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euzoen4‹›crinuIog¿ -‹Y 245 -255 (197t}

Effect of Monosodinm Gluteaiate on Some Endocrine


T.W. REDDING, A. V. S‹I II.1LLY, A. SRI SIUR.h and I. WAKABAYASHI

l'riduc line uuid Polypeptide lmborator)', Veterans Adminisirotion Hospiuil,


and Department of Medicine, Tuliinc University School of Medicine, New Orleans

Neonatal fciniilc und mule r:in of the Sprague- Monos‹›dium glutamate


Des ley strain » erc injected siibcut:incously with B‹›dy weight dectc«s«
a daily dose of MSG (2.W.2 rng}g body wt.)
hcginning on rhe 2rtd by ref life. he rats wefe Endocrine gland atrophy
nutopsied at 40 und 110 days of age. At 4o days Pituitary hormone content decrease
uf age, the b‹›dy weight and nusoanal lengths x-
erc significantly reduced in the f•fSG-treated
rats. /\t 110 ‹lays, the hody lengths of MSG-treated rats wetc approzinintcly ]O—12 ". »
shorter than those of control rats, end cslculetion of the ‘Lee’ ind x indicated a
signific:wit increase in carcass fat. Pu‹›d consumption studies, carried out nt 75 days of age,
showed s signi£cant hypophegiu in some MSG-treated rats. Upon eutripsy at 40 days of
afte, the :ibsoIutc freights ‹if the thyroid and adtenal glands nf both sexes were
significiintly decreased front those of control rats ; but when corrected for body weight,
these differences were marginal. At 110 days, the absolute weights of the adtcnal and
thyroid glands of bnth sexes were significantly reduced from their respective control
levels. Gonadnl v•eights of MSG-treated ruts xvere significnndy reduced at 40 anal 110
days of age. Size and weight of the anterior pituitary glands of both male and female
MSG-tr‹nted mts were significantly reduced trom contrr›l values. There was a marked
decrease in growth hormone and luteinizing hormone convene in ihe anterior pituitnries
of male and female MSG-treated rots at 40 days. However, thyrotropin content of the
anterior pituitary of MSG-treated male rats did not shov any significant change front
control levels st 40 days of age.

Scvcral rcports have suggested that monosodium glutamate (MSG)


may exert n toxic eifect when gfven to both experimental animals and
man. The addition of MSG to food has been implicated in the cause
of the ’Chinese restaurant’ syndrome in man [SCHAUMBURG fJ A/.y

' Suppocced irt pnrE by USPHS Gents z\fi1-U74 ? nnd AM-0^J094.


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Received : Nrivember 13th, 1970. Accepted : Ftbfuary 3rd, 197 t.


REDDfWGj CHALiY/#RfMURN/ hKABAYAS]N

1969]. Recent studies showed that pharmacological doses ‹if tit SG


fed orally to humans precipitated headache, burning sensations, facial
pressure, and chest pains [ScmuxfBURG fl/ o/., 1969]. MSG injected
subcutaneously into neonatal mice has becn shown to damage the
development of the central nervous system and cause failure of the
formati‹›n of the inner nuclear layer of the retina [Pos’s e/ e/., 1960 ;
Over, 1969]. OLwr has also reported that, in mice, MSG selectively’
dcstzoys the preoptic and arcuate nuclei of the hypothnlamus [OcNEv,
1969]. It has also been reported that subcutaneous administration of
MSG to an infant Rhesus monkey resulted in acute degeneratir›n of
hypothalamic neurons [OLxzv and SHARPE, 1969].
It is well-documented that the hypothalamus secretes specific
neurohormones, which are carried to the anterior pituitary gland via
the hypophyseal portal vessels, where they exert stimulntoxy or
inhibitory influences on the synthesis and telense of the trophic hor-
mones [Screw eJ a/., 1968, 1970). Chemical or physical damagc
to the hypothalamus may thus result indirectly in changes in the
content and release of the anterior pituitary hormones and,
consequently, in changes in the weight of the respective target
endocrine organs.
The objective of this study was to determine the effect of ad-
ministration of MSG on the weights of the anterlor pituitary and
other endocrine glands, and on body weight, food consumption,
nasoanal length, and obesity. In addition, the anterior pituitary levels
of growth hormone (GH), luteinizing hotm‹›nc (LH), and thyrotro r in
(TSH) were measured.

Neonatal female and mate fats of the Sprngue-Dawley strain were injected sub-
ciimeously with a dnily dosc of MSG, beginning on the 2nd day of life. The amount
injected was gradually increased ffom 2.2 mg{g body weight on the 1st day until the
10th and final day when 4.2 mg/g body weight was given, as prescribed by Pours e/ a/.
[1960]. Control rats received injections of saline, the volume injected being adjuetnd to
that in which MSG was administered. Litters of rats were marked on the basis of sez
and treatment and, when weaned, they were sepztated fcnm their mothers and grouped
according to sex and trmtmcnt. Food and water were given & fi6i/vm except when food
consumption studies were performed. Food intake wee measured by placing a weighed
amount of food into individual cage food-holders, provided with a trap to catcb spilled
food particles. After 24 h, the remaining tood was removed and weighed together with
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trapped particles. The difference nn the original amount of food end that left after 24 h
was tnken as the amount ingmtcd. At 40 and 110 dnys, rats from each gtoup were
aocrificed and the anterior pimitary gland, thyroid, adrena!s, ovaries, and testes were
removed, carefully cleaned, and weighed on a torsion balance to the nearest 0.1 mg.
hlonosodiuni Glutamate and Endocrine Function 247

8i›dy u’eights and nasoanal length were also recorded. The anterior pituitary glands
u•cre homogenized in egg al6utnfn-phosphate buffer and aliquots taken £or the
determina- tion of GH, LH, and TSI4 content.
’ASH was measured by the mouse assay of Mc Kruziz [1958] and the results ate
npresscd in terms of niilliunits of NH I-TSH-S-5. 1.14 waa measured by the double
antibody radioimmunoassay of Niswznnzn i/ a/. [1968] (00-RAT-RIA), using a crose-
reaction Leith ovinc LH. The amount of LH was expressed in terms of NIH-LI-1-S-i4,
which was obtained by direct rmding on the standard curve. GH wee measured by the
double antibody radioimmunoassay pt 5ciixccii and Raiciizix {1966] and expressed in
terin8 of NI MMD-RAT-GH-R-1. Statistical analyec5 were performed by the Smdent 't’
tcsi | Sxznxcoa, t957].

Table Iݴ shows the changes in wcight, nasoanal length, and the
I.ce index in control and MSG-treated male and female rats at 40 days
of age. Body weight and nasoanal lengths were significantly reduced

’1°ilili IN. Changes in body u eight, length, and obes it)' index in MSG-treated rats at
4t1 days of age

Body weight Nasoanal lengrh I.ec index°


(g -L S. . )‘ (cm i- S.R.) (-L S.R.)
Males Conuols UJ -E0.St M.5+0.2t 0.301*0.t5
(t2)° hlSG-treated t04-L2.S 2L2+O.4S 0.298 40.14
p* 0.00t 0.o0i NS
Females f?outru]s l15*3.0 t6.9 -LO.15 0.302-LO.15
(12) MSG-treatccl 83.2i2.0 14.7 -L0.12 0.295-EO.It
p 0001 0.00t NS

Th IB, Changes in hody weight, length, and obesity indcs in MSG-treated rats at
110 days of age

i \4a Ics tontrr›)s 3586 t6.0 23.0-I-0.15 0.5O7i0.003


(6) ktSG-t c•t<J 322+ 6.9 2t.2-1-0.23 0.322 a
NS 0.OOH 0.002
0.005
Females t:ontrOls 240* 3.7 20.8-L0.t2 0.297 60.001
(6) MSG-treated 228+53.0 t8.4 -0.40 0.33t TO.007
NS 0.00t 0.00t
• A St ndatd error of meen.
*’/BOdy weight in g
'nasoanal length
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* Number of animals in group.


’ Pmhabilicy ns decezmiced by Student’e ‘t’ test.
245

Table If. Pond intake of MSG-treated ruts ov cr a 6-day period from 75 81 dna's ‹›t age

4 5

Das

t?ontrois 26.5 -1-.1 22,(l -i- lLb 23.0 -i- 1.50 21. 5 -£ 1.04 22.7 -£ 1.2s 24.5 -£ 0.2'J

MSG-treatecl 24.fi -1- 2 19,0 1.8 18.7 -i- 0.75 18.75 A 0.25 17.It -1- 0.52 20.0 1.0s
(5)
NS t1,025 0.02.5 t).t)111

Females
Contro)s 17.5 - 0.8 16.0 -L 0,71 17,0 -I- 0.71 T 7.S -E U.9G t6.7 -L I .SO 2t).U *
‹›.’Jt (5)
CISG-trcatcd 14.7 -L I .J 13.7 1 0.g5 \ 4.2 l. I I I 3.7 n.85 14,7 0.25 17.0 -L 0.'\t

0.025 0.0F 0.02J

• -b Standard error of menu.


* Number of animals in group.
* Probability as determined by Student’s 't’ test.

in the MSG-treated rats. Calculation of the f.ee indcx, a measure ‹if


obesity, from the bodY weight and nasr›anal length did not indicate
any increase in carcass fat, and insr ection ‹if the body cavity at
autopsy did not reveal anv significant accumulation of fat in the body
fat d• r ots. As shown in table IB, body wcights of thc MSG-trcatcd
rats had increased by 110 days, but were not significantly different
from thr›se of control rats. Hr›wevex, body length was approximately
10—12 % shorter than that of control rats and calculation of the Lee
index indicated a significant increase in carcass fat. Inspection of the
body cavity at autopsy indicated a striking accumulation of fat in all
the body depots. Food consu r tfon studies, Shown in table II, over
a 6-day period from 75 to 81 days of age, did not indicate h› r er-
phagia in these MSG-treated rats. In fact, most male and female
MSG-treated rats ate less than control rats.
l••• autopsy at 40 and 110 days of age, the absolutc weights of
the th}'roid glands (tablc III) of male and female MSG-treated rats
were significantly decreased from those of control rats ; but when
corrected for body weight, these clifferences were marginal. The
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ur take of 125 I bJ- the thyroid glands of MSG-treatcd rats at 40 days


of age was normal.
Idonoeodium Glutaajstc aod Endocrine function

Table III also shows that the absolute weights of the adrenal
glands of MSG-treated Path at 40 days of age were signifimntly
decreased, but not when corrected foe body weight. However, at 110
days the relative and absolute adrenals weights were significantly
reduced from control levels.
Gooadal weights of the M5G-treated vats were sigpificantly
reduc- ed at 40 and 110 days of age as shown in table IV. The testes
of MSG-treated rats appeared grossly normal, but with an over-all
reduc- tion in mass. Although the absolute weights of the testes at 40
and t10 days were significantly decreased, when corrected for body
weight at 110 days, the differences were not significant. In females
treated with MSG, the ovaries appeared atrophied, with many atretic
follicles.

Table fZf. Thyroid and zdrensl weighu uf control and MSG-treated tels sc 40 and I$0 days

40 days (12)° I IO deyc (6)


T mBwt. T midvr/ Tbyoid n Thyoidm./
mgIEE.• t0OgbeHytt mg+S.E(6) Gogtody«.
*S.E. +lR.
Males
Controls 7.99:£0.31 5.96:£0.13 10.70:£0.63 3.0tA0.25
MSG•treeted 5.92:£0.23 8.64:£0.16 8.78-1-0.33 2.73-i-0.10
p° 0.001 iS 0.025 NS
Females
G.98:£0.30 5.t9:£0.2G t0.t5:£0.70 4.2t-k0.25
4.39-L0.t9 5.31-J-0.26 7.96:£0.55 3.52-E0.3S
0.001 NS 0.05 NS

Adtenal wt. Adeenal. wt.J Adrmal wt. Adrerial wt.J


mg =k S.R.• t00 g body wt: org -k S.E. 100 g body wi.
A S.B. A S.H.

Gontrole SJ.7-1-1.6 21.63:£0.93 4t.1:£2.4 11.58-LO.83


MSG-treated 24.4-£0.8 23.28:£0.50 28.9-kt.3 B.99 :£0.29
p 0.00t NS 0.005 0.025
females
Controls 33.1 -i- L3 H.5 -£ 0.57 7L2 -i-3.t 29.5 A0.88.
ZdGS-tzczud 17.7 -E0.9 21.4 3-0.96 33,8 A4.2 14.8 1 1.TT
p 0.00t 0.025 0.00t .0.001
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• A Standezd error of man.


^ Numbcz of soimxla ia group.
° Fzobabllity as d<tcrafiaod by SNdenc's ’t’ test.
250

There was an appro.ximate 68 'Z» decrease in ovarian weight at 40 days


and 48 % at 110 days of age, and these dif)érences persisted when
corrected for bridy weight.

Tuhlt I U. Gi›nbdn l st cights txt cuntrol and MSG-treated rats at 40 end 110 days

40 days (t2)^ tt0 dsys (6)


Tcstes Tcstcs u t./ Testcs 0“cstca we./
g -E S.E.• 100 g body at. g1 S.E. TOO g body wt-
-I- S.E.

Controls 1.90 £11.07 1.17 -i-11.02 3.27 £ 0.1I 0.93 A 0.09


II 5C-UTatcij 0.G6 -i• 0.08 0.62 -h 0.08 2.60 -k 0.09 0.8 -£ 0.03
p• 0.001 0.001 0.005 NS

* S.E. * S.E.

Females
Conlrr›1a 38.6 -£ 2.9 B.6*l.?2 76.7i2.8 31.9 1.0
kJSG-treated I 2.3-I- 2.R ]4.8i0O2 30.7iG.3 17.2i16
p 0.00t 0.001 0.001 0.001

• -I- Standard error of mosn.


^ Number oF animals in group.
° Probability ss determined by Student’s ‘t’ test.

T bid U. ›\nierior pnuitary weights irt ccntmt and MSG-treated rats at 40 and 110 days

40 days (t2)^ ] IO da}'s (6)


Ant. pit. Ant. pit.wt./ Ant. pit. Ant. pit. v't./
mg A S,E,• t00 g body z t. mg :£ S.L. 100 g body wt.
-k S.F.S.E.

Crunch 4.88zo.15 3.03-£0.0s 7.20 TO.3G 2.02-h0.085


MSG-treated 2.40A0.13 2.27Atl.08 4.32-£0.29 1.34:£0.090
p• o.oot 0.o0l 0.001 0.001
Females
Controls 4.59-ktl.23 3.41:£0.IS IO.11 -EO.57 4.20-£0.20
MSG-treated 2.02-h0.09 2.44-£tLt2 3.80:£0.67 1.68-k0.31
P 0.00t 0.001 0.001

• -£ 5tandard error of mean.


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* Numher of animals in group.


° Probability es determined by Student's 't’ tmt.
’fial ie V sl o»• the t cigl ts ‹›f the antcrior pituitarics from II SCi-
treated and control fats. The size and weight of the anteririr pituttsrv
(glands) ref both male and fema)e N(SG-treated rats wcre significantly’
i’cduccd from c‹iiitrol values. There u,'as a trim i re than 5(1 % reduction
in weight of the antcrl‹ar pituitary glands in b‹›t14 male and fcmalc
ñ UG-treatc‹l rats at 40 days of age, anal this decrease in weight
persistcd t1irouglir›ut the remainder of tlic cxr ° rfnicnts.
It is ‹at interest tr› detcrminc whctlier the changes in weight ‹›f the
:interior pituitary gland and target glancls might be ass‹›ciated »'ith
ci an Ros in content ‹›f tro Phic hornirines ref the nntcri‹ir P ituitary.
Tablc VI show the lcx•cls ref Oil-I and lull in the antcririf pituitarics
of c‹introl and ñfSG-trcatecl male anrl female rats. There was a
marked dccreasc in Gl-I (7t —84 ‘No) c‹ ntent in anterior pituitaries of
malc and female NISC -tfcatcd rats. T‹ital content Gif 1.11 wns als‹›
marLec)ly reduced in make and female NtSC -treated rats. TSH content
ref the anterior pituitaries of hf SCi-treated male rats f:riled tri s1ir›xv
any significant change from controls when mcasured at 40 days of

many r›f the effects pr‹›duccd by MSG in nc‹›natai rats arc similar
tr› a syndrome seen in wcanling rats with electrolytic lesions in the
critrrimcclial nucleus (Vhf N). This synrJrr›mc, as c1cscril›cd lay l'noi i-

“I’ illr U/. itntcri‹›r pituitary content of G14, LI 1, .and ’l’Sl-1 in c‹›n In 1 and hlSG-t rcateil
rat5 at 4tJ cmys

/tg GH total anterior m/ig LH i‹›tal mU TSH tutal antcricir


pit. :£ S.L.• snterlor pit . -1- S.li. pit. -i- S.T:.

i\lnles (3)"
I.ontrols 2d8.5 -!- 3.4 6647 -k 393
CISG-trc:atcJ 82.6 -J- 1742 -£ 173
2?.é› 0.001

3121 + 2b5
I.untruth 318.2 z 12.2 1333 -I- 42
blSG-ttentcd 51.0:£1L3 0.005
p 0.001
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• -£ Standa rci errur of mean.


" Numher of animals in group.
" Probability us determined by Student’s ‘t' test.
252

time r/ n/. [1'9f›9] , cr›nsists of, amt Eni r›tlse r charigcs, a decrease i n
linear gfriu th » ith dccrcasc in r ituitary rind r Jenna GJ-t levels, anal
an increase in carcass fat unassociated with an increase in t‹ ›tal land \
eight rir in food intnkc. In riur studies, ñ4SCi treatment resulted in
an approximately 10—1.5 % decrease in the riasoanal length at 40 anal
1 IO days of age. While upon inspection the MSG-treated rots • r pear-
cd fritter’ at ) 1(1 days, tncrc was no overt ribeslty in terms of incre‹1sctl
b‹ c) y v cigist ‹ rvcr that of the contrr›ls.
/\ rapicl mcans r if cieterminin¿ ubesitj , »‘ith ‹ but sacrificial the
animal, c‹insists ref dividing the cube r‹> ›t of the b‹ad; weigiit by the
nasoanal length. The resulting figure is refcrrcd to as the f,ee’ ‹›r ’‹ahcsity’
in de.x, and it is a measure of i obesity [ BURN.\ R DIS a£itl Kl'1.-
i o>, l'967]. Rcccntl y, BER JNi.I RDis and P.i’r rsnsox | 1***1 •• vc shown
qor›d correlation bctu'ccn thc I.ec indcx and body fat in nits with
clcctr‹›lytic lesions in the Vi’vIN. When rear datn were calculate it
using this formula, there was a significant incrcasc in the J.ce index
u'hcn measured :it 110 days, even th‹›ug1a the weights of MSG-treated nits
diet nr›t exceed the body weights of control rats. There was a
striking increase in fat deposit b‹›tm in the subcutancous aticl bi›dv’
cavity dcP ots. consumptitin measured at 75 t‹› 81 days
alter not su ggest that hj'perphagia vans the cause of this olacsl ti .
intake studies actually inclicate occasionally significant laypopl agia in
these TSC -treatctl rats. As in wean) ing rats made ‹obese b) VEIN
lesions, this r›besitv may result from a metabolic and 'r›r hormonal
imbalance. In a study' of weanling VEIN-1csioncd rats, FRO i r\1.I x r/ n/.
1969] havc shriwn an inrreo se in plasma triglycerides tr› a value
ncarlj' d‹›ublc that r›f cc›ntrr›ls. When plasma triglj cerides » erc mca-
sureil in hfSG -trcatcd rats at 150 days of age, there was an indica-
tion of an increased level in mr›st rats. I loxvcver, the results wcrc
c{u itc variablc.
Gr‹›wth rctardati‹›ti in hlSC›-trcatecl rats possibly rcsultccl fr‹›m
impairment of CMH secretion aridJor synthesis by the anterior pituitary
gland. MSCi-treated rats showed a marked dccrcasc in pituitary GH
contcn t at 40 days of age. There is now gr›‹›cl cs•idcncc that thc
releasc and synthesis of pituitary GH is c‹›ntrr›llcd by G H-rclcasi" fl
h‹›rmonc (GH-RI 1) from the h r othala mus [If r ILLER y/ n/., 1970].
H yr« ›thalami from kittcns with grow th retardation induced by bila-
teral lesions of paravcntricular nuclci showed absence of GH-RH
sctivity [S:ixv.MNO e/ <f., t968]. In rats, destruction rif the sur •aoptic
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nuclei, P rema m millar}' area, and the VMN of the hyP othalamus bj
4Ir›ti‹›xodium Glutnm:itc .iijd f-.ndocriue I 'un‹-ri‹›n

clectrol \’tic 1csi‹ins is also associated with growth rctardati‹m [BER-


S n us r/ »/., I 9(›3 ; I t.tx e/ o/., 1965 ; KR tinier i r/ ml., 196S ; Biiit-
nR uis and S ear. i cx, 1966]. Hypothyr‹›id rats similarly s1u›xv a
ttccrtascd r' Ultary G1-1 content [KNiGcr, 195d]. It is unlilicly that
these ñtSG-treated rats wcrc hypothyroid, since the TSI-I content of
the :tntcrior pituitary was n‹nrmo I and the weight of the thyrr›id and
its uptake t labelled iudinc was not alerted at 40 days of age.
Ti yr‹›trri}3in-releasing lir›rmone (TRI-1), which controls the release
and synthesis of TSFI, may bc prr›duccd in a rathcr diffuse portir›n of
the :intcrior I y otlialamus and m4y 1iax'c escaped darna,ge in the
h1SC)- treated rats [D’s\xcmrta, 19G3].
1n c‹intrabt, both ‹ovaries anal tcstc s r›f MSC*-treated rats wcrc
grc;itly affected. bit 40 dnys, thcrc was n ti8 % dccrcasc in the weight
‹ ›f the ‹ » arics from fiISG -treated rats. "fihis c)ecreasc wss evident
e \’cn when c‹irrccted for b‹›‹1\’ weight ai 4(1 nn‹) ) 1 I) tl.iys. In males,
the tcstcs were normal in nPr C• rancc, but sho ed an civer-all reduc-
tit›n in mass. .'\lasolutc weight ref the tcstes at 11() days »'ns signifi-
cantly’ decreased, but not when ciirrectecl fcir body weight. It is not knr›wn
whether these males or fcmalcs were fertile. It is interesting tri n‹›tc that
pituitary levels ‹if 1.1-1 w'crc decreased in ñfSG -treated rats ‹ ›f both scxes,
when measured at 4tl clnys. Whether f‹›1licle-stimulating horm‹›nc (1'SH)
levels were alsu reduced, v’as not determined. The dccressc in testicular
weight and adrenal weights r›f NI SG-treated rats is in c‹›ntrast tr›
results re r •rtcd in micc by Onsxr [1969]. I n
mice trcatcd north If SCi, the tcstcs wcrc reprinted ro be indistinguish-
able from thr›se of contr‹al mice, and there was a suggcstir›n of mikl
adren‹ cortical hypcrtr‹›{›hy. Pcrha s these discrepancies may be ex-
l• aincd laJ’ a degree of diJfcrence in scnsitivit\• bctwccn mice and rats
to h4S€), i.c., the cxtcnt txt the l4yp‹itha1amic lesion in rats, prr›duccd
try thc ndniinistrnti‹›n txt USG, may bc larger than Ui:it produced in
mice.
\Vc 1iax’c not ruled rout direct toxic effects r›f if SC ‹in the endocrinc
gliinds tlierusclvcs. Similarly, no hist‹alogical studies were perf‹›rmed
in the e• •• iments. In mice, 1iist‹›logical chsnges have been rioted in
the 1iypr›tlia1amus but not in the antcrior pituitary' gland [Onsxr,
i 9G9]. I however, Oc £iY (pcrsr›nu1 ci›mmunication) has stated that
chrt inic injections ‹›f h(SCi in neonatal rats results in histological
changes in the li ›’r othalamus, similar tr› thr›sc seen in mice. These
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d:ita, taken together, suflgest indircct1\• that DISC) treatment in rats


ma y resu It in charities in the areas of tl4c li y Othalamus res rinsiblc
254 REDDIMG/CMAK1.y/ RIMUAA/ xkhBxWama

for elaboration of the hypothalamic releasing hormones that control


release end synthesis of the anterior pituitary hormones. Further
studies on the content of hypothalamic releasing hormones from MSG-
treated rats may be needed to provide conclusive evidence for this
hypothesis. If this concept is correct, then the MSG-treated rat may
prove to be a useful experimental model for studying the effects of
lowered release of hyr othalamic hormones, and the correction of
such effects by replscement therapy.

We are greatly indebted to F...B. Fzacusux, Jr., M.D., for his helpful editorial
udvice on this manuscript. We also xvish tu thnnk Prcr:v Townu fnr her technicnl
services in performing these experiments.

R.efereiicei

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Mailing address: Dr. Asnnzw V, Suit v, Endocrine and Polypeptide I h * lies,


Vetcmns Administration Hospital, t60$ Perdido Stfeet, No»' Orfr°nr, A 88!80 ( A)

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