GASTROENTEROLOGY 77:12-17.
1979
Abnormal Gastric Function in
Longstanding, Insulin-Dependent Diabetic
Patients
MARK FELDMAN, DESMOND B. CORBETT, EDWARD J.
RAMSEY, JOHN H. WALSH, and CHARLES T. RICHARDSON
From the Departments of Internal Medicine. Veterans Administration Hospital. and The
University of Texas Health Science Center at Dallas. Southwestern Medical School. Dallas. Texas.
and the Veterans Administration Hospital. Wadsworth Center. Los Angeles. California
We evaluated gastric function in 8 longstanding, in-
sulin-dependent diabetic patients with nausea and
recur!ent vomiting, as well as in 10 asymptomatic
diabeti c patients and 11 nondiabetic subjects. Gas-
tric vagal function was assessed by measuring the
gastric acid secretory response to sham feeding. Nor-
mal subjects secreted 17.2 ± 3.1 meq/hr, whereas
diabeti c patients with, or without. vomiting secreted
5.4 ± 1.4 and 6.4 ± 2.0 meq/hr, respectively (P <
0.005 vs . normal). Decreased acid secretory re-
sponses in the diabetic patients were not due to hy-
perglycemia, nor were they due to a reduced secre-
tory capacity, since peak acid output to pentagastri.n
was normal in the diabetic patients. Acid secretory
responses to homogenized food infused directly into
the stomach were similar in both groups of diabetic
patients and normal subjects. However, basal and
food-stimulated serum gastrin concentrations were
two- to threefold as high in diabetic patients (with or
without vomiting) as in normal subjects. Diabetic
patients had increased retention of a nonabsorbable
marker that had been added to th e food, suggesting
delayed gastric emptying.
From these studies we conclude that many pa-
tients with longstanding insulin-dependent diabetes
have (a) reduced acid secretory responses to sham
feeding, suggesting vagal neuropathy; (b) normal
Received November 3. 1978. Accepted J anuary 18. 1979.
Address requests for reprints to: Mark Feldman, M.D .. Veterans
Administration Hospital. Gastroenterology. 111B. 4500 S. Lancas-
ter Road. Dallas, Texas 75216.
This work was supported by grants AM16816. AM17328. and
AMl7294 from the National Institutes of Arthritis, Metabolism,
and Diges tive Diseases. Dr. Ramsey was supported by NIH train -
ing grant AM07100.
The authors wish to thank Jeanna W elborn, Kathy Cooper,
Tina Barn ett, and Helen Wong for technical assistance. and Sue
Banks, who prepared the m anuscript.
© 1979 by the American Gastroenterologi cal Association
0016-5085/ 79/070012-06$02.00 . .
acid secretory responses to infused food, despite an
enhanced serum gastrin response; and (c) delayed
gastric emptying. These abnormalities occur both in
diabetic patients with nausea and vomiting and in
asymptomatic diabetic patients.
Patients with diabetes mellitus can develop delayed
gastric emptying without organic obstruction. ' -3
More than 30 yr ago, Hodges et al. observed radio-
logic similarities between the atonic stomachs of
some diabetic patients and the stomachs of surgi-
cally vagotomized patients.' Kassander later specu-
lated that delay ed gastric emptying in diabetes
("gastroparesis diabeticorum") was due to a vagal
neuropathy, in a sense an "autovagotomy."2
Although many patients with gastroparesis diabe-
ticorum are free of gastrointestinal symptoms, some
develop a syndrome characterized by nausea and re-
current vomiting. Clinically symptomatic gastropa-
resis diabeticorum is associated with a grave prog-
nosis, in that approximately one-third of such
patients die within 3 yr.' Diabetics with vomiting
might especially be suspected of having vagal neu-
ropathy. However, this has been confirmed patho-
logically in only one such patient6 and inferred in
another patient who had a reduced gastric acid re-
sponse to insulin-induc~Q. hypoglycemia ,>
In the past 2 yr, B insulin-dependent diabetic pa-
tients have been referred to our clinic because of re-
current vomiting not due to mechanical obstruction.
It was the purpose of the present experiments to as-
sess gastric function in these patients. First, we eval-
uated gastric vagal function by measuring the acid
secretory response to sham feeding. Second, we
measured the acid secretory and serum gastrin re-
sponses to food infused directly into the stomach;
and third , we evaluated gastric emptying of a ho-
July 1979 ABNORMAL GASTRIC FUNCTION IN DIABETIC PATIENTS
Table 1. Mean Age (yr) and Mean (± SE) Acid Secretion Rates (meq/hr) in the Three Groups Studied
Groups n Age (range) BAO"
Diabetic, with vomiting 8 33 (24-57) 3.6 ± 1 .5
Diabetic, without vomiting 10 42 (23-59) 3.6 ± 0 .8
Normal 11 29 (22-45) 3.6 ±1.5
a Basal acid output.
b Peak acid output in response to 12 JLg/kg pentagastrin subcutaneously in diabetic patients and 6 JLg/kg in normal subjects.
c Total I-hr secretion rate for 30 min during and for 30 min after sham feeding.
d Total 2-hr acid secretion rate after homogenized food was infused into the stomach, divided by 2.
e p < 0.005 vs. normal.
mogenized meal. For comparison, we also studied a
group of 10 asymptomatic insulin-dependent dia-
betic patients and 11 healthy, nondiabetic subjects.
Methods
These experiments were approved by a Human Re-
search Review Committee on November 14, 1977, and in-
formed consent was obtained from each patient and sub-
ject.
Patients and Subjects
The ages of the patients and subjects are shown in
Table 1 according to group. In the diabetics with nausea
and vomiting, symptoms had been present for an average
of 23 mo prior to the present studies (range of 2 mo to 6
yr). Vomiting usually occurred daily or, at the least, two to
three times per week. Six patients with vomiting had lost
weight-in three cases:40 lb or more. Their mean duration
of diabetes was 13 yr (range 8-18 yr), and the mean daily
insulin dosage was 46 units (range 20-90 units). The dura-
tion of diabetes in the group with no nausea or vomiting
averaged 18 yr (range 11-29 yr), and the daily insulin dos-
age averaged 42 units (range 30-90 units).
Clinically detectable peripheral neuropathy* was pres-
ent in all 8 diabetics with vomiting and in 5 of 10 diabetics
without vomiting. In addition, peroneal nerve conduction
velocity' was decreased « 40 m/sec B) in all 13 diabetic pa-
tients tested (6 with and 7 without vomiting) . Orthostatic
hypotension (> 20/10 mm Hg fall in blood pressure upon
standing from supine position) was present in 6 of 8 dia-
betic patients with vomiting and in 2 of 10 diabetics with
no vomiting. The serum creatinine was < 2 mg/dl in all 18
diabetic patients.
Acid Secretion
Gastric aspiration studies. On one test day, basal
acid output (BAO), acid output during and after sham
* Deep tendon reflex es, pinprick, light touch, vibratory sensa-
tion , and proprioception were measured in each patient, and pe·
ripheral neuropathy was said to be present if two or more of
these param eters were substantially diminished.
13
PAO b Sham feeding C Infused food d
28.2 ± 4 .0 5.4 ± l.4e 17.1 ± 2 .4
34.9 ± 4.1 6.4 ± 2.0· 21.0 ± 2.4
36.6 ± 5.1 17.2 ± 3.1 20.4 ± 3.6
feeding, and peak acid output (PAO) were measured se-
quentially by gastric aspiration during three I-hr periods.
The test was started between 8:00 and 9:00 AM, after a 12-
hr fast. In the diabetic patients, the morning insulin dos-
age was omitted. Gastric contents were aspirated through
a 16-French Salem sump tube, the tip of which had been
placed under fluoroscopic guidance into the gastric an-
trum. Suction was applied by a Stedman pump (American
Cystoscope Makers and Company, Stanford, Conn.). For
15 min, secretions were collected and discarded. Then,
four 15-min samples were collected during each ensuing
hour. Volume was measured, and the hydrogen ion con-
centration was determined by the method of Moore and
Scarlata. 9 Acid output was calculated by multiplying vol-
ume by hydrogen ion concentration. .
BAO. This was computed by summing the acid out-
puts during the first four 15-min periods.
SHAM FEEDING. After a 60-min basal period, sub-
jects chewed and expectorated for 30 min an appetizing
meal consisting of 227 g of sirloin steak, 142 g of French
fried potatoes, and 300 ml of water. All meals were cooked
in a separate building so that the subjects could not see or
smell food until time for sham feeding. Total I-hr acid se-
cretion during and after sham feeding was computed by
summing the acid outputs during the four 15-min periods.
PAO. At the start of the third hour (after the sham
feeding hour was completed), pentagastrin was injected
subcutaneously. In normal subjects, 6 ltg/kg were given,
while in diabetic patients, 12 ltg/kg were injected. This
higher dose was used in the diabetics, since 12 ltg/kg pen-
tagastrin are required to elicit maximal acid secretion after
truncal vagotomy. to The PAO to pentagastrin was calcu-
lated as the SUIll of the two highest consecutive 15-min
acid outputs, multiplied by 2 to express the results in meq/
hr.
In vivo intragdstric titration studies. On another
test day, acid secretion in response to homogenized food
was measured for 2 hr by in vivo intragastric titration to
pH 5.0. The food consisted of 142 g cooked lean sirloin
steak, 28 g bread, and 5 g butter and contained 12 g of
polyethylene glycol (PEG) as a nonabsorbable marker.
The homogenized food was diluted with water to a final
volume of 600 ml, and pH was adjusted to 5.0 by addition
of 0.1 N hydrochloric acid. Osmolality of the meal was 138
mosmol!kg. Food was infused over a 5-min period into the
stomach through a nasogastric tube. Gastric samples were
obtained every 2 min through the nasogastric tube; pH
14 FELDMAN ET AL.
was measured, and samples were returned to the stomach.
Sodium bicarbonate (0.3 N) was infused through a small
polyvinyl tube at a rate required to maintain pH at 5.0.
The number of milliequivalents of bicarbonate required to
prevent a fall of gastric pH below 5.0 is equal to the num-
ber of milliequivalents of acid secreted."
GASTRIC EMPTYING. The amounts of the original 12
g PEG remaining in the stomach 2 hr after homogenized
food were infused into the stomach were calculated from
the PEG concentration of the gastric contents multiplied
by the final gastric volume. This volume was measured by
removal of the gastric contents by aspiration. PEG concen-
tration was measured turbimetrically,12 and results were
expressed as percentage of the original PEG remaining in
the stomach at 2 hr.
Serum Gastrin
During the infused meal studies, venous blood was
collected through an indwelling catheter (Medicut Lv. can-
nula, A. S. Aloe Co., St. Louis, Mo.) that was kept open by
a slow saline infusion. Blood samples were obtained be-
fore (basal) and 15, 30, 45, 60, 90, and 120 min after the
food infusion. Blood was allowed to clot, and serum was
stored at -20°C until assayed.
Serum gastrin concentrations were measured by radio-
immunoassay. All samples were tested in duplicate. Anti-
body 1296, a rabbit antigastrin prepared by immunization
with gastrin conjugated to bovine serum albumin, ' was
used at a final dilution of 1:300,000. 13 With this antiserum,
human heptadecapeptide gastrins and human big gastrins
are measured on a nearly equimolar basis; big gastrins are
approximately two-thirds as potent as the heptadecapep-
tides. Cross-reactivity with porcine cholecystokinin (CCK)
is < 5%. Results of the serum gastrin assay were expressed
in picograms per milliliter, with natural human heptadeca-
peptide gastrin I used as the standard.
Statistics
Differences in mean values were tested for signifi-
cance by group t-test, and P values < 0.05 were considered
significant.
Results
Acid Secretion
BAG and PAG. As shown in Table 1, BAGs
and PAGs in the diabetic patients. with or without
vomiting, were similar to the BAG and PAG in nor-
mal subjects. None of the differences were statisti-
cally significant.
Sham feeding. Unlike that in normal subjects,
acid secretion in response to sham feeding increased
only slightly above basal rates in diabetic patients
(Figure 1). These secretion rates in the diabetics
were significantly lower than rates in normal sub-
jects at each time period during and after sham ~eed-
GASTROENTEROLOGY Vol. 77, No.1
8 SHAM FEEDING
c::
'E 7
l!)
l ~
&6
cv
E
w 5
tia::
4
z
Q
I- 3
W
a::
u 2
w
CJ)
0
u
<{
15 30 45 60 75 90 105 120
TIME (minutes)
Figure 1. Mean acid secretion rates before, during, and after
sham feeding in 18 patients with diabetes mellitus (DM)
and 11 normal subj ects (NL). Secretion rates during and
after sham feeding in diabetic patients were signifi-
cantly lower than rates in normal subjects at all four
time periods (P < 0.001, P < 0.01, P < 0.005, and P <
0.05, respectively). Inset shows that secretion rates be-
fore, during, and after sham feeding were similar in 8
diabetic patients with vomiting (solid circles) and 10
diabetic patients without vomiting (open circles).
ing. Diabetics with, or without, vomiting had nearly
identical acid secretory responses to sham feeding
(Figure 1, inset). As shown in Table 1, totall-hr acid
secretion rates in response to sham feeding were sig-
nificantly lower in both groups of diabetic patients
than in normal subjects (P < 0.005.)
Because hyperglycemia is thought to inhibit gas-
tric acid secretion," we measured fasting blood glu-
cose levels on the morning of the sham feeding
study. Whether blood glucose levels in the diabetic
patients were normal (arbitriarly defined as :s 130
mg%) or were elevated (::: 140 mg%). total 1-hr acid
secretion rates in response to sham feeding were sig-
nificantly reduced below normal rates. In 8 patients
with normal fasting' glucose levels (averaging 90
mg%). acid secretion during and after sham feeding
averaged 4.8 ± 1.5 meq/hr. (.P < 0.005 vs. normal). In
9' patients with fasting hyperglycemia (averaging 286
mg%). acid secretion averaged 7.1 ± 2.2 meq/hr (P <
0.01 vs. normal).
Infused homogenized food. As shown in Fig-
ure 2, patterns of acid secretion after homogenized
food was infused into the stomach were similar for
diabetic patients and normal subjects. Again, pat-
terns were similar in the two groups of diabetics
(Figure 2, inset). The acid secretion rate during the 2-
hr experiment averaged 17.1 meq/hr in diabetics
July 1979 ABNORMAL GASTRIC FUNCTION IN DIABETIC PATIENTS 15

~
8, f~
HOMOGENIZED FOOD
.fNL with vomiting and 21.0 meq/hr in diabetics without
INFUSED
vomiting (Table 1, P > 0.2). These rates were not sig-
nificantly different from the 2-hr secretion rate of
.~7 /"'-..
~6 >t:::::-_.
/._1
I
20.4 meq/hr in the normal subjects.

15
~4 ,I ·~'DM
\~ Gastrin
Mean basal and food-stimulated gastrin levels
were significantly higher in diabetic patients than in
z normal subjects at each time period (Figure 3).
93 Serum gastrin levels were similar in each diabetic
I-
w group (Figure 3, inset). The serum gastrin rise in re-
n:
~2 sponse to infused food averaged 123 ± 20 pg/ml
(f) above basal levels in diabetics and 46 ± 7 pg/ml in
o 1 ., __ • o 306090120 the normal subjects (P < 0.005).
~
o 15 30 45 60 75 90 105 120 Gastric Emptying and Gastric Volume
TIME (minutes) There was significantly more retention of
Figure 2. Mean acid secretion rates in 18 patients with diabetes PEG 2 hr after homogenized food was infused into
mellitus (DM) and 11 normal subjects (NL) after homog- the stomach in diabetics with, or without, vomiting
enized food was infused into the stomach (see arrow). than in normal subjects (Table 2). In addition, gastric
Basal acid secretion is shown at 0 min. None of the dif-
ferences in secretion rates between diabetic patients
volume at 2 hr was larger in both diabetic groups
and normal subjects were significant. Inset shows that than in normal subjects, although the difference was
secretion rates were similar in diabetic patients with only significant for diabetics with vomiting. Differ-
(solid circles) or without (open circles) v.omiting. ences in percent PEG retention and gastric volume
between the two diabetic groups were not signifi-
cant.

300t::
------
280 ~~~ I":::~=::::::: Discussion
o 30 60 90 120 _ Sham feeding led to significantly lower acid
240 secretion rates in longstanding insulin-dependent

~C\ 200
/--- ---~ OM diabetic patients than in healthy, nondiabetic sub-

J.
jects. These reduced secretion rates were not due to
Q.
hyperglycemia, nor were they due to a reduced se-
z 160 cretory capacity (peak acid output). Because sham
n::

/-._.
I- feeding is thought to stimulate acid secretion via
(f)
~
120 vagal pathways,15.16 a reduced acid response to sham
(!)
feeding is strong evidence for vagal neuropathy
80 •
~N:
("autovagotomy") in our diabetic patients.
Both groups of diabetic patients-those with and
40 those without; vomiting-had similar reductions in
acid responses to sham feeding. Moreover, both
30 45 60 90 120
TIME (minutes) Table 2. Mean (± SE) Percent Retention of Polyethylene
Figure 3. Mean serum gastrin concentrations in response to ho- Glycol (PEG) and Mean (± SE) Gastric Volume
mogenized food in 14 patients with diabetes mellitus 2 Hr after Homogenized Food Was Infused into
(DM) and 11 normal subjects (NL). At 0 min, basal gas- the Stomach
trin was measured and then food was infused into the
PEG Gastric
stomach. At each sampling time, gastrin levels were sig-
retention volume
nificantly greater in the diabetic patients than in normal
Group ("!o) (ml)
subjects. P values were less than 0.001, 0.01, 0.005, 0.001,
0.005, 0.001, and 0.001 at 0, 15, 30, 45, 60, 90, and 120 min, Diabetic, with vomiting 19±4° 304 ± 50 b
respectively. Inset shows that basal and food-stimu- Diabetic, without vomiting 15 ±4° 266 ± 46
lated gastrin levels were similar in diabetic patients Normal subjects 8±1 210 ± 23
with (solid circles) or without (open circles) vomiting.
None of the small differences was significant. ° P < 0.005 vs. normal subjects. b P < 0.05 vs. normal subjects.
16 FELDMAN ET AL.
groups of diabetics had greater than normal gastric
retention of a nonabsorbable meal marker. These
findings support earlier observations that gastric se-
cretory and motor function can be impaired in
asymptomatic diabetics 2,3,17-20 and indicate that gas-
tric vagal neuropathy in diabetics does not necessar-
ily result in nausea and vomiting.
Nausea and vomiting occurs in < 0.04% of hospi-
talized diabetic patients.5 Thus, for every 8 diabetic
patients with vomiting (the number of diabetics with
vomiting in this study), there are approximately
20,000 diabetic patients without nausea or recurrent
vomiting. Although gastric vagal neuropathy prob-
ably contributes to nausea and vomiting, it is not
likely to be the only or even the major pathogenetic
factor, since vagal function was as impaired in a
group of asymptomatic diabetics (randomly selected
from a large diabetic population) as in the 8 diabetic
patients with vomiting. Additional mechanisms that
could lead to vomiting in longstanding diabetics in-
clude: (a) a hypersensitive vomiting center or
chemoreceptor trigger zone; (b) sparing (or irrita-
tion) of specific vagal afferent fibers that initiate
neural reflexes resulting in vomiting; and (c) under-
lying psychopathology. This latter mechanism is un-
likely to explain vomiting, since testing of psy.cho-
logic and personality profiles failed to reveal a
difference between our diabetic patients with, or
without, vomiting (E Abrams, M Feldman, unpub-
lished data).
Despite evidence for an impaired cephalic phase
of acid secretion, the acid secretory response to in-
fused food was normal in the diabetic patients. Be-
cause gastrin accounts for the majority of the acid
response to a protein mea}2' and because parietal
cells are thought to be less responsive to gastrin af-
ter vagotomy,1O,22 it might have been predicted that
acid secretion in response to an infused protein meal
would be reduced in diabetics with "autovagotomy."
However, in our studies, food-stimulated gastrin re-
lease was exaggerated in the diabetics, and the ex-
cessive rise in gastrin concentration may have been
sufficient to overcome reduced responsiveness to
gastrin, resulting in a normal acid response to ho-
mogenized food. It is also possible that delayed gas-
tric emptying led to more gastric distention and to
longer direct stimulation of parietal cells by food
protein in the diabetics than in normal subjects.
These mechanisms (distention and direct chemical
stimulation of parietal cells) contribute to the gastric
phase of acid secretion" and could explain why the
acid secretory response to infused food was normal
in diabetics despite apparent autovagotomy.
There are at least two possible mechanisms for
enhanced food-stimulated gastrin release in long-
standing insulin-dependent diabetics. First, if these
GASTROENTEROLOGY Vol. 77, No. 1
patients have had an "autovagotomy," they may
have destroyed a vagal , inhibitory pathway for gas-
trin release. The existence of such an inhibitory
pathway has been postulated by several workers!4-30
Abnormally high basal gastrin levels in the diabetics
would also be compatible with removal of an inhib-
itory influence. A second explanation for exagger-
ated gastrin release in the diabetics is delayed gas-
tric emptying. Abnormally slow emptying of the
meal from the stomach would be expected to result
in excessive antral distention and in prolonged di-
rect stimulation of antral gastrin cells by food pro-
tein. This mechanism has also been postulated to ex-
plain hypergastrinemia in some patients with gastric
outlet obstruction.'l
In conclusion, we found that longstanding insulin-
dependent diabetic patients with, or without, nausea
and recurrent vomiting secreted significantly less
gastric acid than nondiabetic subjects in response to
sham feeding, suggesting vagal neuropathy ("auto-
vagotomy"). Presumably because of "autova-
gotomy," diabetic patients had a hypergastrinemic
response to food infused into the stomach. However,
hypergastrinemia did not lead to hypersecretion of
acid in response to infused food, probably because
vagotomy also reduced the responsiveness of pa-
rietal cells to endogenous gastrin.
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