Cholocystokinin and satiety

December 1994

studied

CORRESPONDENCE

in the paper

is mentioned

by Yamamoto

in the abstract

is also less likely.

With

et al., although

summary.

and motilin

injections

in the presence

vagal blockade,

absence

personal

do not produce

of pharmacological

this possibility

We suspect

phase III of the MMC is not due to unopposed

this mechanism

phase

Dear Sir:

of the spontaneous

adrenergic

adrenergic

Lieverse et al. report that in human

inhibition6

III-like

activity

blockade

(unpublished

even

3.

4.

5.

6.

of cholecystokinin plasma ings,

observations).

of Phase III activity by acidifying stomach in vagally denervated and innervated dogs with gastric pouches. Gastroenterology 1994; 106:1533-1541. Hall KE, Greenberg GR, El-Sharkawy TY, Diamant NE. Relationship between porcine motilin-induced migrating motor complex-like activity, vagal integrity, and endogenoug motilin release in dogs. Gastroenterology 1984;87:76-85. Miolan JP, Roman C. Discharge of efferent vagal fibers supplying gastric antrum: indirect study by nerve suture technique. Am J Physiol 1978;235:E366-E373. Andrews PLR, Bingham S. Adaptation of the mechanisms controlling gastric motility following chronic vagotomy in the ferret. Exp Physiol 1990:75:811-825. Grundy D, Hutson D, Scratcherd T. A permissive role for the vagus nerves in the genesis of antrc-antral reflexes in the anaesthetized ferret. J Physiol 1986;381:377-384. Chung SA, Valdez DT, Diamant NE. Adrenergic blockade does not restore the canine gastric migrating motor complex during vagal blockade. Gastroenterology 1992; 103:1491-1497.

concentrations,

dance

with

conclusions

McLaughlin Pavihon

Toronto, Ontario MST 2S8, Camah

very much the comments

et al., and we basically

agree with

that the effect of the vagal sensory acidification paper,

is primarily

however,

the stomach

the mechanism stomach

activation

by which

through

the present from gastric

study

elucidated

from gastric

that

the vagally indicate

neurons

induces

phase

in the stomach.

decreases

feeding

decrease

Furthermore,

in food intake

is in accor-

The results

to those of their with

saline infusion.

subjective

criteria

such as desire to eat, hunger

fullness, and prospective

feeding

intentions

Lieverse

et al. conclude

in this former

CCK-33

to plasma

meal does not have a major hunger recent

feelings.” paper

unclear

They

“.

effect on food intake findings

infusion

of

after a fatty

and postprandial

in the discussion

of their

and conclusions

which

are

to us.

Our own studies

support

a role for endogenous

satiety.3 We have also given a CCK-8 dial plasma intake

that

to those observed

do not comment

on these different

feelings,

were not affected by CCK.

study

levels comparable

and

previous

did not produce

CCK-33

compared

feel-

compared

thar “This finding

work in which the same dose of intravenous a significant

in hunger

intentions

effect of CCK.”

are in contrast

infusion

physiological

concentrations

compared

infusion

CCK in control

to reproduce

and shown a significant

of

postpran-

reduction

in food

with saline infusion4

A. B. BALLINGER M. L. CLARK

cholinergic

that activation

pathway. of sensory

that

similar

and that this problem

of motilin’s

action

action

in the is finally

Our findings neurons

in

arising

to turn off the vagal efferent excita-

on the pathway

are identical

us.

that includes

the mechanism

findings,

cannot

the vagova-

by which

antral

be substantially

only because

Lieverse RJ, Jansen JBMJ, Masclee AM, Lamers CBHW. Satiety effects of cholecystokinin in humans. Gastroenterology 1994; 106:1451-1454. Lieverse RJ, Jansen JBMJ, Zwan A vd, Samson L, Masclee AAM, Lamers CBHW. Effects of a physiological dose of cholecystokinin on food intake and postprandial satiation in man. Regul Pept 1993; 43:83-89. Ballinger AB, Clark ML. L-Phenylalanine releases cholecystokinin and is associated with reduced food intake in humans: Evidence for a physiological role of CCK in control of eating. Metabolism 1994;43:735-738. Ballinger AB, McLaughlin L, Medbak S, Clark ML. Cholecystokinin is a satiety hormone at physiological postprandial concentrations. Gut 1993; 34:AlOl.

the pictures

is closely related to the mechanism

Reply.

The regulation

of appetite

control

is complex.

in animals,

regulation

Like Drs. Ballinger

and Clark, we are interested

in the regulation

of food

in humans.

in the role of CCK The recent allowing

development

measurement

and the availability

We have studied plasma

in fasting

subjects,’

Gastrointestinal Research Laboratory

CCK on satiety

Gunma University

decreases

Maebashi, Japan

intentions

CCK-receptor

control

antagonists

delineating

in humans.

subjects.i

of CCK that produced

satiety

we have studied

feelings,

have enabled

the physiological

on preprandial

and on postprandial

after stimulation

in fasting

its

in both lean and obese subjects.

concentrations

in this journal,

in hunger

intake

about

and specific radioimmunoassays

the effect of an infusion

meal.’ In addition

As reported

is known

of the low plasma CCK levels in human plasma of potent

role of CCK in appetite

a preload

of sensitive

a series of experiments

us to perform

physiological

and very little

Most studies

have been performed

0. YAMAMOTO 2. ITOH Institute of Endominology

7BE, England

At present,

III activity

that motilin’s

blocks phase III in the stomach by comparing

In our

fibers inhibit

draw such a conclusion.

appears

We believe

excitation.

these vagal

of inhibitory

motilin

somewhere

gal reflex center. acidification

arising

but it is certain

acidification

tion by motilin

explanation

information

et al. seem to have misunderstood

we cannot

is not known,

mediated

alternate

to turn off vagal efferent

Drs. Diamant

From our experiment

made by Drs. Dia-

their

we did not propose

through

In this respect,

satiety

of this study

London EClA

3 99 Bathurst Street

We appreciate

significant

They conclude

a physiological

produced

Department of Gastroenterology

Toronto Hospital (Wartern Division)

Reply.

induced

an intravenous

which

St. Bartbo/omew’s Hospital

Gastrointestinal Motility Research Laboratory

mant

subjects

(CCK-33),

the wish to eat, and prospective

N. E. DIAMANT S. A. CHUNG K. E. HALL

12-419

33

with saline infusion.’

1. Yamamoto 0, Matsunaga Y, Haga N, Mizumoto A, ltoh Z. Inhibition

2.

1913

with

satiety parameters without,*

intraduodenal

the infusion

and with

the effect of endogenous fat.*

of CCK induced

significant

the wish to eat, and prospective No clear differences

between

feeding lean an