ 233} ti que. A nn
M ed I ntern l 970;121:367-74.
53. W arter I , M #{ 233} tai sP, Berthi er G, Bach A . Trai tement
d une chyl uri e par un r#{ 233} gi mea base de tri gl yceri des
a chal nes moyennes. Pathol Bi ol 1972;20:865-9.
54. Brenner W I , Boal BH, Reed GE. Chyhothorax as a
mani f estati on of rheumati c mi tral stenosi s. I ts post-
operati ve management wi th a di et of medi um-chai n
tri gl yceri de. Chest l 978;73:672-3.
55. Chri stophe A , M atthys F, V erdonk G. Chyl ous-
f l ui d tri gl yceri des and hi poprotei ns i n a pati ent wi th
chyl othorax on a di et of butter or medi um-chai n
tri gl yceri de. A rch I nt Physi ol Bi ochi m 1980;
88:B 17-8.
56. Schwabe A D, Cozzeto Fl , Bennett L R, M el l i nkof f
SM . Esti mati on of f at absorpti on by moni tori ng of
expi red radi oacti ve carbon di oxi de af ter f eedi ng a
radi oacti ve f at. Gastroenterol ogy 1962;42:285-91.
57. W atki ns l B. Schoel l er DA , K l ei n P, Ott DG, New-
comer A D, Hof mann A F. 3C-Tri octanoi n: a non-
radi oacti ve breath test to detect f at mahabsorpti on.
I L ab Cl i n M ed 1977;90:422-30.
58. Thi stl e I L , Carl son GL , Hof mann A F, Babayan
V K . M edi um chai n gl yceri des rapi dl y di ssol ve cho-
l esterol gal l stones i n vi tro, abstracted. Gastroenter-
o l o g y 1 9 7 7 ; 7 2 : A- 1 1 8 / 1 1 4 1 .
59. M ack EA , Sai to C, Gol df arb 5, et al . A new agent
f or gal l stone di ssol uti on: experi mental and cl i ni cal
eval uati on. Surg Forum 1978;29:438-9.
60. Thi stl e I L , Carl son GL , Hof mann A F, et al . M ono-
octanoi n a di ssol uti on agent f or retai ned chol esterol
bi l e duct stones: physi cal properti es and cl i ni cal
appl i cati on. Gastroenterol ogy 1980;78:1016-22.
61. W i tzel L , W i ederhol t I , W ol bergs E. Di ssol uti on of
retai ned duct stones by perf usi on wi th monooctan-
oi n vi a a tef l on catheter i ntroduced endoscopi cal l y.
Gastroi ntest Endosc 198 1;27:63-5.
62. M ack E, Crummy A B, Babayan V K . Percutaneous
transhepati c di ssol uti on of common bi l e duct sto-
nes. Surgery 198 l ;90:584-8.
63. Robi nson A M , W i l l i amson DH. Physi ol ogi cal rol es
of ketone bodi es as substrates and si gnal s i n mam-
mal i an ti ssues. Physi ol Rev 1980;60:l 43-87.
64. Sai l er D, Berg G. Stof f wechsel wi rkung handel s#{ 252} b-
l i cher und ei ner neuentwi ckel ten M CT-hal ti gen
Fettemul si on. I ntensi vmed 1978;15:96-8.
65. Graham GG, Baertl I M , Cordano A , M oral es E.
L actose-f ree, medi um-chai n tri gl yceri de f ormul as
i n severe mal nutri ti on. A m I Di s Chi l d
1973; 126:330-5.
66. Rubal tel l i FF, Enzi G, Debi asi F, Bondi o M , Ron-
di nel hi M . Ef f ect of l i pi d l oadi ng on f etal uptake of
f ree f atty aci ds, gl ycerol and $-hydroxybutyrate.

b
y

g
u
e
s
t

o
n

S
e
p
t
e
m
b
e
r

1
1
,

2
0
1
2
a
j
c
n
.
n
u
t
r
i
t
i
o
n
.
o
r
g
D
o
w
n
l
o
a
d
e
d

f
r
o
m

M EDI UM -CHA I N TRI GL Y CERI DES: UPDA TE 961
Bi ol Neonate 1978;33:320-6.
67. Y eh Y Y , Streuhi UL , Zee P. K etone bodi es serve as
i mportant precursors of brai n l i pi ds i n the devel -
opi ng rat. L i pi ds 1977; 12:957-64.
68. W i throw CD. The ketogeni c di et: mechani sm of
anti convul sant acti on. I n: Gl aser GH, Penry 1K ,
W oodbury DM , eds. A nti epi l epti c drugs: mecha-
ni sms of acti on. New Y ork: Raven Press, 1980:635-
42.
69. W i l der RM . Ef f ect of ketonuri a on course of epi -
hepsy. M ayo Chi n Bul l l 92I ;2:307-l 0.
70. Huttenl ocher PR, W i l bourn A l , Si gnore I M . M e-
di um chai n tri gl yceri des as a therapy f or i ntractabl e
chi l dhood epi l epsy. Neurol ogy 197 I ;2 1:1097-103.
7 1 . Si gnore I M . K etogeni c di et contai ni ng medi um-
chai n tri gl yceri des. I A m Di et A ssoc 1973;62:285-
90.
72. Huttenhocher PR. K etonemi a and sei zures: meta-
bohi c and anti convul sant ef f ects of two ketogeni c
di ets i n chi l dhood epi l epsy. Pedi atr Res
1976; 10:536-40.
73. Gordon N. M edi um-chai n tri gl yceri des i n a keto-
geni e di et. Dcv M ed Chi l d Neurol 1977;19:535-8.
74. L i vi ngston 5, Pauhi L L , Pruce I . K etogeni c di et i n
the treatment of epi l epsy. Dcv M ed Chi l d Neurol
l 977;19:833-4.
75. Cl ark BJ, House FM . M edi um chai n tri gl yceri de
oi l ketogeni c di ets i n the treatment of chi l dhood
epi l epsy. I Hum Nutr 1978;32:1 11-6.
76. Berman W . M edi um-chai n tri gl yceri de di et i n the
treatment of i ntractabl e chi l dhood epi l epsy. Dcv
M ed Chi l d Neurol 1978;20:249-50.
77. Hahn TI , Hal stead L R, Devi vo DC. Di sordered
mi neral metabol i sm produced by ketogeni c di et
therapy. Cal ci f Ti ssue I nt 1979;28:17-22.
78. Border JR. Burns GP, Rumph C, Schenk W G.
Carni ti ne l evel s i n severe i nf ecti on and starvati on:
a possi bl e key to the prol onged catabol i c state.
Surgery 1970;68: 175-9.
79. Neuf el d HA , Pace I A , W hi te FE. The ef f ect of
bacteri al i nf ecti ons on ketone concentrati ons i n rat
bl ood. M etabol i sm 1976;25:877-84.
80. Sai l er D, M ul l er M . M edi um chai n tri gl yceri des i n
parenteral nutri ti on. I PEN 198l ;5:1 15-9.
81. Eckart I , A dol ph M . van der M uhl en U, Naab V .
Fat emul si ons contai ni ng medi um chai n tri gl ycer-
i des i n parenteral nutri ti on of i ntensi ve care pa-
ti ents. I PEN 1980;4:360-6.
82. Babayan V K . M edi um chai n l ength f atty aci d esters
and thei r medi cal and nutri ti onal appl i cati ons. I
A m Oi l Chem Soc 1981;58:49A -51A .
83. Rath F, Sk#{ 225} l aI , Nathov#{ 225} E. M etabol i c aspects of
the use of medi um chai n tri gl yceri des i n the treat-
ment of obesi ty. Z Ern#{ 228} hrungswi ss 1972:
13(suppl ):l 16-24.
84. Stewart JW , W i ggers K D, l acobson NL , Berger P1.
Ef f ect of vari ous tri gl yceri des on bl ood and ti ssue
chol esterol of cal ves. I Nutr 1978;108:561-6.
85. Furman RH, Howard RP, Brusco 01, A l aupovi c P.
Ef f ects of medi um chai n l ength tri gl yceri de (M CT)
on serum l i pi ds and l i poprotei ns i n f ami l i al hyper-
chyl omi cronemi a (di etary f at-i nduced l i pemi a) and
di etary carbohydrate-accentuated l i pemi a. I L ab
Cl i n M ed 1965;66:912-26.
86. L i eber CS, Decarhi L M . Study of agents f or the
preventi on of the f atty l i ver produced by prol onged
al cohol i ntake. Gastroenterohogy 1966:50:316-22.
87. Theuer RC, M arti n W H, Fri day TJ, Zoumas BL ,
Sarett HP. Regressi on of al cohol i c f atty l i ver i n the
rat by medi um-chai n tri gl yceri des. A m I Cl i n Nutr
1972:25:175-81.
88. M al mros H, Ni l sson I M , Sternby NH, A rvi dson 0,
K ockum I . Coagul ati on def ects and atheroscl erosi s
i nduced i n rabbi ts by a di et contai ni ng medi um
chai n tri gl yceri des. A cta M ed Scand 1972;192:201-
12.
89. Hashi moto 5, Dayton S. Uti l i zati on of gl ucose,
octanoate and pal mi tate by normal rat aorta, and
the ef f ect of these aci ds and of al bumi n on gl ucose
metabol i sm. Proc Soc Exp Bi ol M ed 1968:129:35-
41.
90. K auni tz H. Cl i ni cal uses of medi um-chai n tri gl yc-
eri des. Drug Therapy l 978;8:9I -9.
91. Hornstra G, L ussenburg RN. Rel ati onshi p between
the type of di etary f atty aci d and arteri al thrombosi s
tendency i n rats. A theroscl erosi s 1975;22:499-516.
92. K auni tz H, I ohnson RE. I nf l uence of di etary f ats
on di sease and l ongevi ty. I n: Chavez A , Bourges H,
Basta 5, eds. Proceedi ngs of the 9th I nternati onal
Congress on Nutri ti on, M exi co, 1972. Basel : K ar-
ger, 1975;l :362-73.
93. M i tchel l M E. Carni ti ne metabol i sm i n human sub-
j ects. I I I . M etabol i sm i n di sease. A m I Cl i n Nutr
1978:31:645-59.
94. A ngel i ni C, L #{ 252} cke5, Cantarutti F. Carni ti ne def i -
ci ency of skel etal muscl e: report of a treated case.
Neurol ogy 1976;26:633-7.
95. Smyth D, L ake BD, M acdermot I , W i l son I . I nborn
error of carni ti ne metabol i sm (carni ti ne def i ci ency)
i n man. L ancet 1975;1:l l 98-9.
96. Hoski ng GP, Cavanagh NPC, Smi th DPI , W i l son
I . Oral treatment of carni ti ne myopathy. L ancet
1977; 1:853.
97. A ngehi ni C, Govoni E, Bragagl i a M M , V ergani L .
Carni ti ne def i ci ency: acute postpartum cri si s. A nn
Neurol 1978;4:558-61.
98. Carrol l I E, Brooke M H, Devi vo DC, K ai ser K K ,
Hagberg I M . Bi ochemi cal and physi ol ogi c conse-
quences of carni ti ne pal mi tyl transf erase def i ci ency.
M uscl e Nerve 1978;1:103-10.
99. Bertori ni T, Y eh Y Y , Trevi san C, Stadl an E, Sa-
besi n 5, Di M auro S. Carni ti ne pal mi tyl transf erase
def i ci ency: myogl obi nuri a and respi ratory f ai l ure.
Neurol ogy 1980;30:263-7 I .
100. Harki ns RW , Sarett HP. Nutri ti onal eval uati on of
medi um-chai n tri gl yceri des i n the rat. I A m Oi l
Chem Soc 1968;45:26-30.
101. Sti ckney RR, A ndrews 1W . Ef f ects of di etary l i pi ds
on growth, f ood conversi on, l i pi d and f atty aci d
composi ti on of channel catf i sh. I Nutr
1 9 7 2 ; 1 0 2 : 2 4 9 - 5 8 .
102. W i l ey I H, L evei hl e GA . M etabol i c consequences of
di etary medi um-chai n tri gl yceri des i n the rat. I
Nutr 1973; 103:829-35.
103. Takase 5, M ori moto A , M uto Y , Hosoya N. Ef f ect
of medi um chai n tri gl yceri de (M CT) on l i pi d me-
tabohi sm i n rats wi th respect to obesi ty. I n: Pro-
ceedi ngs Subcommi ttee, eds. Tenth I nternati onal
Congress of Nutri ti on, I apan, 1975. K yoto: Pro-
ceedi ngs of Subcommi ttee of X I CN 1976:549

b
y

g
u
e
s
t

o
n

S
e
p
t
e
m
b
e
r

1
1
,

2
0
1
2
a
j
c
n
.
n
u
t
r
i
t
i
o
n
.
o
r
g
D
o
w
n
l
o
a
d
e
d

f
r
o
m

962 BA CH A ND BA BA Y A N
(abstr).
104. Schemmel R. Physi ol ogi cal consi derati ons of l i pi d
storage and uti l i zati on. A m Zool 1976;16:661-70.
105. Travi s D, M i nenna A , Fri er H. Ef f ects of medi um
chai n tri gl yceri de on energy metabol i sm and body
composi ti on i n the rat. Fed Proc 1979;38:561.
106. Del eted i n proof .
107. Fi no JH, Schemmel R, M i ckel sen 0. Ef f ect of
di etary tri gl yceri de chai n l ength on energy uti l i za-
ti on and obesi ty i n rats f ed hi gh f at di ets. Fed Proc
1973;32:933 (abstr).
108. K auni tz H, Sl anetz CA , Johnson RE, Babayan V K ,
Barsky G. Rel ati on of saturated, medi um- and
l ong-chai n tri gl yceri des to growth, appeti te, thi rst
and wei ght mai ntenance requi rements. I Nutr
1958;64:5 13-24.
109. K auni tz H, Cotton RH, Johnson RE. Compari son
of medi um-chai n tri gl yceri des and other f ats i n a
reduci ng di et. I n: Proceedi ngs Subcommi ttee, eds.
Tenth I nternati onal Congress i n Nutri ti on, Japan
1975, K yoto: Proceedi ngs Subcommi ttee of X I CN
1976:63-4 (abstr).
110. Bach A , Schi rardi n H, Chanussot F, Bauer M ,
W eryha A . Ef f ects of medi um- and l ong-chai n
tri gl yceri de di ets i n the geneti cal l y obese Zucker
rat. I Nutr 1980; 110:686-96.
I 1 1. L au HC, Fl ai m E, Ri tchey SI . Body wei ght and
depot f at changes as i nf l uenced by exerci se and
di etary f at sources i n adul t BHE rats. I Nutr
1979; 109:495-500.
1 12. Turkenkpof I , M aggi o C, Greenwood M RC. M e-
di um chai n tri gl yceri dees reduce wei ght, but not
obesi ty i n young (f af a) rats. Fed Proc 198 l ;40:842.
1 13. Baba N, Bracco EF, Seyl ar 1, Hashi m SA . En-
hanced thermogenesi s and di mi ni shed deposi ti on
of f at i n response to overf eedi ng wi th di et contai n-
i ng medi um chai n tri gl yceri de. A m I Chi n Nutr
198 l ;34:624 (abstr).
114. Bray GA , L ee M , Bray TL . W ei ght gai n of rats f ed
medi um-chai n tri gl yceri des i s l ess than rats f ed
l ong-chai n tri gl yceri des. l nt I Obesi ty 1980;4:27-
32.
115. Bach A , Chanez M , Boi s-Joyeux B, Del homme B,
Schi rardi n H, Peret I . Regi mes hyperprot#{ 233} i ques et
hyperl i pi di ques (L CT ou M CT) chez l e rat Zucker
genCti quement obese. R#{ 233} sul tats prul i mi nai res. Pre-
sented at the Reuni on Soci #{ 233} tC Nutri ti on Di CtCti que,
L angue Fran#{ 231} ai se, Pari s, France, Dec 7, 1981.
1 16. Babayan V K . M odi f i cati on of f ood to control f at
i ntrke. I A m Oi l Chem Soc 1974;51:260-4.
1 17. Gordon EE, Duga I . Experi mental hyperosmol ar
di abeti c syndrome. K etogeni c response to medi um-
chai n tri gl yceri des. Di abetes 1975;24:301-6.
1 18. Guy DO, Tul ey RI . Ef f ects of di ets hi gh i n carbo-
hydrate, soy oi l , medi um-chai n tri gl yceri des or tri -
pel argoni n on bl ood and l i ver l i pi d and gl ucose
i ntermedi ates i n meal -eati ng rats. I Nutr 1981;
111:1437-45.
1 19. L i nscheer W G, Castel l DO, Pl att RR. A new
method f or eval uati on of portosystemi c shunti ng.
The rectal octanoate tol erance test. Gastroenterol -
o g y 1 9 6 9 ; 5 7 : 4 1 5 - 2 3 .
120. Trauner DA , Huttenl ocher PR. Short chai n f atty
aci d-i nduced central hyperventi l ati on i n rabbi ts.
Neurol ogy 1978;28:940-4.
121. Rabi nowi tz I L , Staef f en I , A umoni er P. et al . The
ef f ects of i ntravenous sodi um octanoate on the
Rhesus M onkey. A m I Gastroenterol 1978;69:I 87-
90.
122. A shbrook I D, Spector A A , Fl etcher I E. M edi um
chai n f atty aci d bi ndi ng to human pl asma al bumi n.
I Bi ol Chem 1972;247:7043-50.
123. L i nscheer W G, Bhum A L , Pl att RR. Transf er of
medi um chai n f atty aci ds f rom bl ood to spi nal f l ui d
i n pati ents wi th ci rrhosi s. Gastroenterol ogy 1970;
5 8 : 5 0 9 - 1 5 .
124. Shi l s M E, Bl och A S, Chernof f R. L i qui d f ormul as
f or oral and tube f eedi ng. 2nd ed. New Y ork:
M emori al Sl oan-K etteri ng Cancer Center, 1979.
125. Bach A , Gui sard D, Debry 0, M #{ 233} tai sP. M etabol i c
ef f ects f ol l owi ng a medi um chai n tri gl yceri des l oad
i n dogs. V . I nf l uence of the perf usi on rate. A rch I nt
Physi ol Bi ochi m 1974;82:705-l 9.
126. K auni tz H, Sl anetz CA , Johnson RE, Babayan V K .
M edi um-chai n and l ong-chai n saturated tri gl ycer-
i des and l i nol ei c aci d requi rements. I Nutr
1960;7 1:400-4.
127. Hi rono H, Suzuki H, I garashi Y , K onno T. Essen-
ti al f atty aci d def i ci ency i nduced by total parenteral
nutri ti on and by medi um-chai n tri gl yceri de f eed-
i ng. A m I Chi n Nutr 1977;30:1670-6.
128. W i l l i ams M L , Oski FA . V i tami n-E status of i nf ants
f ed f ormul a contai ni ng medi um-chai n tri gl yceri des.
I Pedi atr 1980;96:70-2.

b
y

g
u
e
s
t

o
n

S
e
p
t
e
m
b
e
r

1
1
,

2
0
1
2
a
j
c
n
.
n
u
t
r
i
t
i
o
n
.
o
r
g
D
o
w
n
l
o
a
d
e
d

f
r
o
m