THE EFFECT OF GLUCOSE FEEDING UPON THE QUANTITA-

TIVE RELATIONSHIP BETWEEN /3-HYDROXYRUTYRIC

ACID AND ACETOACETIC ACID IN ULOOD AND URINE*
BY IRENE E. STARK AND MICHAEL SOMOGYI
(From the Laboratory of the Jewish Hospital of St. Louis, St. Louis)

(Received for publication, January 5, 1943)

Ketosis that is caused in healthy individuals by fasting or by a carbo-

hydrate deficiency in the food readily subsides in a few hours after the

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administration of carbohydrates. When, as a result, ketonuria diminishes,
fi-hydroxybutyric acid disappears from the urine more rapidly than aceto-
acetic acid; as Kennaway expressed it (l), the @ratio, (100 X P-hydroxy-
butyric acid)/(total ketone bodies), gradually decreases. This observation
of several earlier workers (1, 2) was confirmed in part in our laboratory.
Since it is possible, however, that interconversion between acetoacetic acid
and /3-hydroxybutyric acid may take place in the kidneys, we followed the
changes of the p ratio not only in the urine but also in the blood. In view
of our observations that in the postabsorptive state the ketone bodies are
unevenly distributed between corpuscles and plasma and, furthermore,
that the distribution of acetoacetic acid and of P-hydroxybutyric acid shows
substantial differences (3), we have studied all of these relationships during
the process of recession of ketosis resulting from carbohydrate feeding.
Healthy Subjects
For observations on non-diabetic ketosis, three healthy young men were
fasted for 62, 38, and 64 hours, respectively. All of them showed marked
ketonuria at the end of the fasting period. At this point blood samples
were obtained directly before and at hourly intervals after the administra-
tion of 100 gm. of glucose. The ketone bodies were determined in whole
blood and in plasma by a procedure outlined in a preceding publication
(3). The values for the corpuscles were calculated from these analytical
data and the cell volume.
The data presented in Table I show that, as previously reported (3),
the corpuscles contain considerably smaller amounts of ketone bodies than
doesthe plasma; in our three subjects the concentration in the plasma was
from 2 to 3 times as high as in the cells. The administration of glucose,
however, effected changesin the distribution. Thus in Subject 1 the distri-
bution ratio (ketone body concentration in the cells)/(ketone body concen-
tration in the plasma), which in the fasting state was 0.39, rose to 1.06
* This work was aided by the Helen Yonkers Rcscarch Fund.
721
722 DISTRIBUTION OF KETONE BODIES

during the 3rd, and to 4.50 during the 4th hour after glucose feeding; that
is to say, the ratio was inverted, and the concentration of ketone bodies in
the corpuscles ultimately increased to more than 4-fold the concentration in
the plasma. Subjects 2 and 3 showed changes of much the same character.
We interpret this fact as follows: Hyperketonemia occurs when the liver
transmits ketone bodies into the blood stream at a higher rate than the
extrahepatic tissues are able to consume them. After glucose feeding the
liver begins to catabolize carbohydrate in preference to fat and protein,
so that the production of ketone bodies is gradually arrested. In conse-
quence the blood receives from the liver smaller amounts of ketone bodies
than it gives up to the extrahepatic tissues (and to some extent to the urine),

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TABLE I
E$ect of Glucose Feeding upon Distribution of Total Ketone Bodies between Corpuscles
and Plasma in Normal Subjects

Total ketone bodies in Ketones in

Time sine Time after COIpUSCltX
Subject No. last meal ;” 6lucose feedi
Whole blood
Ketonesin
Corpuscles PlZWIUl plasma

hrs. hrs. ?ng . per cent nzg. per cent mg. per cent
62 0 23.1 13.1 33.7 0.39
1 21.5 14.1 28.8 0.49
2 5.80 5.63 5.95 0.95
3 1.61 1.65 1.55 1.06
4 0.58 0.90 0.20 4.50
38 0 17.9 9.24 26.0 0.36
1 9.31 5.66 13.2 0.43
2 3.57 3.50 3.56 1.00
3 2.51 3.32 1.43 2.32
4 1.53 2.20 0.42 5.20
64 0 68.4 48.8 87.9 0.56
1 58.2 47.3 70.0 0.67
3 17.2 18.3 16.4 1.11

and the ketonemic level recedes. As a matter of course this change affects
primarily the concentration of plasma ketones, and thereby, secondarily,
induces a diffusion of ketone bodies from cells to plasma. The diffusion
apparently lags behind the rate of decrease in the plasma and, as a result,
the distribution ratio shifts in favor of the corpuscles.
In the same three subjects we also examined the possible effect of glucose
feeding upon the relationship between &hydroxybutyric acid and aceto-
acetic acid (0 ratio) both in corpuscles and in plasma. The results, given
in Table II, show a continual decline of the /3 ratio in the plasma as well as
in the corpuscles. It has markedly decreased already during the 1st hour
after the administration of glucose, and in the 3rd and 4th hours it dropped
 I. E. STARK AND M. SOMOGYI 723

to zero. This means the complete disappearance of /3-hydroxybutyric acid

at these periods; so that the ketone bodies in the blood were represented
solely by acetoacetic acid both in corpuscles and plasma. The complete
disappearance of /3-hydroxybutyric acid occurred in the corpuscles earlier
than in the plasma in Subjects 2 and 3, but later in Subject 1. An in-
teresting fact is that, whereas the concentration of @-hydroxybutyric acid
in the plasma usually remained higher than in the cells, the concentration
TABLE II
Effect of Glucose Feeding upon Distribution of Acetoacetic and P-Hydroxybutyric
Acids in Blood of Normal Subjects

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‘ime afte. r
glucose Aceto- I Total Aceto- I Total
acetic ketone I ratio acetic ketone ratio
acid bodies acid bodies
_- -
w. m. w. w?.
hrs.
*Z%,t +er cent @?r cent per cent flercent perw.cent
0 4.08 9.01 13.1 70 5.47 28.2 33.7 84
1 6.75 7.32 14.1 52 7.02 21.8 28.8 76
2 3.95 1.68 5.63 30 2.65 3.30 5.95 56
3 0.98 0.67 1.65 40 1.55 0 1.55 0
4 0.90 0 0.90 0 0.20 0 0.20 0
0 5.32 3.92 9.24 43 8.36 17.6 26.0 68
1 5.66 0 5.66 0 5.51 7.60 13.2 58
2 3.18 0.32 3.50 9 2.86 0.70 3.56 20
3 3.32 0 3.32 0 1.43 0 1.43 0
4 2.20 0 2.20 0 0.42 0 0.42 0
0 26.1 22.7 48.8 42 21.8 66.1 87.9 75
1 27.3 20.0 47.3 42 29.5 40.5 70.0 60
3 18.3 0 18.3 0 13.3 3.1 16.4 19
0 0.25 0.70 0.95 74
2 0.12 0.10 0.22 45
0 0.11 0.27 0.38 71
2 0.24 0.11 0.35 33

* Fasted 62 hours.
t Fasted 38 hours.
$ Fasted 64 hours.
$ In postabsorptive state, 14 hours after last meal.

of acetoacetic acid tended to shift in favor of the corpuscles, especially in

the 3rd and 4th hours after glucose feeding. In Subjects 1 and 2, for
instance, the acetoacetic acid in the corpuscles eventually became from 2
to 5 times as high as in the plasma. A possible cause of this phenomenon
is that the cells tend to retain acetoacetic acid more firmly than p-hydroxy-
butyric acid under conditions that cause a rapid decline in the ketone body
concentration of the plasma.
‘724 DISTRIBUTION OF KETONE BODIES

As regards Subjects 4 and 5 in Table II, these were normally nourished

healthy individuals in the postabsorptive st,ate (14 hours after the last
meal) when subjected to the experiment. In view of the large quantities
of blood required for analysis in such cases, only twg samples were taken,
one before and one 2 hours after glucose feeding. We have previously
described the observation that glucose feeding measurably depresses the
ketonemic level of the well nourished healthy individual just as it does in
the instance of fasting ketosis (4). Subjects 4 and 5 show that the response
of the two groups is similar also in regard to changes in the /3 ratio. Even
in Subject 5, whose basal ketonemic level was so low (0.38 mg. per cent)
that its probable decrease after glucose feeding may have eluded measure-

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TABLE III
E$ect of Glucose Feeding on Relationship between Acetoacetic Acid and
p-Hydroxybutyric Acid in Urine of Normal Subjects

T;rime after
glucose Acetoacetic acid B-Hydroxybutyric acid Total ketone bodies rsI ratio
hrs. ng.per cent mg. #er hr. :g. per celz, wg. per hr. g. per ceni ng. per hr.
0 96.5 20.7 131.0 28.0 227.5 48.7 58
1 129.0 36.3 85.0 23.8 214.0 64.1 40
2 38.5 8.86 0 0 38.5 8.86 0
3 5.90 1.89 5.12 1.64 11.0 3.52 46
4 2.95 0.74 5.58 1.40 8.53 2.14 71
0 30.6 11.5 74.7 28.0 105.3 39.5 72
1 16.5 6.61 15.1 6.05 31.6 12.7 48
2 5.73 1.60 0 0 5.73 1.60 0
3 3.33 7.33 1.43 3.58 4.76 10.9 31
4 3.00 6.90 0.84 1.93 3.84 8.83 22
0 70.0 58.1 149.0 124.0 219.0 182.1 68
1 15.5 8.27 13.6 7.27 29.1 15.5 47
2.5 91.7 149.2 0 0 91.7 149.2 0
-

ment, the drop in t,he p ratio was still great enough to be detected. In
Subject 4 the ketonemic level was high enough (0.95 mg. per cent) for
reliable measurement; here it is clearly shown that the p ratio decreased
materially as the ketonemic level was depressed by glucose feeding, in the
same manner as in fasting ketosis.
Changes in the relationship between acetoacetic acid and P-hydroxy-
butyric acid were examined at hourly intervals in urine samples which
were collected simultaneously with the blood samples. The results, given
in Table III, show that the /3 ratio declined in urine faster than in the blood.
This tendency was evident as early as in the 1st hour, and quite conspicuous
during the 2nd hour after glucose feeding; at this time /3-hydroxybutyric
 I. E. STARK AND M. SOMOGYI 725

acid completely disappeared in the urine, which was 1 hour earlier than
in the blood in all three of our fasted subjects. The difference between
blood and urine was further accentuated when P-hydroxybutyric acid
emerged again in the urine during the 3rd and 4th hours, when it was
completely absent from the blood.
TABLE IV
Effect of Glucose Feeding upon Distribution of Total Ketone Bodies between Corpuscles
and Plasma in Diabetic Subjects

Total ketone bodies in Ketones in

Time after I corpuscles
Subject No.

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glucose feeding Ketonesin
Whole blood Corpuscles Plasma pl&Sl%3

hrs. mg. per cent mg. per cent cent

nzf. fler
6 0 25.4 8.49 38.7 0.22
0.5 41.0 28.6 49.8 0.57
1 35.5 21.9 50.6 0.43
2 33.2 18.7 44.4 0.42
3 38.3 48.3 29.8 1.62
4 43.1 36.5 49.8 0.73
0 68.0 60.2 78.8 0.76
1.5 82.0 67.7 95.4 0.71
3.5 101.3 95.9 105.6 0.91
0 4.78 4.78 4.78 1.00
1 3.98 1.53 6.10 0.25
2 4.04 4.26 3.80 1.12
3 4.16 2.36 6.10 0.39
4 3.67 2.90 4.40 0.66
9 0 63.8 52.9 71.9 0.74
0.5 62.9 25.9 87.6 0.29
1 70.7 66.4 73.7 0.90
2 58.0 37.6 70.7 0.53
3 55.3 31.3 72.1 0.43
4 43.0 20.8 56.8 0.37

Diabetic Subjects
On the basis of previous studies we divide diabetic subjects, with respect
to their response to glucose feeding, into two main categories. Those in
the first exhibit a tendency towards rising ketonemic levels; those in the
second show a rather consistent decrease of ketonemia. Patients belonging
to the latter group behave much like the healthy individuals whose ketosis
resulted from fasting or a carbohydrate-deficient diet. In a previous
paper, this difference was attributed to differences in the liver function of
the patients (5).
Tables IV to VI contain results of observations on representative cases
of the first category. As may be seen in Table IV, the distribution of total
726 DISTRIBUTION OF KETONE BODIES

ketone bodies between corpuscles and plasma showed changes quite dif-
ferent from those observed in healthy individuals (cf. Table I); i.e., instead
of a consistent increase of the distribution ratio in favor of the corpuscles,
considerable and rather irregular fluctuations occurred. In Subject 7 the
ratio showed a tendency to increase at the end, somewhat as in healthy
subjects, but in Subjects 8 and 9 the opposite tendency was in evidence
during the 3rd and 4th hours after glucose feeding.
TABLE V

Effect of Glucose Feeding upon Distribution of Acetoacetic and p-Hydroxybutyric

Acids in Blood of Diabetic Subjects

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Corpuscles PlWIla

‘ime after
glUCOSe Aceto- Aceto-
I I
acetic
acid
c? ratio acetic
acid
? ratio

hrs. WT. “g. w. mg. %c. WT.

per cent per cent $3er cent per cent jwr cent per cent
0 8.47 0.02 8.49 0.2 7.20 31.5 38.7 81
0.5 12.4 16.1 28.6 57 9.10 40.7 49.8 82
1 4.87 17.0 21.9 78 14.3 36.3 50.6 72
2 10.0 8.69 18.7 47 11.8 32.6 44.4 73
3 9.00 39.3 48.3 81 9.00 20.8 29.8 70
4 11.9 24.5 36.5 67 15.3 34.5 49.8 69
0 29.1 31.1 60.2 52 19.1 59.8 78.8 76
1.5 39.2 28.5 67.7 42 23.5 71.9 95.4 75
3.5 54.5 41.4 95.9 43 23.8 81.8 1105.6 63
0 1.31 3.47 4.78 73 1.31 3.47 4.78 73
1 0.43 1.20 1.63 62 1.40 4.70 6.10 78
2 1.76 2.50 4.26 59 0.80 3.00 3.80 78
3 1.20 1.16 2.36 49 1.70 4.40 6.10 74
4 1.04 1.86 2.90 64 1.20 3.10 4.40 72
0 23.3 29.6 52.9 56 21.2 50.7 71.9 71
0.5 10.7 15.2 25.9 59 24.9 62.7 87.6 71
1 27.1 39.3 66.4 59 21.5 52.2 73.7 71
2 22.7 14.9 37.6 40 20.3 50.4 70.7 71
3 10.9 20.4 31.3 65 21.7 50.4 72.1 70
4 8.30 12.5 20.8 60 16.1 40.7 56.8 72
-
Likewise, the response was entirely different from the normal as regards
the changes in the relationship between ,&hydroxybutyric acid and aceto-
acetic acid. As may be noted in Table V, the p ratio showed at no time
any appreciable decrease either in the corpuscles or in the plasma, and the
actual amount of @-hydroxybutyric acid tended to increase at such periods
at which it completely disappeared in non-diabetic ketosis. The main-
tenance of high p ratios was more consistent in the plasma than in the
corpuscles.
 I. E. STARK AND M. SOMOGYI 727

The difference between this group of diabetic patients and healthy in-
dividuals was just as marked in the urine as in the blood. As it may be
seen in Table VI, the relative quantities of fl-hydroxybutyric acid have not
appreciably changed in the course of the entire 4 hours after glucose feeding.
During the 2nd hour, when fl-hydroxybutyric acid had completely disap-
peared from the urines of healthy subjects (cf. Table III), the three diabetic
subjects showed p ratios of 73, 70, and 82, respectively, values of the same
order of magnitude as one finds in fasting or in postabsorptive states.
Diabetic patients belonging to the second category, who respond to
glucose feeding with a progressive decline of the ketonemic level, as do

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TABLE VI
Effect of Glucose Feeding on Relationship between Acetoacetic Acid and
&Hydroxybutyric Acid in Urine of Diabetic Subjects
-
Time after
glucose Acetoacetic acid /8.Hydroxybutyric acid Total ketone bodies I 9 ratio

hrs. fng. #er ten ;i: mg. per hr. *ng. per m m mg. per hr. 1 ng. per Cm
6 0 55.0 120.0 175.0 69
1 28.1 45.6 96.2 156.0 124.0 201.6 77
2 16.5 43.4 44.0 116.3 60.5 159.7 73
3 16.6 78.5 43.8 206.7 60.4 285.2 73
4 20.0 78.8 118.0 460.4 138.0 539.2 85
7 0 48.6 167.0 215.3 78
1 54.0 184.0 139.0 471 .o 193.0 655.0 72
2 53.0 249.0 123.0 579.0 176.0 829.0 70
3 40.0 209.0 129.0 672.0 169.0 881 .o 76
4 50.0 111 .o 131.0 287.0 181.0 398.0 73
10 0 47.0 47.0 145.0 145.0 192.0 192.0 76
1 53.0 127.0 187.0 448.0 240.0 575.0 78
2 68.0 60.6 298.0 269.0 366.0 329.0 82
3 65.0 51.9 278.0 223.0 343.0 275.0 76
4 109.0 65.5 371.0 223.0 480.0 287.0 77
- - - -

healthy men (although at a lower rate), also show tendencies in the direc-
tion of normal as regards the changes in the relationship between ,&hy-
droxybutyric acid and acetoacetic acid, both in blood and urine. This
fact is illustrated by an example, Subject 11, in Table VII. As may be
seen, in the blood the /3 ratio began to decrease during the 2nd hour after
glucose feeding, and continued to decline throughout the 4 hour period.
This decrease was more delayed and distinctly less extensive than in non-
diabetic subjects. A similar change has occurred in the urine; namely,
the fl-hydroxybutyric acid has at no time disappeared as in fasting ketosis,
and yet the /I ratio dropped from the postabsorptive level of 70 to 53 during
the 1st hour after glucose feeding. This drop was then followed by an
728 DISTRIBUTION OF KETONE BODIES

increase during the remainder of the 4 hour period (cf. Table III). It may
be stated then that in this group of diabetic individuals glucose feeding
elicits changes both in ketonemia and ketonuria that show the same
tendency as the changes in healthy subjects. There is only a quantitative
difference, in that the changes in the diabetic proceed at a diminished rate.
Subject 12 was included in Table VII to emphasize further the great
differences between blood and urine in the changes in the /3 ratio after
glucose feeding. This individual belongs to the first category of diabetics;
namely, to the group that does not respond with a consistent decrease in
TABLE VII

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Comparison of Efect of Glucose Feeding on Changes of p Ratio in Blood and Urine of
Diabetic Subjects
-~
, Whole blood Urine
I-
T ‘ime r’
%Yt glUCOSe
afte

acetic
Total
lietone I ratio
Aceto-
acetic 1 ratio
acid bodies acid
--
“f;,pt”’ nq. per mg. per mg. per mg. per
hrs. cent cent cent cent
* *
11 0 2.60 8.40 11.0 76 70
0.5 2.00 4.46 6.45 69 47.4 70.6 1118.0 70
1 2.00 5.30 7.30 76 13.5 30.5 57.4 53
2 1.60 2.90 4.50 64 28.0 32.9 60.9 55
3 1.50 3.00 4.50 67 17.4 37.8 55.1 69
4 1.90 2.80 4.70 60 11.9 17.8 29.7 60
0 1.63 5.17 6.80 76 * * * 36
12
0.5 1.12 3.80 4.92 77
1 1.15 4.17 5.32 78 3.88 0.05 3.93 I
2 1.59 5.17 6.76 76 11.1 0.64 11.7 6
3 1.59 4.66 6.25 75 4.34 1.98 6.32 31
4 1.14 3.05 4.19 73 4.54 4.72 9.26 51

* The interval of time during which the specimen was excreted is unknown; hence
the rate of excretion of ketone bodies could not be calculated. The concentration of
acetoacetic acid and P-hydroxybutyric acid at 0 hour was as follows: in Subject 11,
25.0 and 57.3 mg. per cent; in Subject 12, 7.71 and 6.32 mg. per cent.

the ketonemic level. As in other cases of this group, the /3 ratio in the
blood remained virtually unaltered during the 4 hour period after the
administration of glucose. The changes in the urine, on the other hand,
were entirely unexpected. Here the /3 ratio (which was already excep-
tionally low in the postabsorptive state) dropped steeply in the first 2 hours
and then increased, much as in the fasting ketosis of healthy subjects.
The divergence between the changes of the p ratio in the blood and urine
after glucose feeding was conspicuous enough in our non-diabetic subjects
(cf. Table III). It is evidently due to a reversible conversion between
 I. E. STARK AND M. SOMOGYI 729

acetoacetic acid and P-hydroxybutyric acid, which has been known to occur
in the kidney. Subject 12 (Table VII) vividly illustrates how extensive
this effect of the kidney can be. It is a warning against the injudicious
use of data of urine analysis as the basis of conclusions concerning the
changes of the ketone bodies in the living organism. To explore these
changes one must resort to the analysis of blood and other tissues.
The most notable change in the blood, recorded in this report, is the
rapid decrease and eventual complete disappearance of @-hydroxybutyric
acid* while measurable amounts of acetoacetic acid are still present. This
occurs when glucose feeding exerts its fat- (and protein-) sparing effect

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in the liver and, in consequence, the liver ceases to produce and transmit
to the blood excessive amounts of ketone bodies. In other words, two
facts, namely the suppression of hepatic ketone production and the disap-
pearance of P-hydroxybutyric acid from the blood, appear to be in a simple
causal connection, implying that the ketone body supplied by the liver is
mainly, if not exclusively, /3-hydroxybutyric acid. This inference is at
variance with the widely held view that the parent ketone body formed in
the tissues is acetoacetic acid. In our opinion no evidence presented thus
far to support either of the two conflicting views can be regarded as con-
clusive and unequivocal.

SUMMARY

In postabsorptive states the ratio of P-hydroxybutyric acid to aceto-

acetic acid in blood and urine, as also of the distribution of the two acids be-
tween corpuscles and plasma, is independent of the ketonemic level; in this
respect no difference exists between healthy and diabetic subjects. Glucose
feeding elicits the following changes.
1. In the blood of healthy persons, in the state of hunger ketosis, the
concentration of ketone bodies decreases faster in the plasma than in the
corpuscles; this leads to an inversion of the distribution ratio (total ketone
bodies in corpuscles)/(total ketone bodies in plasma), which in the post-
absorptive state is below unity.
2. The fi ratio (100 X P-hydroxybutyric acid)/(total ketone bodies)
decreases consistently and drops to zero during the 3rd and 4th hours after
glucose feeding, so that at these intervals the ketone bodies are represented
by acetoacetic acid alone. This change proceeds faster in the plasma
than in the corpuscles.
1 It is in order, perhaps, to remark here that the disappearance of P-hydroxybutyric
acid can be demonstrated only by analytical methods that are sufficiently selective
for acetone. By simply measuring the mercury content of the Deniges precipitate,
as for example in Crandall’s technique (6), one always obtains positive values for
p-hydroxybutyric acid.
730 DISTRIBUTION OF KETONE BODIES

3. In the urine of these subjects the p ratio decreases more rapidly than
in the blood and the fi-hydroxybutyric acid completely disappears about
an hour earlier than in the blood. In contrast to the blood, however, it
emerges again at an increasing rate during the 3rd and 4th hours.
4. Diabetic patients, whose livers have retained to an appreciable degree
the ability to utilize carbohydrate, respond to glucose feeding as do healthy
individuals, with a difference only in the rate of the process.
5. Diabetic patients of another category, i.e. those whose livers areun-
able to utilize appreciable amounts of carbohydrate and, in consequence,
maintain (or more often increase) their ketonemic level after glucose feed-

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ing, show no significant changes in the blood. The distribution ratio be-
tween corpuscles and plasma, as well as the /? ratio, remains substantially
the same as that in the postabsorptive state. As a rule, this applies also
to urines of these patients, but there are exceptions.
6. The frequent divergence between the changes in blood and urine, due
to oxidation-reduction processes in the kidney, suggests that studies of the
metabolism of ketone bodies should include analyses of blood and of other
tissues, since data derived from the urine alone may be misleading.

BIBLIOGRAPHY

1. Kennaway, E. L., B&hem. J., 8, 355 (1914).

2. Forssner, G., Xkand. Arch. Physiol., 23, 305 (1910).
3. Stark, I. E., and Somogyi, M., J. Biol. Chem., 14’7, 319 (1943).
4. Somogyi, M., J. Biol. Chem., 146, 575 (1942).
5. Somogyi, M., and Weichselbaum, T. E., J. Biol. Chem., 146, 567 (1942).
6. Crandall, L. A., Jr., J. Biol. Chem., 133, 539 (1940).
THE EFFECT OF GLUCOSE FEEDING
UPON THE QUANTITATIVE
RELATIONSHIP BETWEEN β
-HYDROXYBUTYRIC ACID AND
ACETOACETIC ACID IN BLOOD AND
URINE
Irene E. Stark and Michael Somogyi
J. Biol. Chem. 1943, 147:721-730.

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